Heart Failure Archives - Cardionerds: Recent Episodes

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The following question refers to Sections 7.3.3 and 7.3.6 of the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure.

The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by UTSW AHFT Cardiologist & CardioNerds FIT Ambassador Dr. Natalie Tapaskar, and then by expert faculty Dr. Robert Mentz.

Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz has been a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

American Heart Association’s Scientific Sessions 2024* As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here! * When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #39

| Ms. Kay Lotsa is a 48-year-old woman with a history of CKD stage 2 (baseline creatinine ~1.2 mg/dL) & type 2 diabetes mellitus. She has recently noticed progressively reduced exercise tolerance, leg swelling, and trouble lying flat. This prompted a hospital admission with a new diagnosis of decompensated heart failure. A transthoracic echocardiogram reveals LVEF of 35%. Ms. Lotsa is diuresed to euvolemia, and she is started on carvedilol 25mg BID, sacubitril/valsartan 49-51mg BID, and empagliflozin 10mg daily, which she tolerates well. Her eGFR is at her baseline of 55 mL/min/1.73 m2 and serum potassium concentration is 3.9 mEq/L. Your team is anticipating she will be discharged home in the next one to two days and wants to start spironolactone. Which of the following is most important regarding her treatment with mineralocorticoid antagonists? | | A | Spironolactone is contraindicated based on her level of renal impairment and should not be started | | B | Serum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactone | | C | Eplerenone confers a higher risk of gynecomastia than does spironolactone | | D | The patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin |

Answer #39

| Explanation | The correct answer is B – after starting a mineralocorticoid receptor antagonist (MRA), it is important to closely monitor renal function and serum potassium levels.MRA (also known as aldosterone antagonists or anti-mineralocorticoids) show consistent improvements in all-cause mortality, HF hospitalizations, and SCD across a wide range of patients with HFrEF.The RALES trial of spironolactone vs. placebo in highly symptomatic HFrEF (LVEF ≤ 35%, NYHA III-IV), trial of eplerenone vs placebo post-MI in patients with LVEF ≤ 40%, and EMPHASIS-HF trial of eplerenone vs placebo in less symptomatic HFrEF (LVEF ≤ 35%, NYHA II) altogether suggest MRAs confer improvements in all-cause mortality, HF hospitalizations, and sudden cardiac death in patients with HFrEF. Importantly, these benefits have been demonstrated across a wide range of HFrEF severity and etiologies, including ischemic cardiomyopathy (Option D).Therefore, in patients with HFrEF and NYHA class II to IV symptoms, an MRA (spironolactone or eplerenone) is recommended to reduce morbidity and mortality, if eGFR is >30 mL/min/1.73 m2 and serum potassium is <5.0 mEq/L. Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation and closely monitored thereafter to minimize risk of hyperkalemia and renal insufficiency (Class 1, LOE A). MRA therapy in this context provides high economic value.Adverse Effects of MRAsBoth spironolactone and eplerenone are excreted by the kidney and due to their inhibition of aldosterone signaling, reduce potassium excretion in the urine. For these reasons, the initiation of MRAs is contraindicated in patients with eGFR of ≤30 mL/min/1.73m2 or serum potassium levels of ≥5.0 mEq/L. After starting or intensifying MRA therapy, serum potassium levels and renal function should be rechecked at approximately 1 week, at 4 weeks, and every 6 months thereafter, provided clinical stability. Hyperkalemia can increase the risk of ventricular arrhythmias and death. Unfortunately, this often results in de-escalation or discontinuation of RAASi and a subsequent loss of long-term cardiorenal benefits of maximally tolerated GDMT.The utility of prescribing potassium binders (e.g., patiromer, sodium zirconium cyclosilicate) to improve outcomes by facilitating continuation of Patiromer and sodium zirconium cyclosilicate remove potassium by exchanging cations leading to increased fecal excretion and thereby lowering serum potassium levels. These have been FDA approved for treatment of hyperkalemia for patients receiving RAASi.Therefore, the use of potassium binders (patiromer, sodium zirconium cyclosilicate) to improve outcomes by facilitating the continuation of RAASi therapy in patients with HF who experience hyperkalemia (serum potassium level ≥5.5 mEq/L) received a Class 2b recommendation (LOE B-R), but overall utility remains uncertain.In the DIAMOND trial, patients with HFrEF and hyperkalemia were randomized to patiromer vs. control. In the run-in phase, all patients were started on patiromer, and subsequently, RAASi therapy was initiated/optimized. After this, patients were randomized to continue vs stop patiromer. Hard clinical primary endpoints of time to CV death or first CV hospitalization were changed to mean change in serum potassium due to challenges with recruitment related to the COVID-19 pandemic. There was a significant reduction in the mean change of potassium (0.03 mEq/L in the patiromer group vs. 0.13 mEq/L in the control). Additionally, 85% of the patiromer arm was able to be optimized on RAASi.Aside from hyperkalemia, troublesome side effects of MRAs include gynecomastia and vaginal bleeding. Eplerenone results in lower rates of these side effects than spironolactone given greater specificity for the aldosterone receptor (Option C). | | Main Takeaway | Mineralocorticoid receptor antagonists, like spironolactone and eplerenone, reduce all-cause mortality, HF hospitalizations, and sudden cardiac death in a wide range of patients with HFrEF. Monitoring renal function and potassium levels while on MRA therapy is imperative. | | Guideline Loc. | Section 7.3.3 Section 7.3.6 |

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The following question refers to Sections 7.4 and 7.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Randall Starling.

Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

American Heart Association’s Scientific Sessions 2024* As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here! * When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #38

| Mrs. M is a 65-year-old woman with non-ischemic dilated cardiomyopathy (LVEF 40%) and moderate to severe mitral regurgitation (MR) presenting for outpatient follow-up. Despite improvement overall, she continues to experience dyspnea on exertion with two flights of stairs and occasional PND. She reports adherence with her medication regimen of sacubitril-valsartan 97-103mg twice daily, metoprolol succinate 200mg daily, spironolactone 25mg daily, empagliflozin 10mg daily, and furosemide 80mg daily. A transthoracic echocardiogram today shows an LVEF of 35%, an LVESD of 60 mm, severe MR with a regurgitant fraction of 60%, and an estimated right ventricular systolic pressure of 40 mmHg. Her EKG shows normal sinus rhythm at 65 bpm and a QRS complex width of 100 ms.What is the most appropriate recommendation for management of her heart failure? | | A | Continue maximally tolerated GDMT; no other changes | | B | Refer for cardiac resynchronization therapy (CRT) | | C | Refer for transcatheter mitral valve intervention |

Answer #38

| Explanation | Choice C is correct. The 2020 ACC/AHA Guidelines for the management of patients with valvular heart disease outline specific recommendations.In patients with chronic severe secondary MR related to LV systolic dysfunction (LVEF <50%) who have persistent symptoms (NYHA class II, III, or IV) while on optimal GDMT for HF (Stage D), M-TEER is reasonable in patients with appropriate anatomy as defined on TEE and with LVEF between 20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure ≤70 mmHg (Class 2a, LOE B-R).Conversely, mitral valve surgery may have a role in the following contexts:* Severe secondary MR when CABG is planned (Class 2a, LOE B-NR) * Chronic severe secondary MR related to atrial annular dilation with preserved LV systolic function (LVEF ≥50%) who have severe persistent symptoms (NYHA class III or IV) despite therapy for HF and therapy for associated AF or other comorbidities (Stage D) (Class 2b, LOE B-NR) * Chronic severe secondary MR related to LV systolic dysfunction (LVEF <50%) who have persistent severe symptoms (NYHA class III or IV) while on optimal GDMT for HF (Stage D) (Class 2b, LOE B-NR).

Choice A is incorrect. GDMT has been shown to improve MR and LV dimensions in patients with HFrEF and secondary MR, and it is a Class 1 recommendation (LOE B-R) to optimize GDMT before any intervention for secondary MR related to LV dysfunction. This includes both medical GDMT and cardiac resynchronization therapy (CRT) where appropriate. Our patient is still having symptoms despite being on the maximally tolerated doses of medical GDMT. This highlights the importance of a multidisciplinary approach to the management of valvular heart disease in patients with HF in accordance with clinical practice guidelines to prevent worsening of HF and adverse clinical outcomes (Class 1, LOE B-R). A cardiologist with expertise in the management of HF is integral in the shared decision-making for valve intervention and should guide optimization of GDMT to ensure that medical options for HF and secondary MR have been effectively applied for an appropriate time-period and exhausted before considering intervention.Choice B is incorrect. While CRT has been shown to improve MR, LV dimensions, and outcomes in patients with HFrEF and secondary MR in appropriately selected patients, our patient would not be a candidate given that her QRS duration was < 120ms (Class 3: no benefit, LOE B-R). | | Main Takeaway | In patients with severe secondary MR and reduced ejection fraction with persistent symptoms despite GDMT, M-TEER is reasonable in patients with appropriate anatomy as defined on TEE and with LVEF between 20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure ≤70 mmHg. Conversely, surgery may be appropriate for some patients. HF ad VHD should be managed in a multidisciplinary fashion. | | Guideline Loc. | Sections 7.4-7.5Figure 10Also: Section 7.3 from “Otto, C. M., Nishimura, R. A., Bonow, R. O., Carabello, B. A., rwin, J. P., Gentile, F., Jneid, H., Krieger, ric v., Mack, M., McLeod, C., O’Gara, P. T., Rigolin, V. H., Sundt, T. M., Thompson, A., & Toly, C. (2021). 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. In Circulation (Vol. 143, Issue 5, pp. E72–E227). Lippincott Williams and Wilkins. https://doi.org/10.1161/CIR.0000000000000923” |

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The following question refers to Section 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Clyde Yancy.

Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the ACC/AHA Joint Committee on Clinical Practice Guidelines.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

American Heart Association’s Scientific Sessions 2024* As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here! * When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #37

| Mr. S is an 80-year-old man with a history of hypertension, type II diabetes mellitus, and hypothyroidism who had an anterior myocardial infarction (MI) treated with a drug-eluting stent to the left anterior descending artery (LAD) 45 days ago. His course was complicated by a new LVEF reduction to 30%, and left bundle branch block (LBBB) with QRS duration of 152 ms in normal sinus rhythm. He reports he is feeling well and is able to enjoy gardening without symptoms, though he experiences dyspnea while walking to his bedroom on the second floor of his house. Repeat TTE shows persistent LVEF of 30% despite initiation of goal-directed medical therapy (GDMT). What is the best next step in his management? | | A | Monitor for LVEF improvement for a total of 60 days prior to further intervention | | B | Implantation of a dual-chamber ICD | | C | Implantation of a CRT-D | | D | Continue current management as device implantation is contraindicated given his advanced age |

Answer #37

| Explanation | Choice C is correct. Implantation of a CRT-D is the best next step.In patients with nonischemic DCM or ischemic heart disease at least 40 days post-MI with LVEF ≤35% and NYHA class II or III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year,ICD therapy is recommended for primary prevention of SCD to reduce total mortality (Class 1, LOE A). A transvenous ICD provides high economic value in this setting, particularly when a patient’s risk of death from ventricular arrhythmia is deemed high and the risk of nonarrhythmic death is deemed low.In addition, for patients who have LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration ≥150 ms, and NYHA class II, III, orambulatory IV symptoms on GDMT, cardiac resynchronization therapy (CRT) is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. Cardiac resynchronization provides high economic value in this setting.Mr. S therefore meets criteria for both ICD and CRT.Choice A is incorrect. All patients should be on maximally tolerated doses of GDMT prior to consideration of device implantation to allow for assessment of LVEF recovery. Patients who have experienced myocardial infarction should be reassessed 40 days after the event and after achieving maximally tolerated doses of GDMT. Choice B in incorrect. For patients in sinus rhythm with a LBBB morphology and QRS duration >150 ms with an LVEF ≤35%, there were significant improvements in 6-minute walk test performance, quality of life, NYHA classification, and LVEF after implantation of CRT. Mortality and hospitalizations were also found to be decreased in patients with CRT-P & CRT-D. Overall, CRT has been shown to have high economic value in these patients.It should be noted that CRT has the most benefit in patients with a wide QRS (>150 ms), LBBB morphology, and LVEF ≤35%, though trials have shown a modest benefit in special populations. CRT has a Class 2a recommendation (LOE B-NR) in patients with LVEF ≤35%, sinus rhythm, and NYHA Class II, III, or ambulatory IV symptoms on GDMT, with either:a) Non-LBBB pattern with a QRS duration ≥150 msb) LBBB with a QRS duration of 120 to 149 msChoice D is incorrect. If LVEF remains ≤35% in a patient with a life expectancy >1 year, trials have shown that ICD placement for primary prevention reduces sudden cardiac death and also has a high economic value. There is no indication that this patient has a life expectancy < 1 year. | | Main Takeaway | In patients 40 days post-MI on GDMT with an LVEF that remains ≤35%, ICD therapy for primary prevention is appropriate and cost effective. For those additional with a LBBB and QRS >150 ms, CRT-D is also appropriate and cost effective. | | Guideline Loc. | Section 7.4 |

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The following question refers to Sections 2.1and 4.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by CardioNerds Academy Intern Dr. Adriana Mares, answered first by CardioNerds FIT Trialist Dr. Christabel Nyange, and then by expert faculty Dr. Shelley Zieroth.

Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She has been a PI Mentor for the CardioNerds Clinical Trials Program.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

American Heart Association’s Scientific Sessions 2024* As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here! * When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #36

| A 50-year-old woman presents to establish care. Her medical history includes COPD, prediabetes, and hypertension. She is being treated with chlorthalidone, amlodipine, lisinopril, and a tiotropium inhaler. She denies chest pain, dyspnea on exertion, or lower extremity edema.On physical exam, blood pressure is 154/88 mmHg, heart rate is 90 beats/min, and respiration rate is 22 breaths/min with an oxygen saturation of 94% breathing ambient room air. BMI is 36 kg/m2. Jugular venous pulsations are difficult to assess due to her body habitus. Breath sounds are distant, with occasional end-expiratory wheezing. Heart sounds are distant, and extra sounds or murmurs are not detected. Extremities are warm and without peripheral edema. B-type natriuretic peptide level is 28 pg/mL (28 ng/L).A chest radiograph shows increased radiolucency of the lungs, flattened diaphragms, and a narrow heart shadow consistent with COPD. An electrocardiogram shows evidence of left ventricular hypertrophy. The echocardiogram showed normal LV and RV function with no significant valvular abnormalities.In which stage of HF would this patient be classified? | | A | Stage A: At Risk for HF | | B | Stage B: Pre-HF | | C | Stage C: Symptomatic HF | | D | Stage D: Advanced HF |

Answer #36

| Explanation | The correct answer is A – Stage A or at risk for HF.This asymptomatic patient with no evidence of structural heart disease or positive cardiac biomarkers for stretch or injury would be classified as Stage A or “at risk” for HF.The ACC/AHA stages of HF emphasize the development and progression of disease with specific therapeutic interventions at each stage. Advanced stages and disease progression are associated with reduced survival. The stages were revised in this edition of guidelines to emphasize new terminologies of “at risk” for Stage A and “pre-HF” for Stage B.At Stage A, emphasis is placed on the prevention of structural heart disease by aggressive risk factor modification. Healthy lifestyle habits, including regular physical activity, maintaining a normal weight, healthy dietary habits, and avoiding smoking, help reduce the future risk of HF.For patients with established hypertension, coronary disease, or diabetes, optimal control of risk factors is crucial.For hypertension, the SPRINT trial and subsequent meta-analysis of 35 BP-lowering trials have demonstrated a substantial reduction in incident HF and mortality with aggressive BP control.For diabetes, SGLT2 inhibitors have demonstrated reductions in HF hospitalizations regardless of baseline HF status.Screening patients “at risk” for HF for disease progression may be beneficial. The STOP-HF study randomized patients with risk factors but without established LV systolic dysfunction or symptomatic HF to screening with BNP testing or usual care. Screening with BNP followed by an echocardiogram and referral to a cardiovascular specialist for those with levels ≥50 pg/mL led to a reduction in the composite endpoint of incident asymptomatic LV dysfunction with or without newly diagnosed HF. Accordingly, BNP or NT–proBNP–based screening followed by team-based care, including a cardiovascular specialist, has a Class 2a (LOE B-R) recommendation in patients at risk of developing HF to prevent the development of LV dysfunction or new-onset HF.Our patients should be counseled on healthy lifestyles, smoking cessation, and weight loss. Her anti-hypertensive regimen should be intensified for blood pressure optimization. Her ASCVD risk should be calculated, and counseling regarding statin use should be provided accordingly. If she develops overt diabetes, she should be started on an SGLT-2 inhibitor. Given her BNP level, she does not currently warrant further evaluation with an echocardiogram or referral to a specialist. | | Main Takeaway | Patients with Stage A HF are those who are at risk for HF but are without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury. At this stage, the emphasis should be on identifying and modifying risk factors. | | Guideline Loc. | Sections 2.1 and 4.2 |

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The following question refers to Section 2.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by University of Chicago advanced heart failure cardiologist and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Mark Drazner.

Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #35

| A 50-year-old woman with a history of congestive heart failure, hypertension, type 2 diabetes mellitus, and obstructive sleep apnea presents to the outpatient clinic to follow up on her heart failure management. One year prior, echocardiogram showed an ejection fraction of 30% with an elevated BNP, for which she was started on appropriate GDMT. Repeat echocardiogram today showed an EF of 50%. Which of the following best describes her heart failure status? | | A | HFrEF (HF with reduced EF) | | B | HFimpEF (HF with improved EF) | | C | HFmrEF (HF with mildly reduced EF) | | D | HFpEF (HF with preserved EF) |

Answer #35

| Explanation | The correct answer is B – HFimpEF, or heart failure with improved ejection fraction, best describes her current heart failure status.Left ventricular ejection fraction is an important factor in classifying heart failure given differences in prognosis, response to treatment, and use in clinical trial enrollment criteria.The classification of heart failure by EF (adopted from the Universal Definition of HF):– HFrEF (HF with reduced EF): LVEF ≤40%– HFimpEF (HF with improved EF): previous LVEF ≤40%, a ≥10% increase from baseline LVEF, and a second measurement of LVEF >40%.– HFmrEF (HF with mildly reduced EF): LVEF 41%–49%, andevidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)– HFpEF (HF with preserved EF): LVEF ≥50%, and evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)Patients with HFmrEF are usually in a dynamic state of improving from HFrEF or deteriorating towards HFrEF. Therefore, patients with HFmrEF may benefit from follow-up evaluation of systolic function and etiology of sub-normal EF.Improvements in EF are associated with better outcomes but do not indicate full myocardial recovery or normalization of LV function. Indeed, structural and functional abnormalities such as LV dilation and systolic or diastolic dysfunction often persist. Moreover, EF may remain dynamic with fluctuations in either direction depending on factors such as GDMT adherence and re-exposure to cardiotoxic agents. As such, the term heart failure with “improved EF” was deliberately chosen over “recovered EF” and “preserved EF”. Importantly, in patients with HFimpEF while on GDMT, the EF may decrease after withdrawal of GDMT. | | Main Takeaway | Classification of Heart failure helps direct and track management. | | Guideline Loc. | Section 2.2 |

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CardioNerds Cofounder Dr. Amit Goyal, Chair of the CardioNerds Heart Failure Committee Dr. Jenna Skowronski, and Episode FIT Lead Dr. Shazli Khan discuss iron deficiency and its impact on heart failure with Dr. Robert Mentz, Chief of Heart Failure at Duke University and principal investigator of the HEART-FID trial. In this case-based discussion, they cover the diagnostic criteria of iron deficiency in heart failure, epidemiology, and strengths and limitations of different iron formulations. They also review clinical trials examining the impact of iron deficiency on quality of life, heart failure hospitalizations, and mortality. Importantly, they stress the relevance of iron metabolism in heart failure, irrespective of the presence of anemia. They also discuss the approach to addressing outpatient management of iron in heart failure and future directions of research needed in this domain.

Notes were drafted by Dr. Shazli Khan, and Dr. Daniel Ambinder engineered episode audio.

Click here for CME.

This episode was created in collaboration with the Cardiometabolic Health Congress and is supported by an educational grant from American Regent. Please follow the link in the show notes for free CME. All CardioNerds education is planned, produced, and reviewed by CardioNerds.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Pearls – Iron Deficiency in Heart Failure Think about iron deficiency in ALL patients with heart failure and send appropriate diagnostic labs, even if there is no evidence of anemia! * Iron deficiency in heart failure* has a specific and distinguished definition, defined as a ferritin level of <100 ng/mL, or a ferritin level between 100-300 ng/mL with a transferrin saturation of <20%. * Data thus far suggests that treatment of iron deficiency in heart failure results in improved quality of life, as well as a probable reduction in heart failure hospitalizations, and that administration of intravenous iron has a favorable safety profile. * Not all formulations of iron are created equal – intravenous iron formulations have been shown to be effective in this population, but oral iron therapy has not. * Management of iron deficiency in the outpatient setting is an evolving area of research, but patients should typically receive surveillance labs and additional treatment with IV iron if indicated.

Show notes – Iron Deficiency in Heart FailureHow is iron deficiency in heart failure defined, and how prevalent is iron deficiency in this patient population?

• Iron deficiency is common in patients with heart failure, with an estimated prevalence of 50-60%.
  • Iron deficiency in heart failure is associated with worse outcomes, including increased hospitalization and mortality and poorer functional status and quality of life.
  • Iron deficiency in heart failure is defined as a ferritin level of <100 ng/mL or a ferritin level of 100-300 ng/mL plus a transferrin saturation of <20%.
  • There is an evolving school of thought that suggests transferrin saturation alone may be the best indicator of iron deficiency in heart failure, but more data are needed.

Importantly, iron deficiency in heart failure can be seen in patients with both reduced and preserved ejection fraction. Which patients should be screened for iron deficiency?

• There is a class I indication to send iron studies in all patients with heart failure as a part of the initial diagnostic work-up for the underlying etiology of the cardiomyopathy, as well as to assess for the presence of iron deficiency.
  • The presence of anemia is not required to check iron studies, as many patients with iron deficiency in heart failure may not have concomitant anemia.
  • That is, all patients with heart failure should be evaluated for iron deficiency, irrespective of the presence of anemia.

What are the hypothesized mechanisms of iron deficiency in heart failure, and how does iron deficiency impact patients with heart failure?

• Mechanisms causing iron deficiency in heart failure are multifactorial, including reduced oral intake, reduced gut absorption, reduced iron availability due to sequestration, and increased loss due to higher rates of bleeding.
  • Nutritional variation is one proposed mechanism, as patients living with heart failure tend to take in less iron in their diet, and the iron consumed tends to be less easily absorbed.
  • Due to chronic inflammation, there are increased levels of iron sequestration in cells in patients with heart failure, rendering the available iron stores unable to be used.
  • Patients with chronic heart failure also tend to be on anti-platelet agents and/or anticoagulants (due to often-occurring comorbidities), which may potentially lead to bleeding complications, consequently causing iron deficiency.
  • Iron deficiency has been associated with decreased exercise tolerance and functional status, worse quality of life, and increased risk of heart failure hospitalizations.

What are the key takeaways of the clinical trials done in patients with heart failure and iron deficiency?

• The FAIR-HF trial published in 2009 demonstrated that treatment with IV ferrous carboxymaltose (FCM) in patients with heart failure led to improved symptoms and quality of life with an acceptable safety profile. These benefits were verified in a follow-up study known as CONFIRM-HF, demonstrating improvement in 6MWT and functional capacity.
  • The AFFIRM-AHF trial investigated IV FCM in patients with iron deficiency and a left ventricular ejection fraction of <50%. It was a neutral trial with no significant improvement in their primary endpoint, a composite of hospitalization and death. The trial did demonstrate the safety of FCM and decreased hospitalizations. Of note, this trial was significantly impacted by the COVID pandemic, which may have affected the results.
  • The IRONMAN trial was similar in design to AFFIRM-AHF but used a different iron formulation (iron derisomaltose) and had similar findings.
  • The HEART-FID trial was a larger study including 3000 patients with HFrEF investigating treatment with IV ferric carboxymaltose every six months if the patients remained iron deficient. The primary endpoint was a hierarchical composite of death within 12 months after randomization, hospitalizations for heart failure within 12 months after randomization, or change from baseline to 6 months in the 6-minute walk distance. While it was considered a neutral trial with a p=0.019 with a prespecified significance level of 0.01, it demonstrated a trend to improved mortality and six-minute walk.

Which patients should we treat with iron, and with what formulation? What do the guidelines recommend?

• Patients who have chronic heart failure on maximally tolerated guideline-directed medical therapy with iron deficiency are candidates for intravenous iron supplementation with the goal of improving quality of life and reducing heart failure hospitalizations.
  • Intravenous iron has been shown to be effective, but oral iron therapy has shown no benefit in trials.
  • Per the updated 2023 ESC guidelines, there is a class IA recommendation to provide intravenous iron supplementation in symptomatic patients with heart failure with reduced and mid-range ejection fraction with iron deficiency to both alleviate HF symptoms and improve quality of life.
  • There is a class IIA recommendation to provide supplementation to reduce heart failure hospitalizations.
  • Surveillance labs in the outpatient setting, combined with continued treatment for persistent iron deficiency, are likely beneficial in patients with heart failure.

References – Iron Deficiency in Heart Failure1. Packer M, Anker SD, Butler J, et al. Identification of three mechanistic pathways for iron-deficient heart failure. Eur Heart J. 2024;45(26):2281-2293. doi:10.1093/eurheartj/ehae284. https://academic.oup.com/eurheartj/article/45/26/2281/7668668 * Salah HM, Savarese G, Rosano GMC, et al. Intravenous iron infusion in patients with heart failure: a systematic review and study-level meta-analysis. ESC Heart Fail. 2023;10(2):1473-1480. doi:10.1002/ehf2.14310. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10053151/ * Ponikowski P, Kirwan BA, Anker SD, et al. Ferric carboxymaltose for iron deficiency at discharge after acute heart failure: a multicentre, double-blind, randomised, controlled trial. Lancet. 2020;396(10266):1895-1904. doi:10.1016/S0140-6736(20)32339-4. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)32339-4/abstract * Kalra PR, Cleland JGF, Petrie MC, et al; IRONMAN Study Group. Intravenous ferric derisomaltose in patients with heart failure and iron deficiency in the UK (IRONMAN): an investigator-initiated, prospective, randomised, open-label, blinded-endpoint trial. Lancet. 2022;400(10369):2199-2209. doi:10.1016/S0140-6736(22)02083
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)02083-9/fulltext * Mentz RJ, Garg J, Rockhold FW, et al; HEART-FID Investigators. Ferric Carboxymaltose in Heart Failure with Iron Deficiency. N Engl J Med. 2023;389(11):975-986. doi:10.1056/NEJMoa2304968. https://www.nejm.org/doi/full/10.1056/NEJMoa2304968 * McDonagh TA, Metra M, Adamo M, et al; ESC Scientific Document Group. 2023 Focused Update of the 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2023;44(37):3627-3639. doi:10.1093/eurheartj/ehad195. Erratum in: Eur Heart J. 2024;45(1):53. doi:10.1093/eurheartj/ehad613. https://academic.oup.com/eurheartj/article/44/37/3627/7246292?login=false * Anker SD, Comin Colet J, Filippatos G, et al. Ferric Carboxymaltose in Patients with Heart Failure and Iron Deficiency. N Engl J Med. 2009;361(25):2436-2448. doi:10.1056/NEJMoa0908355. https://www.nejm.org/doi/full/10.1056/NEJMoa0908355 * Ponikowski P, van Veldhuisen DJ, Comin-Colet J, et al. Beneficial effects of long-term intravenous iron therapy with ferric carboxymaltose in patients with symptomatic heart failure and iron deficiency. Eur Heart J. 2015;36(11):657-668. doi:10.1093/eurheartj/ehu385. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4359359/

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The following question refers to Sections 6.1 and 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by University of Chicago advanced heart failure cardiologist and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Mark Drazner.

Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #34

| Question Stem | A 72-year-old woman with a history of hypertension, type 2 diabetes mellitus, and a recent myocardial infarction is seen in your clinic. Two months previously, she was hospitalized with a myocardial infarction and underwent successful revascularization of the left anterior descending artery with a drug-eluting stent. Following her myocardial infarction, an echocardiogram revealed an ejection fraction of 17%, and she was discharged on metoprolol succinate, lisinopril, spironolactone, and dapagliflozin with escalation to maximal tolerated doses over subsequent visits. A repeat echocardiogram performed today in your clinic reveals an ejection fraction of 26%. An electrocardiogram reveals normal sinus rhythm with a narrow QRS at a heart rate of 65 beats per minute. She is grateful for her cardiac rehabilitation program and reports no ongoing symptoms. Which of the following devices is indicated for placement at this time? | | Answer choices | A | Implantable loop recorder | | B | ICD | | C | CRT-D | | D | CRT-P |

Answer #34

| Explanation | The correct answer is B.This patient suffered a myocardial infarction more than 40 days ago and has been on appropriate guideline-directed medical therapy since that time. Her left ventricular ejection fraction has improved but remains under 30%. For patients who have suffered a myocardial infarction over 40 days prior with LVEF ≤ 30% and NYHA Class I symptoms while receiving GDMT and have a reasonable expectation of meaningful survival for >1 year, an ICD is recommended for primary prevention of sudden cardiac death to reduce total mortality (Class I, LOE B-R).The MADIT-II trial enrolled 1,232 patients with a prior myocardial infarction and LVEF ≤ 30% to prophylactic ICD or medical therapy. At a median follow-up of 20 months, the trial was terminated early for reduced all-cause mortality with prophylactic ICD. The DINAMIT trial later investigated the implantation of ICD in patients with MI and an LVEF of ≤ 35% at 6 to 40 days after the initial myocardial infarction. This trial found no differences in all-cause mortality between the two groups. Therefore, the current recommendation is to wait at least 40 days with GDMT prior to re-evaluation of left ventricular ejection fraction before proceeding with ICD implantation.Cardiac resynchronization therapy entails implanted pacemakers to simultaneously pace both the RV and LV in order to improve electrical synchrony and generally provides benefit in those with systolic dysfunction and a wide left bundle branch block. Specifically, for patients who have LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration ≥150 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT, CRT is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL (Class I, LOE B-R). CRT implantation provides high economic value in this setting. CRT implantation carries a Class 2a recommendation for those with reduced LVEF (≤35%) and either a non-LBBB pattern with a QRS ≥150 ms or a LBBB with QRS duration 120-149ms. This patient with a narrow QRS does not have indications for CRT placement at this time. | | Main Takeaway | ICD implantation is recommended as primary prophylaxis against ventricular arrhythmias for patients with LVEF ≤30% after 40 days following myocardial infarction despite use of GDMT. | | Guideline Loc. | Section 6.1 and 7.4 |

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The following question refers to Section 5.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by advanced heart failure faculty at the University of Chicago and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Biykem Bozkurt.

Dr. Bozkurt is the Mary and Gordon Cain Chair, Professor of Medicine, Director of the Winters Center for Heart Failure Research, and an advanced heart failure and transplant cardiologist at Baylor College of Medicine in Houston, TX. She is former President of HFSA, former senior associate editor for Circulation, and current Editor-In-Chief of JACC Heart Failure. Dr. Bozkurt was the Vice Chair of the writing committee for the 2022 Heart Failure Guidelines.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #33

| A 63-year-old man with a past medical history of hypertension and type 2 diabetes mellitus presents for routine follow-up. He reports feeling in general good health and enjoys 2-mile walks daily. A review of systems is negative for any symptoms. Which of the following laboratory studies may be beneficial for screening? | | A | NT-proBNP | | B | CK-MB | | C | Troponin | | D | C-reactive protein | | E | None of the above |

Answer #33

| Explanation | The correct answer is A – NT-proBNP.This patient is at risk for HF (Stage A) given the presence of risk factors (hypertension and type 2 diabetes mellitus) but the absence of signs or symptoms of heart failure.Patients at risk for HF screened with BNP or NT-proBNP followed by collaborative care, diagnostic evaluation, and treatment in those with elevated levels can reduce combined rates of LV systolic dysfunction, diastolic dysfunction, and HF.The STOP-HF (St Vincent’s Screening to Prevent Heart Failure) study was a large single-center trial of patients at risk of HF that showed BNP-based screening reduced the composite endpoint of incident asymptomatic LV dysfunction with or without newly diagnosed HF.Therefore, for patients at risk of developing HF, natriuretic peptide biomarker-based screening followed by team-based care, including a cardiovascular specialist optimizing GDMT, can be useful toprevent the development of LV dysfunction (systolic or diastolic) or new-onset HF (Class 2a, LOE B-R).There is no indication for measuring troponin, CK-MB, or CRP at this time. | | Main Takeaway | In patients at risk for HF, screening for pre-HF using natriuretic peptide testing followed by team-based care may be helpful for preventing disease progression. | | Guideline Loc. | Section 5.1 |

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The following question refers to Section 13 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Faculty Dr. Dinu Balanescu, and then by expert faculty Dr. Harriette Van Spall.

Dr. Van Spall is an Associate Professor of Medicine, cardiologist, and Director of E-Health at McMaster University. Dr Van Spall is a Canadian Institutes of Health Research-funded clinical trialist and researcher with a focus on heart failure, health services, and health disparities.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #32

| Palliative and supportive care has a role for patients with heart failure only in the end stages of their disease. | | TRUE | | FALSE |

Answer #32

| Explanation | The correct answer is FalsePalliative care is patient- and family-centered care that optimizes health-related quality of life by anticipating, preventing, and treating suffering and should be integrated into the management of all stages of heart failure throughout the course of illness. The wholistic model of palliative care includes high-quality communication, estimation of prognosis, anticipatory guidance, addressing uncertainty, shared decision-making about medically reasonable treatment options, advance care planning; attention to physical, emotional, spiritual, and psychological distress; relief of suffering; and inclusion of family caregivers in patient care and attention to their needs during bereavement.As such, for all patients with HF, palliative and supportive care—including high-quality communication, conveyance of prognosis, clarifying goals of care, shared decision-making, symptom management, and caregiver support—should be provided to improve QOL and relieve suffering (Class 1, LOE C-LD).For conveyance of prognosis, objective risk models can be incorporated along with discussion of uncertainty since patients may overestimate survival and the benefits of specific treatments – “hope for the best, plan for the worst.”For clarifying goals of care, the exploration of each patient’s values and concerns through shared decision-making is essential in important management decisions such as when to discontinue treatments, when to initiate palliative treatments that may hasten death but provide symptom management, planning the location of death, and the incorporation of home services or hospice.It is a Class I indication that for patients with HF being considered for, or treated with life-extending therapies, the option for discontinuation should be anticipated and discussed through the continuum of care, including at the time of initiation, and reassessed with changing medical conditions and shifting goals of care (LOE C-LD).Caregiver support should also be offered to family members even beyond death to help them cope with the grieving process.A formal palliative care consult is not needed for each patient, but the primary team should exercise the above domains to improve processes of care and patient outcomes.Specialist palliative care consultation can be useful to improve QOL and relieve suffering for patients with heart failure—particularly those with stage D HF who are being evaluated for advanced therapies, patients requiring inotropic support or temporary mechanical support, patients experiencing uncontrolled symptoms, major medical decisions, or multimorbidity, frailty, and cognitive impairment (Class 2a, LOE B). Studies have been mixed on if the palliative team itself improves quality of life and well-being so these interventions should be tailored to each patient and caregiver.For patients with HF, execution of advanced directives can be useful to improve documentation of treatment preferences, delivery of patient-centered care, and dying in a preferred place (Class 2a, LOE C-LD).In patients with advanced HF with expected survival < 6 months, timely referral to hospice can be useful to improve QOL (Class 2a, LOE C-LD) | | Main Takeaway | In summary, the core principles of palliative care that include communication, transparency on prognosis, clarification of goals of care, shared decision-making, symptom management, and caregiver support should be integrated into each patient’s treatment plan regardless of the stage of heart failure | | Guideline Loc. | Section 13, Figure 15, Table 32 |

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The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Keck School of Medicine USC medical student & former CardioNerds Intern Hirsh Elhence, answered first by Vanderbilt Cardiology Fellow and CardioNerds Academy Faculty Dr. Breana Hansen, and then by expert faculty Dr. Javed Butler.

Dr. Butler is an advanced heart failure and transplant cardiologist, President of the Baylor Scott and White Research Institute, Senior Vice President for the Baylor Scott and White Health, and Distinguished Professor of Medicine at the University of Mississippi

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #31

| Mrs. Hart is a 70-year-old woman who was admitted to the CICU two days ago for signs and symptoms consistent with cardiogenic shock. Since her admission, she has been on maximal diuretics, requiring greater doses of intravenous dobutamine. Unfortunately, her liver and renal function continue to worsen, and urine output is decreasing. A right heart catheterization reveals elevated biventricular filling pressures with a cardiac index of 1.7 L/min/m2 by the Fick method.What is the next best step? | | A | Continue current measures and monitor for improvement | | B | Switch from dobutamine to norepinephrine | | C | Place an intra-aortic balloon pump (IABP) | | D | Resume guideline directed medical therapy |

Answer #31

| Explanation | The Correct answer is C – Place an intra-aortic balloon pump.This patient is between the SCAI Shock Stages C and D with elevated venous pressures, decreased urine output, and worsening signs of hypoperfusion. She has been started on appropriate therapies, including diuresis and inotropic support. The relevant Class 2a recommendation is that in patients with cardiogenic shock, temporary MCS is reasonable when end-organ function cannot be maintained by pharmacologic means to support cardiac function (LOE B-NR). Thus, the next best step is a form of temporary MCS. IABP is appropriate to help increase coronary perfusion and offload the left ventricle. In fact, for patients who are not rapidly responding to initial shock measures, triage to centers that can provide temporary MCS may be considered to optimize management (Class 2b, LOE C-LD).The guidelines further state that in patients presenting with cardiogenic shock, placement of a pulmonary arterial line may be considered to define hemodynamic subsets and appropriate management strategies (Class 2B, LOE B-NR). And so, if time allows escalation to MCS should be guided by invasively obtained hemodynamic data via PA catheterization. Several observational experiences have associated PA catheterization use with improved outcomes, particularly in conjunction with short-term MCS. Additionally, PA catheterization is useful when there is diagnostic uncertainty as to the cause of hypotension or end-organ dysfunction, particularly when the patient in shock is not responding to empiric initial measures, such as in this patient.There are additional appropriate measures at this time that are more institution-dependent. An institutional shock team would be very helpful here as they often comprise multidisciplinary teams of heart failure and critical care specialists, interventional cardiologists, surgeons, and palliative care specialists. As such, there is a Class 2a recommendation that in patients with cardiogenic shock, management by a multidisciplinary team experienced in shock is reasonable (LOE B-NR). Most documented experiences have suggested outcomes improve after shock teams are instituted. For instance, in one such experience, using a shock team was associated with improved 30-day all-cause mortality (HR, 0.61; 95% CI, 0.41–0.93) and reduced in-hospital mortality (61.0% vs. 47.9%; P=0.041).Choice A – Continue current measures and monitor for improvement – is incorrect. This patient has been deteriorating on current measures since admission and is at higher risk for SCAI Shock Stage E – extremis, refractory hypotension/hypoperfusion, and cardiac arrest and, therefore requires escalation of therapyChoice B- Switch from dobutamine to norepinephrine – is incorrect. The Class 1 LOE B-NR recommendation is that in patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and maintain end-organ performance. Dobutamine is a more potent inotropic agent than norepinephrine. Stopping dobutamine in the setting of her low cardiac index would be incorrect.Choice D – Resume guideline-directed medical therapy – is incorrect. This patient’s shock is getting worse. The Class 1 LOE B-NR recommendation is that in patients with HFrEF, GDMT should be initiated during hospitalization after clinical stability is achieved. Restarting medications now would be premature. | | Main Takeaway | In patients with cardiogenic shock, temporary MCS is reasonable when end-organ function cannot be maintained by pharmacologic means to support cardiac function. | | Guideline Loc. | Section 9.5 |

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The following question refers to Section 8.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by University of Southern California cardiology fellow and CardioNerds FIT Trialist Dr. Michael Francke, and then by expert faculty Dr. Shashank Sinha.

Dr. Sinha is an Assistant Professor of Medical Education at the University of Virginia School of Medicine and an advanced heart failure, MCS, and transplant cardiologist at Inova Fairfax Medical Campus. He currently serves as both the Director of the Cardiac Intensive Care Unit and Cardiovascular Critical Care Research Program at Inova Fairfax. He is also a Steering Committee member for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network and an Associate Editor for the Journal of Cardiac Failure, the official Journal of the Heart Failure Society of America.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #30

| Ms. V. Tea is a 55-year-old woman with a history of cardiac sarcoidosis, heart failure with mildly reduced ejection fraction (HFmrEF – EF 40%), and ventricular tachycardia with CRT-D who presents with recurrent VT. She has undergone several attempts at catheter ablation of VT in the past and previously had been trialed on amiodarone which was discontinued due to hepatotoxicity. She now continues to have episodic VT requiring anti-tachycardia pacing and ICD shocks despite medical therapy with mexiletine, metoprolol, and sotalol. Her most recent PET scan showed no active areas of inflammation. Currently, her vital signs are stable, and labs are unremarkable. What is the best next step for this patient? | | A | Evaluation for heart transplant | | B | Evaluation for LVAD | | C | Dobutamine | | D | Prednisone | | E | None of the above |

Answer #30

| Explanation | The correct answer is A – evaluation for heart transplant.For selected patients with advanced heart failure despite GDMT, cardiac transplantation is indicated to improve survival and quality of life (Class 1, LOE C-LD). Heart transplantation, in this context, provides intermediate economic value.Clinical indicators include refractory or recurrent ventricular arrhythmias with frequent ICD shocks. Patient selection for heart transplant includes assessment of comorbidities, goals of care, and various other factors. The United Network of Organ Sharing Heart Transplant Allocation Policy was revised in 2018 with a 6-tiered system to better prioritize unstable patients and minimize waitlist mortality. VT puts the patient as a Status 2 on the transplant list. There was a contemporary analysis of patients with end-stage cardiomyopathy due to cardiac sarcoidosis, published in Journal of Cardiac Failure, in 2018 that demonstrated similar 1-year and 5-year survival after heart transplant between patients with and without cardiac sarcoidosis.Choice B (evaluation for LVAD) is incorrect. While bridge to transplant with LVAD is definitely a potential next step in patients with cardiac sarcoidosis, it is not recommended in patients presenting primarily with refractory ventricular arrhythmias due to granuloma-induced scarring. In this situation, patients benefit from direct heart transplant rather than bridge to transplant LVAD approach. The same study, described before in the Journal of Cardiac Failure, also showed similar 1-year and 5-year survival after bridge-to-transplant mechanical circulatory support between patients with and without cardiac sarcoidosis. Since cardiac sarcoidosis is not just limited to the left ventricle, patients being considered for LVAD need hemodynamic assessment to determine the risk of post-LVAD RV failure.Choice C (dobutamine) is incorrect. The patient is currently not decompensated in terms of contractility nor is showing signs of cardiogenic shock. Further, dobutamine may worsen arrhythmia burden.Choice D (prednisone) is incorrect as there is no sign of active inflammation on the PET scan. The recurrent ventricular arrhythmias are being driven by granuloma-induced scar. | | Main Takeaway | Cardiac transplantation has a Class 1 (LOE C-LD) recommendation for eligible patients with advanced HF despite GDMT to improve survival and quality of life. Specifically, direct heart transplantation is the best next step in patients with cardiac sarcoidosis and refractory ventricular arrhythmias rather than a bridge-to-transplant approach. | | Guideline Loc. | Section 8.5 |

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The following question refers to Section 7.8 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Stony Brook University Hospital medicine resident and CardioNerds Intern Dr. Chelsea Tweneboah, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Michelle Kittleson.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #29

| A 69-year-old man was referred to the cardiology clinic after being found to have a reduced left ventricular ejection fraction and left ventricular hypertrophy. For the last several months he has been experiencing progressively worsening fatigue and shortness of breath while getting to the 2nd floor in his house. He has a history of bilateral carpal tunnel syndrome and chronic low back pain. He takes no medications. On exam, his heart rate is 82 bpm, blood pressure is 86/60 mmHg, O2 saturation is 97% breathing ambient air, and BMI is 29 kg/m2. He has a regular rate and rhythm with normal S1 and S2, bibasilar pulmonary rales, and 1+ pitting edema in both legs. EKG shows normal sinus rhythm with a first-degree AV delay and low voltages. Transthoracic echocardiogram shows a moderately depressed LVEF of 35-39%, severe concentric hypertrophy with a left ventricular posterior wall thickness of 1.5 cm and strain imaging showing globally reduced longitudinal strain with apical sparring. There is also biatrial enlargement and a small pericardial effusion. A pharmacologic nuclear stress test did not reveal any perfusion defects. A gammopathy panel including SPEP, UPEP, serum and urine immunofixation studies, and serum free light chains are unrevealing. A 99mTc-Pyrophosphate scan was positive with grade 3 uptake. In addition to starting diuretics, what is the next most appropriate step for managing for this patient? | | A | Start metoprolol succinate | | B | Start sacubitril/valsartan | | C | Perform genetic sequencing of the TTR gene | | D | Perform endomyocardial biopsy |

Answer #29

| Explanation | The correct answer is C – perform genetic sequencing of the TTR gene.This patient has findings which raise suspicion for cardiac amyloidosis. There are both cardiac (low voltages on EKG and echocardiogram showing marked LVH with biatrial enlargement and small pericardial effusion as well as a characteristic strain pattern) and extra-cardiac (bilateral carpal tunnel syndrome and low back pain) features to suggest amyloidosis. The diagnosis of cardiac amyloidosis requires a high index of suspicion and most commonly occurs due to a deposition of monoclonal immunoglobulin light chains (AL-CM) or transthyretin (ATTR-CM). ATTR may cause cardiac amyloidosis as either a pathogenic variant (ATTRv) or as a wild-type protein (ATTRwt).Patients for whom there is a clinical suspicion for cardiac amyloidosis should have screening for serum and urine monoclonal light chains with serum and urine immunofixation electrophoresis and serum free light chains (Class 1, LOE B-NR). Immunofixation electrophoresis (IFE) is preferred because serum or urine plasma electrophoresis (SPEP or UPEP) are less sensitive. Together, measurement of serum IFE, urine IFE, and serum FLC is >99% sensitive for AL amyloidosis. Negative studies as in our patient essentially exclude AL amyloidosis from consideration.In patients with high clinical suspicion for cardiac amyloidosis, without evidence of serum or urine monoclonal light chains, bone scintigraphy should be performed to confirm the presence of transthyretin cardiac amyloidosis (Class 1, LOE B-NR). As in this patient’s case, the 99mTc-Pyrophosphate scan with a grade 2/3 cardiac uptake in the absence of a serum or urinary monoclonal protein has a very high specificity and positive predictive value for ATTR-CM. This allows for a noninvasive diagnosis of ATTR-CM, obviating the need for an endomyocardial biopsy and so option D is inaccurate.In patients for whom a diagnosis of transthyretin cardiac amyloidosis is made, genetic testing with TTR gene sequencing is recommended to differentiate hereditary variant from wild-type transthyretin cardiac amyloidosis (Class 1, LOE B-NR). Differentiating ATTRv from ATTRwt is important because confirmation of ATTRv would trigger genetic counseling and potential cascade screening of family members and TTR silencer therapies, such as inotersen and patisiran (currently only approved for the treatment of polyneuropathy caused by ATTRv amyloidosis).Routine guideline-directed medical treatment (GDMT) for neurohormonal blockade may be poorly tolerated in patients with ATTR-CM and EF ≤40%. Due to restrictive physiology, they may be predisposed to more hypotension with ARNi, ACEi, and ARB. Similarly, patients with ATTR-CM rely on their heart rate response to preserve the cardiac output, thus BB may worsen HF symptoms. In this case, our patient already has a borderline blood pressure without these medications. Both options A and B are false. | | Main Takeaway | In patients for whom a diagnosis of transthyretin cardiac amyloidosis is made, TTR gene sequencing is recommended to differentiate pathologic variant (ATTRv) from wild-type transthyretin cardiac amyloidosis (ATTRwt). This has implications in terms of screening for family members and management options for ATTRv.For patients with ATTR-CM and EF ≤40%, GDMT may be poorly tolerated. | | Guideline Loc. | Section 7.8, Figure 13 |

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The following question refers to Section 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by Hopkins Bayview medicine resident & CardioNerds Academy Faculty Dr. Ty Sweeny, and then by expert faculty Dr. Gregg Fonarow.

Dr. Fonarow is the Professor of Medicine and Interim Chief of UCLA’s Division of Cardiology, Director of the Ahmanson-UCLA Cardiomyopathy Center, and Co-director of UCLA’s Preventative Cardiology Program.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #28

| Mr. Gene D’aMeTi, a 53-year-old African American man with ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 30-35%), is recently admitted with acutely decompensated heart failure and acute kidney injury on chronic kidney disease stage III. His outpatient regiment includes sacubitril-valsartan 97-103mg BID, carvedilol 25mg BID, and hydralazine 50mg TID.Sacubitril-valsartan was held because of worsening renal function. Despite symptomatic improvement with diuresis, his renal function continues to decline. He is otherwise well perfused & with preservation of other end organ function.Throughout this hospitalization, he has steadily become more hypertensive with blood pressures persisting in the 170s/90s mmHg. What would be an appropriate adjustment to his medication regimen at this time? | | A | Resume Losartan only | | B | Start Amlodipine | | C | Increase current Hydralazine dose | | D | Start Isosorbide dinitrate therapy | | E | Both C & D |

Answer #28

| Explanation | The correct answer is E – both increasing the current hydralazine dose (C) and starting isosorbide dinitrate therapy (D).Although ACEI/ARB therapy (choice A) has shown a mortality and morbidity benefit in HFrEF, caution should be used in patients with renal insufficiency. In this patient with ongoing decline in renal function, RAAS-inhibiting therapies (ACEi, ARB, ARNI, MRA) should be avoided. In this case, as his RAAS-I has been stopped, it would be reasonable to increase current therapies to target doses (or nearest dose tolerated), as these demonstrated both safety and efficacy in trials (Class 1, LOE A). Considering that his high dose ARNI was stopped, it is unlikely that either hydralazine or isosorbide dinitrate alone, even at maximal doses, would be sufficient to control his blood pressure (Options C and D, respectively). Interestingly, in the original study by Massie et. Al (1977), the decision was made to combine these therapies as the result was thought to be superior to either medication alone. ISDN would provide preload reduction, while Hydralazine would decrease afterload. Consequently, we do not have data looking at the individual benefit of either medication in isolation.In self-identified African Americans with NYHA class III or IV HFrEF already on optimal GDMT, the addition of hydralazine & isosorbide dinitrate is recommended to improve symptoms and reduce mortality and morbidity (Class 1, LOE A). In this case, as the patient has evidence of progressive renal disfunction, we are limited in using traditional RAAS-I, such as ACEI, ARB, or ARNI. In patients with current or previously symptomatic HFrEF who cannot be given first-line agents (like ARNi, ACEi, ARB) due to intolerance or renal insufficiency, combination therapy of hydralazine & isosorbide dinitrate might be considered to reduce morbidity and mortality (Class 2b, LOE C-LD).Dihydropyridine calcium channel blockers such as Amlodipine (choice B) are not recommended for treatment of HFrEF (COR 3, LOE A), though may be considered for treating elevated blood pressure despite optimization of GDMT. | | Main Takeaway | In self-identified African Americans, the addition of hydralazine & isosorbide dinitrate to GDMT has additional mortality & morbidity benefits.Should a patient have drug intolerances or renal dysfunction that precludes the use of ACEi/ARB/ARNi, hydralazine & isosorbide dinitrate is a reasonable alternative. | | Guideline Loc. | · Section 7.3.5-8· Table 14, Table 15 |

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The following question refers to Section 4.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by […]

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The following question refers to Section 4.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by […]

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The following question refers to Sections 10.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy House Faculty Leader Dr. Dinu Balanescu, and then by expert faculty Dr. Ileana Pina. […]

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The following question refers to Sections 10.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy House Faculty Leader Dr. Dinu Balanescu, and then by expert faculty Dr. Ileana Pina. […]

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Dr. Amit Goyal (CardioNerds co-founder), Dr. Jessie Holtzman (House Faculty in CardioNerds Academy and cardiology fellow at UCSF), and Dr. Megan McLaughlin (CardioNerds Scholar and cardiology fellow at UCSF) discuss stimulant-associated cardiomyopathy with Dr. Jonathan Davis (Associate Professor at UCSF the Director of the Heart Failure Program at Zuckerberg San Francisco General Hospital) and Dr. […]

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The following question refers to Section 9.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Cedars Sinai medicine resident, soon to be Vanderbilt Cardiology Fellow, and CardioNerds Academy Faculty Dr. Breanna Hansen, and then […]

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The following question refers to Section 8.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by University of Southern California cardiology fellow and CardioNerds FIT Trialist Dr. Michael Francke, and then by expert faculty Dr. Prateeti Khazanie. […]

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The CardioNerds and Pulm PEEPs have joined forces to co-produce this important episode, delving into the management of decompensated right ventricular failure in pulmonary arterial hypertension. Joining us for this informative discussion are Pulm PEEPs co-founders, Dr. David Furfaro and Dr. Kristina Montemayor, along with Dr. Leonid Mirson (Internal Medicine Resident at Johns Hopkins Osler […]

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The following question refers to Section 7.6 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by premedical student and CardioNerds Intern Pacey Wetstein, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Nancy Sweitzer.

Dr. Sweitzer is Professor of Medicine, Vice Chair of Clinical Research for the Department of Medicine, and Director of Clinical Research for the Division of Cardiology at Washington University School of Medicine. She is the editor-in-chief of Circulation: Heart Failure. Dr. Sweitzer is a faculty mentor for this Decipher the HF Guidelines series.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Clinical Trials TalksQuestion #21

| Ms. Betty Blocker is a 60-year-old woman with a history of alcohol-related dilated cardiomyopathy who presents for follow up. She has been working hard to improve her health and is glad to report that she has just reached her 5-year sobriety milestone. Her current medications include metoprolol succinate 100mg daily, sacubitril-valsartan 97-103mg BID, spironolactone 25mg daily, and empagliflozin 10mg daily. She is asymptomatic at rest and up to moderate exercise, including chasing her grandchildren around the yard. A recent transthoracic echocardiogram shows recovered LVEF from previously 35% now to 60%. Ms. Blocker does not love taking so many medications and asks about discontinuing her metoprolol. Which of the following is the most appropriate response to Ms. Blocker’s request? | | A | Since the patient is asymptomatic, metoprolol can be stopped without risk | | B | Stopping metoprolol increases this patient’s risk of worsening cardiomyopathy regardless of current LVEF or symptoms | | C | Because the LVEF is now >50%, the patient is now classified as having HFpEF and beta-blockade is no longer indicated; metoprolol can be safely discontinued | | D | Metoprolol should be continued, but it is safe to discontinue either ARNi or spironolactone |

Answer #21

| Explanation | The correct answer is D – continue current therapy.The patient described above was initially diagnosed with HFrEF and experienced significant symptomatic improvement with GDMT, so she now has heart failure with improved ejection fraction (HFimpEF). In patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic (Class 1, LOE B-R). Although symptoms, functional capacity, LVEF and reverse remodeling can improve with GDMT, structural abnormalities of the LV and its function do not fully normalize, causing symptoms and biomarker changes to persist or recur if treatment is deescalated. Improvements in EF do not always reflect sustained recovery; rather, they signify remission.Of note, HF relapse can be defined by at least 1 of the following:o A drop in the EF by >10% and to < 50%o An increase in LVEDV by >10% and to higher than the normal rangeo A 2-fold rise in NT-proBNP concentration and to > 400 ng/Lo Clinical evidence of HF on examinationChoice A is incorrect as it would be incorrect to discontinue spironolactone. A potassium of 5.1 is still within the acceptable limit in a patient who has been on Spironolactone for two years, and this medication is an important part of GDMT for HFrEF.Despite the improvement in Hb A1c, empagliflozin should be continued for heart failure with improved ejection fraction, as it is part of routine GDMT of HFrEF even in the absence of diabetes. Choice B is thus incorrect.Similarly, carvedilol should be continued at the same dose as the patient’s heart rate is within the desired range. Furthermore, all GDMT should be continued in patients with HFimpEF, as emphasized above. Choice C is therefore also incorrect. | | Main Takeaway | In patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic. (Class 1, LOE B-R). | | Guideline Loc. | Section 7.6.2 |

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The following question refers to Sections 7.3.2, 7.3.8, and 7.6.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by Hopkins Bayview medicine resident & CardioNerds Academy Fellow Dr. Ty Sweeny, and then by expert faculty Dr. Robert Mentz.

Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz is a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #20

| Ms. Betty Blocker is a 60-year-old woman with a history of alcohol-related dilated cardiomyopathy who presents for follow up. She has been working hard to improve her health and is glad to report that she has just reached her 5-year sobriety milestone. Her current medications include metoprolol succinate 100mg daily, sacubitril-valsartan 97-103mg BID, spironolactone 25mg daily, and empagliflozin 10mg daily. She is asymptomatic at rest and up to moderate exercise, including chasing her grandchildren around the yard. A recent transthoracic echocardiogram shows recovered LVEF from previously 35% now to 60%. Ms. Blocker does not love taking so many medications and asks about discontinuing her metoprolol. Which of the following is the most appropriate response to Ms. Blocker’s request? | | A | Since the patient is asymptomatic, metoprolol can be stopped without risk | | B | Stopping metoprolol increases this patient’s risk of worsening cardiomyopathy regardless of current LVEF or symptoms | | C | Because the LVEF is now >50%, the patient is now classified as having HFpEF and beta-blockade is no longer indicated; metoprolol can be safely discontinued | | D | Metoprolol should be continued, but it is safe to discontinue either ARNi or spironolactone |

Answer #20

| Explanation | The correct answer is B – stopping metoprolol would increase her risk of worsening cardiomyopathy.Heart failure tends to be a chronically sympathetic state. The use of beta-blockers (specifically bisoprolol, metoprolol succinate, and carvedilol) targets this excess adrenergic output and has been shown to reduce the risk of death in patients with HFrEF. Beyond their mortality benefit, beta-blockers can improve LVEF, lessen the symptoms of HF, and improve clinical status. Therefore, in patients with HFrEF, with current or previous symptoms, use of 1 of the 3 beta blockers proven to reduce mortality (e.g., bisoprolol, carvedilol, sustained-release metoprolol succinate) is recommended to reduce mortality and hospitalizations (Class 1, LOE A). Beta-blockers in this setting provide a high economic value.Table 14 of the guidelines provides recommendations for target doses for GDMT medications. Specifically for beta blockers, those targets are 25-50mg twice daily for carvedilol (or 80mg once daily for the continuous release formulation), 200mg once daily for metoprolol succinate, and 10mg once daily for bisoprolol.While we should be cognizant of pill-burden and other barriers to our patients’ quality of life, we must counsel them about the risks of discontinuing any element of guideline directed medical therapy (GDMT). The 2022 heart failure guidelines recommend the long-term use of beta blockers for patients diagnosed with HFrEF, even if symptoms improve (Option A). Conversely, long-term treatment should also be maintained even if symptoms do not improve to reduce the risk of major cardiovascular events. Importantly, the abrupt withdrawal of beta blockers can lead to clinical deterioration.Our patient here has heart failure with improved ejection fraction (HFimpEF) defined as having a previous LVEF ≤ 40% and a ≥ 10-point increase from baseline with a follow-up measurement of LVEF > 40%. HFimpEF is distinct from HFpEF and was proposed in the “Universal Definition and Classification of Heart Failure” by Bozkurt et al published in JCF 2021 in order to distinguish those who benefit from continued GDMT. Accordingly, in patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic (Class 1, LOE B-R). While GDMT may improve symptoms, functional capacity, LVEF, and reverse remodeling in patients with HFrEF, these favorable changes do not reflect full and sustained recovery but rather remission with susceptibility to worsening with GDMT withdrawal. Therefore, stopping any element of her GDMT (BB, ARNi, or MRA) would be incorrect (Options A, C, D). | | Main Takeaway | In patients with HFrEF who experience improvement in heart failure symptoms and cardiac function on GDMT (develop HFimpEF), it is important to continue optimizing GDMT to prevent relapse, even if asymptomatic. | | Guideline Loc. | Section 7.3.2Section 7.3.8, Table 14Section 7.6.2 |

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The following question refers to Section 7.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by New York Medical College medical student and CardioNerds Intern Akiva Rosenzveig, answered first by Lahey Hospital and Medical Center internal medicine resident and CardioNerds Academy House Faculty Leader Dr. Ahmed Ghoneem, and then by expert faculty Dr. Clyde Yancy.

Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the ACC/AHA Joint Committee on Clinical Practice Guidelines.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #19

| Ms. M is a 36-year-old G1P1 woman 6 months postpartum who was diagnosed with peripartum cardiomyopathy at the end of her pregnancy. She is presenting for a follow up visit today and notes that while her leg edema has resolved, she continues to have dyspnea when carrying her child up the stairs. She also describes significant difficulty sleeping, though denies orthopnea, and notes she is not participating in hobbies she had previously enjoyed. She is currently prescribed a regimen of sacubitril-valsartan, metoprolol succinate, spironolactone, and empagliflozin. What are the next best steps? | | A | Screen for depression | | B | Counsel her to follow a strict low sodium diet with goal of < 1.5g Na daily | | C | Recommend exercise therapy and refer to cardiac rehabilitation | | D | A & C |

Answer #19

| Explanation | The correct answer is D – both A (screening for depression) and C (referring to cardiac rehabilitation) are appropriate at this time.Choice A is correct. Depression is a risk factor for poor self-care, rehospitalization, and all-cause mortality among patients with HF. Interventions that focus on improving HF self-care have been reportedto be effective among patients with moderate/severe depression with reductions in hospitalization and mortality risk. Social isolation, frailty, and marginal health literacy have similarly been associated with poor HF self-care and worse outcomes in patients with HF. Therefore, in adults with HF, screening for depression, social isolation, frailty, and low healthliteracy as risk factors for poor self-care is reasonable to improve management (Class 2a, LOE B-NR). Choice C is correct. In patients with HF, cardiac rehabilitation has a Class 2a recommendation (LOE B-NR) to improve functional capacity, exercise tolerance, and health-related QOL; exercise training (or regular physical activity) for those able to participate has a Class 1 recommendation (LOE A) to improve functional status, exercise performance, and QOL.Choice B is incorrect. For patients with stage C HF, avoiding excessive sodium intake is reasonable to reduce congestive symptoms (Class 2a, LOE C-LD). However, strict sodium restriction does not have strong supportive data and is not recommended. There are ongoing studies to better understand the impact of sodium restriction on clinical outcomes and quality of life. The AHA currently recommends a reduction of sodium intake to <2300 mg/d for general cardiovascular health promotion; however, there are no trials to support this level of restriction in patients with HF. | | Main Takeaway | Depression is a risk factor for poor HF self-care and worse outcomes in patients with heart failure and so it is reasonable to screen for depression in these patients. Exercise therapy and cardiac rehabilitation have been shown to improve outcomes in HF patients. While avoiding excess sodium intake is reasonable in HF patients to reduce congestive symptoms, there is no specific strict sodium level recommended. | | Guideline Loc. | Section 7.1 |

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The following question refers to Sections 3.2, 4.1, 4.3, and 4.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Baylor University cardiology fellow and CardioNerds FIT Trialist Dr. Shiva Patlolla, and then by expert faculty Dr. Shelley Zieroth.

Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She is a steering committee member for PARAGLIE-HF and a PI Mentor for the CardioNerds Clinical Trials Program.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #18

| Ms. AH is a 48-year-old woman who presents with a 3-month history of progressively worsening exertional dyspnea and symmetric bilateral lower extremity edema. She has no history of recent upper respiratory symptoms or chest pain.She denies any tobacco, alcohol, or recreational drug use. There is no family history of premature CAD or HF.On exam, her blood pressure is 110/66 mmHg, heart rate is 112 bpm, and respiration rate is 18 breaths/min with oxygen saturation of 98% on ambient room air. She has jugular venous distention of about 12cm H2O, bibasilar crackles, an S3 heart sound, and bilateral lower extremity edema.Complete blood count, serum electrolytes, kidney function tests, liver chemistry tests, glucose level, iron studies, and lipid levels are unremarkable.An electrocardiogram shows sinus tachycardia with normal intervals and no conduction delays. A transthoracic echocardiogram demonstrates a left ventricular ejection fraction of 25%, normal right ventricular size and function, and no valvular abnormalities.Which of the following diagnostic tests has a Class I indication for further evaluation? | | A | Cardiac catheterization | | B | Referral for genetic counseling | | C | Thyroid function studies | | D | Cardiac MRI |

Answer #18

| Explanation | The correct answer is C – thyroid function studies have a Class 1 indication for the evaluation of HF. The common causes of HF include coronary artery disease, hypertension, and valvular heart disease. Other causes may include arrhythmia-associated, toxic, inflammatory, metabolic including both endocrinopathies and nutritional, infiltrative, genetic, stress induced, peripartum, and more. It is important to evaluate for the etiology of a given patient’s heart failure as diagnosis may have implications for treatment, counseling, and family members.For patients who are diagnosed with HF, laboratory evaluation should include complete blood count, urinalysis, serum electrolytes, blood urea nitrogen, serum creatinine, glucose, lipid profile, liver function tests, iron studies, and thyroid-stimulating hormone to optimize management (Class 1, LOR C-EO). These studies provide important information regarding comorbidities, suitability for and adverse effects of treatments, potential causes or confounders of HF, and severity and prognosis of HF.HF is often caused by coronary atherosclerosis, and evaluation for ischemic heart disease can help in determining the presence of significant coronary artery disease (CAD). Noninvasive stress imaging with echocardiography or nuclear scintigraphy can be helpful in identifying patients likely to have obstructive CAD. Invasive or computed tomography coronary angiography can detect and characterize the extent of CAD. Therefore, in patients with HF, an evaluation for possible ischemic heart disease can be useful to identify the cause and guide management (Class 2a, LOE B-NR).Familial cardiomyopathy is increasingly recognized and may be the underlying etiology of patients previously classified as having idiopathic dilated cardiomyopathy. A detailed family history may provide the first clue to a genetic basis. A 3-generation family pedigree obtained by genetic health care professionals improved the rate of detection of a familial process as compared with routine care. Furthermore, a family history of cardiomyopathy, as determined by a 3-generation pedigree analysis, was associated with findings of gadolinium enhancement on cardiac magnetic resonance imaging (MRI) and increased major adverse cardiac events. The possibility of an inherited cardiomyopathy provides the impetus for cascade screening of undiagnosed family members, thereby potentially avoiding preventable adverse events in affected relatives by implementation of GDMT and other management that otherwise would not be initiated. Therefore, in patients with cardiomyopathy, a 3-generation family history should be obtained or updated when assessing the cause of the cardiomyopathy to identify possible inherited disease (Class 1, LOE B-NR). In selecting patients with nonischemic cardiomyopathy, referral for genetic counseling and testing is reasonable to identify conditions that could guide treatment for patients and family members (Class 2a, LOE B-NR).CMR provides noninvasive characterization of the myocardium that may provide insights into HF cause. Registry data show that CMR findings commonly impact patient care management and provide diagnostic information in patients with suspected myocarditis or cardiomyopathy. However, routine screening with CMR is not recommended. The OUTSMART HF trial recently demonstrated routine cardiac MRI use did not yield more specific HF causes than a selective strategy based on echocardiographic and clinical findings. The guidelines give a Class 2a recommendation for the use of CMR in diagnosis or management in patients with HF or cardiomyopathy (LOE B-NR). | | Main Takeaway | The common causes of HF include ischemic heart disease, hypertension, and valvular heart disease. When a patient presents with new-onset heart failure, a complete initial evaluation including laboratory testing for potentially reversible causes such as thyroid disease, or other endocrine, metabolic, and nutritional causes should be performed. | | Guideline Loc. | Section 3.2, 4.1, 4.3, and 4.4Table 5 |

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The following question refers to Section 5.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Greater Baltimore Medical Center medicine resident / Johns Hopkins MPH student and CardioNerds Academy House Chief Dr. Alaa Diab, and then by expert faculty Dr. Biykem Bozkurt.

Dr. Bozkurt is the Mary and Gordon Cain Chair, Professor of Medicine, Director of the Winters Center for Heart Failure Research, and an advanced heart failure and transplant cardiologist at Baylor College of Medicine in Houston, TX. She is former President of HFSA, former senior associate editor for Circulation, and current Editor-In-Chief of JACC Heart Failure. Dr. Bozkurt was the Vice Chair of the writing committee for the 2022 Heart Failure Guidelines.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #17

| A 63-year-old man with CAD s/p CABG 3 years prior, type 2 diabetes mellitus, hypertension, obesity, and tobacco use disorder presents for routine follow-up. His heart rate is 65 bpm and blood pressure is 125/70 mmHg. On physical exam, he is breathing comfortably with clear lungs, with normal jugular venous pulsations, a regular rate and rhythm without murmurs or gallops, and no peripheral edema. Medications include aspirin 81mg daily, atorvastatin 80mg daily, lisinopril 20mg daily, and metformin 1000mg BID. His latest hemoglobin A1C is 7.5% and recent NT-proBNP was normal. His latest transthoracic echocardiogram showed normal biventricular size and function. Which of the following would be a good addition to optimize his medical therapy? | | A | DPP-4 inhibitor | | B | Dihydropyridine calcium channel blocker | | C | SGLT2 inhibitor | | D | Furosemide |

Answer #17

| Explanation | The correct answer is C: SGLT2 inhibitor.This patient is at risk for HF (Stage A) given absence of signs or symptoms of heart failure but presence of coronary artery disease and several risk factors including diabetes, hypertension, obesity, and tobacco smoking. At this stage, the focus should be on risk factor modification and prevention of disease onset.Healthy lifestyle habits such as maintaining regular physical activity; normal weight, blood pressure, and blood glucose levels; healthy dietary patterns, and not smoking have been associated with a lower lifetime risk of developing HF.Multiple RCTs in patients with type 2 diabetes who have established CVD or are at high risk for CVD, have shown that SGLT2i prevent HF hospitalizations compared with placebo. The benefit for reducing HF hospitalizations in these trials predominantly reflects primary prevention of symptomatic HF, because only approximately 10% to 14% of participants in these trials had HF at baseline.As such, in patients with type 2 diabetes and either established CVD or at high cardiovascular risk, SGLT2i should be used to prevent hospitalizations for HF (Class 1, LOE A).The mechanisms for the improvement in HF events from SGLT2i have not been clearly elucidated but seem to be independent of glucose lowering. Proposed mechanisms include reductions in plasma volume, cardiac preload and afterload, alterations in cardiac metabolism, reduced arterial stiffness, and interaction with the Na+/H+ exchanger. SGLT2i are generally well tolerated, but these agents have not been evaluated in those with severe renal impairment (estimated glomerular filtration rate [eGFR] <25 mL/min/1.73 m2). | | Main Takeaway | It is important to identify patients who are at risk for HF (Stage A) and focus on risk factor optimization to prevent disease onset and progression. | | Guideline Loc. | Section 5.1 |

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The following question refers to Sections 11.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Johns Hopkins Osler internal medicine resident and CardioNerds Academy Fellow Dr. Justin Brilliant, and then by expert faculty Dr. Harriette Van Spall.

Dr. Van Spall is Associate Professor of Medicine, cardiologist, and Director of E-Health at McMaster University. Dr Van Spall is a Canadian Institutes of Health Research-funded clinical trialist and researcher with a focus on heart failure, health services, and health disparities.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #16

| Ms. Augustin is a 33 y/o G1P1 woman from Haiti who seeks counseling regarding family planning as she and her husband dream of a second child. Her 1st pregnancy 12 months ago was complicated by pre-eclampsia and peripartum cardiomyopathy (LVEF 35%). Thankfully she delivered a healthy baby via C-section. She has no other past medical history and is currently on losartan 25 mg daily and metoprolol succinate 200 mg daily. She has been asymptomatic. Which of the following statements is recommended to medically optimize Ms. Augustin prior to her 2nd pregnancy? | | A | No medical optimization or preconception planning is needed as her 1st pregnancy resulted in a healthy infant. | | B | Discontinue losartan and metoprolol with no other needed pregnancy planning | | C | Change her medication regimen, consider repeat TTE, and provide patient-centered counseling regarding risk of a future pregnancy | | D | Continue losartan and metoprolol and advise against repeat pregnancy |

Answer #16

| Explanation | The correct answer is C – change her medication regimen, consider repeat TTE, and provide patient-centered counseling regarding risk of a future pregnancy.Heart failure may complicate pregnancy either secondary to an existing pre-pregnancy cardiomyopathy or as a result of peripartum cardiomyopathy. In women with history of heart failure or cardiomyopathy, including previous peripartum cardiomyopathy, patient-centered counseling regarding contraception and the risks of cardiovascular deterioration during pregnancy should be provided (Class I, LOE C-LD)Peripartum cardiomyopathy (PPCM) is defined as systolic dysfunction, typically LVEF < 45%, often with LV dilation, occurring in late pregnancy or early postpartum with no other identifiable etiology. PPCM occurs worldwide, with the highest incidences in Haiti, Nigeria, and South Africa. Other clinical risk factors include maternal age > 30 years, African ancestry, multiparity, multigestation, preeclampsia/eclampsia, anemia, diabetes, obesity, and prolonged tocolysis.The pathogenesis of peripartum cardiomyopathy is complex and it is likely a multifactorial process. The combination of hemodynamic changes of pregnancy, inflammation of the myocardium, hormonal changes, genetic factors, and an autoimmune response have all been proposed as possible mechanisms and these may certainly be interrelated.While pregnancy is generally well-tolerated in women with cardiomyopathy and NYHA class I status pre-pregnancy, clinical deterioration can occur and so counseling and shared decision-making are important. In fact, the ROPAC study of pregnancy outcomes for women with structural heart disease showed that women with pre-pregnancy or previous peripartum CM had the highest mortality rate at 2.4%. Subsequent pregnancies for women with previous peripartum cardiomyopathy have been associated with further decreases in LV function, maternal death, and adverse fetal outcomes. LVEF < 50% prior to a subsequent pregnancy is the strongest prognostic determinant.Different strategies are needed to optimize the cardiovascular health of women with a prior history of PPCM before embarking on a subsequent pregnancy including pre-conception counseling regarding risk of subsequent pregnancies, pharmacologic strategies, and a multi-disciplinary approach to expectant management.Pre-conception counseling: can utilize cardiovascular risk tools including ZAHARA I and CARPREG II scores (which predict outcomes during pregnancy in women with prior heart disease) and obtain a baseline TTE prior to conception to inform shared decision making. Pharmacologic strategies: in women with HF or cardiomyopathy who arepregnant or currently planning for pregnancy, ACEi, ARB, ARNi, MRA, SGLT2i, ivabradine, and vericiguat should not be administered because of significant risks of fetal harm (Class 3: Harm, LOE C-LD). Beta blockers (preferably metoprolol), hydralazine, and nitrates are considered acceptable during pregnancy, when guided by multidisciplinary shared decision-making regarding benefits and potential risks. Diuretic dosing should be discussed (if applicable) to minimize the risk of placental hypoperfusion. A repeat TTE should be performed 3 months following changes in heart failure medicine regimen. Of note, postpartum women who breastfeed can start an ACEi (enalapril or captopril are preferred), and metoprolol remains the preferred beta blocker.Multidisciplinary care may include consultations with genetics, gynecology, and maternal-fetal medicine teams, as appropriate to the outcome of shared decision making. During pregnancy, for women with decompensated HF or evidence of hemodynamic instability antepartum, delivery planning will include obstetrics and maternal-fetal medicine, cardiac anesthesia, cardiology, and neonatology teams.Therefore, answer choice C is correct because pre-conception counseling is essential to guide pertinent discussions on risk stratification prior to subsequent pregnancies. Additionally, her medications need to be modified by discontinuing her ARB prior to conception.Choice A is incorrect because she is high risk for worsening cardiomyopathy and repeat preeclampsia in her next pregnancy.Choice B is incorrect because shared decision making and risk stratification prior to 2nd pregnancy are essential.Choice D is incorrect because, although she is at high risk for complications including worsening cardiomyopathy, preeclampsia/eclampsia, and neonatal demise, repeat pregnancy is not absolutely contraindicated and should be an informed decision after appropriate education within the construct of a multidisciplinary team.See Heart Failure and Pregnancy Infographic created by Dr. Alaa Diab, CardioNerds Academy Chief. | | Main Takeaway | In summary, when a patient with history of peripartum cardiomyopathy is planning on a repeat pregnancy, patient-centered counseling regarding risks and management strategies should be provided with guidance from a multidisciplinary team and medications should be adjusted to balance GDMT for heart failure against risks to fetal development. | | Guideline Loc. | Section 11.3, Table 30 |

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The following question refers to Section 10.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Boston University cardiology fellow and CardioNerds Ambassador Dr. Alex Pipilas, and then by expert faculty Dr. Ileana Pina.

Dr. Pina is Professor of Medicine and Quality Officer for the Cardiovascular Line at Thomas Jefferson University, Clinical Professor at Central Michigan University, and Adjunct Professor of Biostats and Epidemiology at Case Western University. She serves as Senior Fellow and Medical Officer at the Food and Drug Administration’s Center for Devices and Radiological Health.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #15

| Mrs. Framingham is a 65-year-old woman who presents to her cardiologist’s office for stable angina and worsening dyspnea on minimal exertion. She has a history of non-insulin dependent type 2 diabetes mellitus and hypertension. She is taking metformin, linagliptin, lisinopril, and amlodipine. Blood pressure is 119/70 mmHg. Labs are notable for a hemoglobin of 14.2 mg/dL, iron of 18 mcg/dL, ferritin 150 ug/L, transferrin saturation 15%, and normal creatine kinase. An echocardiogram shows reduced left ventricular ejection fraction of 25%. Coronary angiography shows obstructive lesions involving the proximal left anterior descending, left circumflex, and right coronary arteries. In addition to optimizing GDMT, which of the following are recommendations for changes in management? | | A | Anticoagulation, percutaneous revascularization, and IV iron | | B | A change in her diabetic regimen, percutaneous revascularization, and PO iron | | C | A change in her diabetic regimen, surgical revascularization, and IV iron | | D | A change in her diabetic regimen, medical treatment alone for CAD, and PO iron | | E | Anticoagulation and surgical revascularization |

Answer #15

| Explanation | The correct answer is C – a change in her diabetic regimen, surgical treatment and IV iron.Multimorbidity is common in patients with heart failure. More than 85% of patients with HF also have at least 2 additional chronic conditions, of which the most common are hypertension, ischemic heart disease, diabetes, anemia, chronic kidney disease, morbid obesity, frailty, and malnutrition. These conditions can markedly impact patients’ tolerance to GDMT and can inform prognosis.Not only was Mrs. F found with HFrEF (most likely due to ischemic cardiomyopathy), but she also suffers from severe multi-vessel coronary artery disease, hypertension, and non-insulin dependent type 2 diabetes mellitus.In addition to starting optimized GDMT for HF, specific comorbidities in the heart failure patient warrant specific treatment strategies. Mrs. Framingham would benefit from a change in her diabetic regimen, namely switching from linagliptin to an SGLT2 inhibitor (e.g., empagliflozin, dapagliflozin). In patients with HF and type 2 diabetes, theuse of SGLT2i is recommended for the management of hyperglycemia and to reduce HF related morbidity and mortality (Class 1, LOE A).Furthermore, as she has diabetes, symptomatic severe multi-vessel CAD, and LVEF≤35%, surgical revascularization with coronary artery bypass grafting is warranted to improve symptoms, cardiovascular hospitalizations, and long-term all-cause mortality (Class 1, LOE B-R). Given the severity of her coronary disease, presence of diabetes mellitus, and coronary anatomy suitable for bypass, percutaneous (i.e., PCI) or medical treatment alone are inappropriate (options B, D).Although she does not have anemia, she may benefit from IV iron. IV iron supplementation has been shown in the FAIR-HF, IRONOUT HF, and AFFIRM-AHF trials to significantly improve NYHA functional class, 6-minute walk test, quality of life, and decrease hospitalizations for HF, independently of anemia. These effects were not seen with iron given orally (options B, D). Iron deficiency is usually defined as ferritin level <100 μg /L or 100 to 300 μg/L, if the transferrin saturation is <20%. Therefore, in patients with HFrEF and iron deficiency with or without anemia, intravenous iron replacement is reasonable to improve functional status and QOL (Class 2a, LOE B-R).Although HF is a pro-thrombotic state, anticoagulation is not warranted empirically in Mrs. F, who has no evidence of thrombus or high-risk features suggesting impending thrombus (options A, E). | | Main Takeaway | In summary, multimorbidity is frequent in heart failure patients and treatment targeted to specific morbidities is warranted. In patients with heart failure and diabetes, an SGLT2 inhibitor should be part of the medication regimen. Intravenous iron supplementation should be considered in iron-deficient patients independent of anemia. In patients with heart failure with LVEF≤35% and severe coronary artery disease with suitable anatomy, coronary artery bypass grafting is recommended. | | Guideline Loc. | Section 10.1, Figure 14 |

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The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Duke University cardiology fellow and CardioNerds FIT Ambassador Dr. Aman Kansal, and then by expert faculty Dr. Javed Butler.

Dr. Butler is an advanced heart failure and transplant cardiologist, President of the Baylor Scott and White Research Institute, Senior Vice President for the Baylor Scott and White Health, and Distinguished Professor of Medicine at the University of Mississippi.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #14

| Mrs. Hart is a 70-year-old woman hospitalized for a 2-week course of progressive exertional dyspnea, increasing peripheral edema, and mental status changes. She has a history of coronary artery disease, hypertension, and heart failure for which she takes aspirin, furosemide, carvedilol, lisinopril, and spironolactone. On physical exam, the patient is afebrile, BP is 80/60 mmHg, heart rate is 120 bpm, and respiratory rate is 28 breaths/min with O2 saturation of 92% breathing room air. She is sitting upright and is confused. Jugular venous pulsations are elevated. Cardiac exam reveals an S3 gallop. There is ascites and significant flank edema on abdominal exam. Her lower extremities have 2+ pitting edema to her knees and are cool to touch. Her labs are significant for an elevated serum Creatinine of 3.0 from a baseline of 1.0 mg/dL, lactate of 3.0 mmol/L, and liver enzyme elevation in the 300s U/L.Which of the following is the most appropriate initial treatment? | | A | Increase carvedilol | | B | Start dobutamine | | C | Increase lisinopril | | D | Start nitroprusside |

Answer #14

| Explanation | The Correct answer is B – start dobutamine.This patient with progressive congestive symptoms, mental status changes, and signs of hypoperfusion and end-organ dysfunction meets the clinical criteria of cardiogenic shock. The Class 1 recommendation is that in patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and maintain end-organ performance (LOE B-NR). Their broad availability, ease of administration, and clinician familiarity favor such agents as first line when signs of hypoperfusion persist. Interestingly, despite their ubiquitous use for management of cardiogenic shock, there is a lack of robust evidence to suggest the clear benefit of one agent over another. Therefore, the choice of a specific agent is guided by additional factors including vital signs, concurrent arrhythmias, and availability. For this patient, dobutamine is the only inotrope listed. Although she is tachycardic, her lack of arrhythmia makes dobutamine relatively lower risk and does not outweigh the potential benefits.Choice A – Increase carvedilol – is not correct. Beta-blockers should be continued in HF hospitalization whenever possible; however, in a patient with low cardiac output and signs of shock, beta-blockers should be discontinued due to their negative inotropic effects.Choice C – Increase lisinopril – is not correct. Afterload reduction is reasonable to decrease myocardial oxygen demand. However, given the hypotension and renal dysfunction, increasing lisinopril could be potentially dangerous by further exacerbating hypotension and renal dysfunction. Furthermore, given her tenuous hemodynamic status, it would be more beneficial to start an IV medication that is easier to monitor and rapidly titrate.Choice D – Start nitroprusside – is not correct. Intravenous Vasodilators are helpful for improving cardiac output in high SVR states when the patient is normotensive or even hypertensive. However, this patient is HYPOtensive and so vasodilators should be held. | | Main Takeaway | In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ performance. | | Guideline Loc. | Section 9.5 |

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The following question refers to Section 9.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Duke University cardiology fellow and CardioNerds FIT Ambassador Dr. Aman Kansal, and then by expert faculty Dr. Anu Lala.

Dr. Lala is an advanced heart failure and transplant cardiologist, associate professor of medicine and population health science and policy, Director of Heart Failure Research, and Program Director for the Advanced Heart Failure and Transplant fellowship training program at Mount Sinai. Dr. Lala is deputy editor for the Journal of Cardiac Failure. Dr. Lala has been a champion and role model for CardioNerds. She has been a PI mentor for the CardioNerds Clinical Trials Network and continues to serve in the program’s leadership. She is also a faculty mentor for this very 2022 heart failure decipher the guidelines series.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #13

| Mrs. Hart is a 63-year-old woman with a history of non-ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 20-25%) presenting with 5 days of worsening dyspnea and orthopnea. She takes carvedilol 12.5mg BID, sacubitril-valsartan 24-46mg BID, empagliflozin 10mg daily, and furosemide 40mg daily and reports that she has been able to take all her medications. What is the initial management for Mrs. H? | | A | Assess her degree of congestion and hypoperfusion | | B | Search for precipitating factors | | C | Evaluate her overall trajectory | | D | All of the above | | E | None of the above |

Answer #13

| Explanation | The correct answer is D – all of the above.Choice A is correct because in patients hospitalized with heart failure, the severity of congestion and adequacy of perfusion should be assessed to guide triage and initial therapy (Class 1, LOE C-LD). Congestion can be assessed by using the clinical exam to gauge right and left-sided filling pressures (e.g., elevated JVP, S3, edema) which are usually proportional in decompensation of chronic HF with low EF; however, up to 1 in 4 patients have a mismatch between right- and left-sided filling pressures. Hypoperfusion can be suspected from narrow pulse pressure and cool extremities, intolerance to neurohormonal antagonists, worsening renal function, altered mental status, and/or an elevated serum lactate. For more on the bedside evaluation of heart failure, enjoy Episode #142 – The Role of the Clinical Examination in Patients With Heart Failure – with Dr. Mark Drazner.Choice B, searching for precipitating factors is also correct. In patients hospitalized with HF, the common precipitating factors and the overall patient trajectory should be assessed to guide appropriate therapy (Class 1, LOE C-LD). Common precipitating factors include ischemic and nonischemic causes, such as acute coronary syndromes, atrial fibrillation and other arrhythmias, uncontrolled HTN, other cardiac disease (e.g., endocarditis), acute infections, anemia, thyroid dysfunction, non-adherence to medications or new medications. When initial clinical assessment does not suggest congestion or hypoperfusion, symptoms of HF may be a result of transient ischemia, arrhythmias, or noncardiac disease such as chronic pulmonary disease or pneumonia, and more focused assessments may be warranted.Lastly, Choice C, evaluation of a patient’s trajectory is correct as hospitalization for HF is a sentinel event that signals worse prognosis and provides key opportunities to redirect the disease trajectory – including establishment of optimal volume status before and after discharge. During the HF hospitalization, the approach to management should include and address precipitating factors, comorbidities, and previous limitations to ongoing disease management related to social determinants of health. The disease trajectory for patients hospitalized with reduced EF is markedly improved by optimization of recommended medical therapies, which should be initiated or increased toward target doses once the efficacy of diuresis has been shown. | | Main Takeaway | In summary, when a patient is admitted for acute decompensated heart failure, initial management involves assessing the patient’s degree of congestion and hypoperfusion, identifying and addressing precipitating factors, and evaluating overall patient trajectory to guide appropriate triage and therapy. | | Guideline Loc. | Section 9.1, Table 21 |

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CardioNerds (Dr. Amit Goyal), Dr. Sonu Abraham (CardioNerds Ambassador from Lahey Hospital and Medical Center, Burlington, MA) discuss left ventricular assist devices (LVAD) and the implications of renal dysfunction with Dr. Brian Houston and Dr. Nisha Bansal. This episode will focus on the intersection of left ventricular assist devices and renal dysfunction. Patients with a combination of heart failure and renal dysfunction overall have a guarded prognosis and their management poses unique challenges to the clinician. We initially discuss the basics of an LVAD and general approach to LVAD candidacy evaluation. We then discuss specific implications of acute kidney injury, presence of preexisting CKD, and end stage renal disease in patients with/being considered for an LVAD. Risk factor identification and prognostication allows for appropriate selection of the right candidates for an LVAD in the context of renal disease. Dr. Brian Houston is the Director of the Mechanical Circulatory Support program at Medical University of South Carolina. Dr. Nisha Bansal is an Associate Professor and the Arthur Stach Family Endowed Professor in the Division of Nephrology, an investigator at the Kidney Research Institute, the Director of Nephrology Clinical and Research Education, and the Director of the Kidney-Heart Service at the University of Washington. Notes were drafted by Dr. Sonu Abraham and episode audio was edited by student Dr. Chelsea Amo-Tweneboah.

Check out the CardioNerds ~~Failure~~ Heart Success Series Page for more heart success episodes and content!

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Pearls – Left Ventricular Assist Devices and Renal Dysfunction1. End stage renal disease (CKD on dialysis) is considered an absolute contraindication for LVAD implantation. Select young patients who are being considered for heart-kidney transplantation in the near future may be candidates for an LVAD as a bridge to heart-kidney transplantation. 2. LVAD implantation can improve kidney function in the short term in patients with AKI primarily caused by cardio-renal syndrome. 3. Patients with pre-existing CKD (not dialysis dependent) have a greater risk of developing AKI after LVAD implantation. 4. Several dialysis modalities including in-center hemodialysis, home hemodialysis, and peritoneal dialysis are available for LVAD patients. However, there are several challenges associated with each modality. 5. An AV graft is a useful vascular access option in LVAD patients undergoing hemodialysis due to a lower risk of infection and ease of immediate use. 6. Causes for anemia in patients with an LVAD and renal dysfunction include anemia of chronic disease, gastrointestinal bleeding, and pump thrombosis leading to hemolysis.

Show notes – Left Ventricular Assist Devices and Renal DysfunctionNotes: (drafted by Dr. Sonu Abraham)

What is a left ventricular assist device (LVAD) and what are its components?

An LVAD supports circulation by unloading the left ventricle and providing increased cardiac output to help support organ perfusion. Use in properly selected patients is associated with improved quality of life and increased survival. The current iteration of LVADs offer continuous flow, as opposed to the older versions which employed pulsatile flow.

Components of the LVAD:

• Inflow cannula (sucks blood from the LV)
• Pump
• Outflow cannula (dumps blood into the aorta)
• Percutaneous driveline
• Electrical controller

How is a patient evaluated for LVAD candidacy?

The 2 main questions to be answered during the evaluation of a patient for an LVAD are:

1. Are they sick enough? Do they have end stage heart failure?

2. Do we expect the benefits of an LVAD to outweigh the risks?

3. Presence/absence of right ventricular failure

4. Other life limiting organ failure: Kidney failure/lung disease/liver failure/vascular disease
5. Anatomic concerns (ex. LV size)
6. Surgical risk (ex. Prior sternotomies, calcified aorta, etc)
7. Psychosocial aspects
8. Shared decision making (Does the patient want the device?)

What are the outcomes of patients with end stage renal disease (chronic kidney disease on dialysis) after LVAD implantation?

• Patients with ESRD have a high burden of comorbidities. 40% of dialysis patients have heart failure.
• The combination of heart failure and ESRD propounds a poor prognosis. Patients with ESRD without heart failure have a 40% survival in 5 years. Conversely, those with ESRD and heart failure have a < 20% survival in 5 years.
• A retrospective analysis of the United States Renal Data System revealed that 50% patients on dialysis who received an LVAD died during the index hospitalization, compared to those not on dialysis whose in hospital mortality was <10%. The median survival was ~3 weeks. By 6 months after LVAD implantation, ~70% of patients on dialysis had died.
• Based on INTERMACS data, kidney function is one of the strongest predictors of outcomes in patients with an LVAD.

What are the specific situations in which an LVAD might be offered to a patient with ESRD?

• We may consider LVAD implantation in ESRD patients under specific circumstances.
• Young patients with good functional status and good end organ function otherwise, who may be a candidate for heart-kidney transplantation in the near future, may be considered for LVAD implantation as a bridge to heart-kidney transplantation.
• If it is felt that the patient’s renal dysfunction can be improved by augmenting cardiac output and the hemodynamics suggest cardio-renal syndrome, in very select patients on recently initiated dialysis LVAD implantation may be considered. Renal imaging showing absence of scarring and the absence of proteinuria suggest a better prognostic sign and may suggest cardio-renal syndrome.

In patients with acute kidney injury (with no prior history of CKD) being evaluated for LVAD implantation, what is the effect of an LVAD on kidney function?

• Effect of an LVAD on kidney function: There is typically an initial improvement in kidney function, particularly in the first month post-implantation, due to restoration of normal hemodynamics with improvement in cardiac output and relieving renal venous congestion. Long term data, however, suggests gradual deterioration of kidney function in the long term. This is possibly due to kidney insults from the LVAD itself. The continuous flow of the LVAD can lead to periarteritis, hyperplasia of the renal arterial smooth muscle cells, and neurohormonal activation of the RAAS system leading to kidney injury over time.
• Creatinine may not be the best marker of kidney function in these patients. Cystatin C and tubular kidney injury markers, soon to be commercially available, may be better markers of kidney function.

Does having chronic kidney disease (not dialysis dependent) increase the risk of worsening kidney function after LVAD implantation?

The occurrence of AKI after LVAD worsens outcomes. The presence of CKD prior to LVAD implantation increases this risk of AKI after LVAD implantation. Patients with CKD stage 3 or more have a 1-year mortality of >30% after LVAD implantation. In patients who have AKI after LVAD implantation, 30-day mortality is 18% and 1 year mortality is 40% with increased risk of infection, multisystem organ failure, and longer length of stay.

Common causes of AKI after LVAD implantation include:

1. Right ventricular failure
2. Bleeding requiring blood products and crystalloids, contributing to congestion.
3. Longer cardio-pulmonary bypass

Hemolysis

Based on a 10-year case series from the Mayo clinic, 15% of patients with LVAD require renal replacement therapy. If GFR<45 and there is proteinuria, the risk increased to 40%.

The 4 risk factors to predict AKI and RRT requirement after LVAD:

• Presence of a low GFR
• Proteinuria
• Increased RA pressure
• Longer cardio-pulmonary bypass time
• The HEARTMATE III Risk Score provides individual survival prediction at 1- and 2-years post LVAD implantation – includes BUN and sodium levels

What are the options available to patients in terms of long-term dialysis once LVAD patients are dialysis dependent?

• There are 3 main options for long term RRT:
  • In-center hemodialysis
  • Home hemodialysis
  • Peritoneal dialysis
• Considerations:
  • In center Hemodialysis:
    • Challenges: large ultrafiltration rates can lead to lower MAPs, anticoagulation considerations (bleeding complications), high risk of infection (central venous catheter), pragmatic challenges (technical expertise of the dialysis staff, comfort of the attending nephrologist, transportation issues).
  • Peritoneal dialysis:
    • Benefits: decreased risk of infection (however anatomical considerations with respect to proximity to the driveline should be taken into account), more physiological and less hemodynamic instability, no need for anticoagulation.
    • Challenge: home based therapy (burden on the patient and family members)

What are the options in terms of vascular access in patients with an LVAD who are started on hemodialysis?

• Central venous HD catheters – high risk of infection and therefore, not preferred.
• AV fistula – low rates of infection, however, it takes 2-3 months for fistula maturation.
• AV graft – preferred due to lower risk of infection, ability to use immediately.

What are the causes for anemia in patients with an LVAD and renal dysfunction?

• Anemia of chronic disease
• Increased risk of gastrointestinal bleed
  • Anticoagulation requirement
  • Acquired Von Willebrand deficiency
  • Higher burden of arterio-venous malformations
• Pump thrombosis can lead to hemolysis

What are the implications of blood transfusions and use of erythropoietin stimulating agents (ESAs) in these patients?

• Judicious use of blood transfusions is advised particularly in patients waiting for a heart transplantation due to increased risk of antigen sensitization which can limit their potential donor pool.
• Those who receive ESAs have a dose-dependent increased risk of pump thrombosis and all-cause mortality. This was however, studied in patients with a HEARTMATE II (axial flow device) as opposed to the currently most commonly used pump which is the HEARTMATE III (centrifugal flow device) known to have an overall lower risk of pump thrombosis.

References 1. Peritoneal Dialysis Following Left Ventricular Assist Device Placement and Kidney Recovery: A Case Report Kidney Med. 2021;3(3):438-441. Published 2021 Feb 17. doi:10.1016/j.xkme.2020.12.009 2. Bansal N, Hailpern SM, Katz R, et al. Outcomes Associated With Left Ventricular Assist Devices Among Recipients With and Without End-stage Renal Disease. JAMA Intern Med. 2018;178(2):204-209. doi:10.1001/jamainternmed.2017.4831 3. Butler J, Geisberg C, Howser R, et al. Relationship between renal function and left ventricular assist device use. Ann Thorac Surg. 2006;81(5):1745-1751. doi:10.1016/j.athoracsur.2005.11.061 4. Haglund NA, Feurer ID, Dwyer JP, et al. Does renal dysfunction and method of bridging support influence heart transplant graft survival?. Ann Thorac Surg. 2014;98(3):835-841. doi:10.1016/j.athoracsur.2014.05.059 5. Jawaid O, Gaddy A, Omar HR, Guglin M. Ventricular Assist Devices and Chronic Kidney Replacement Therapy: Technology and Outcomes. Adv Chronic Kidney Dis. 2021;28(1):37-46. doi:10.1053/j.ackd.2021.01.002 6. Ootaki C, Yamashita M, Ootaki Y, et al. Reduced pulsatility induces periarteritis in kidney: role of the local renin-angiotensin system. J Thorac Cardiovasc Surg. 2008;136(1):150-158. doi:10.1016/j.jtcvs.2007.12.023 7. Patel AM, Eduardo Rame J, Rudnick MR. How does the nephrologist manage an LVAD patient on chronic maintenance dialysis?. Semin Dial. 2014;27(3):284-288. doi:10.1111/sdi.12229 8. Roehm B, Vest AR, Weiner DE. Left Ventricular Assist Devices, Kidney Disease, and Dialysis. Am J Kidney Dis. 2018;71(2):257-266. doi:10.1053/j.ajkd.2017.09.019 9. Sandner SE, Zimpfer D, Zrunek P, et al. Renal function and outcome after continuous flow left ventricular assist device implantation. Ann Thorac Surg. 2009;87(4):1072-1078. doi:10.1016/j.athoracsur.2009.01.022 10. Wettersten N, Estrella M, Brambatti M, et al. Kidney Function Following Left Ventricular Assist Device Implantation: An Observational Cohort Study. Kidney Med. 2021;3(3):378-385.e1. Published 2021 Apr 2. doi:10.1016/j.xkme.2021.01.009 11. Yalcin YC, Muslem R, Veen KM, et al. Impact of Continuous Flow Left Ventricular Assist Device Therapy on Chronic Kidney Disease: A Longitudinal Multicenter Study. J Card Fail. 2020;26(4):333-341. doi:10.1016/j.cardfail.2020.01.010 12. Yoshioka D, Sakaguchi T, Saito S, et al. Predictor of early mortality for severe heart failure patients with left ventricular assist device implantation: significance of INTERMACS level and renal function. Circ J. 2012;76(7):1631-1638. doi:10.1253/circj.cj-11-1452

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CardioNerds (Amit and Dan) join Dr. Khaled Abdelrahman, Dr. Gurleen Kaur, and Dr. Danny Pipilas from the Brigham and Women’s Hospital Residency Program for Italian food and cannolis at the North End in Boston as they discuss the case of an elderly man with primary cardiac lymphoma. They review an approach to intracardiac masses, discuss advantages and disadvantages of various imaging modalities for the evaluation of intracardiac masses, and also delve into anthracycline toxicity. The E-CPR segment is provided by Dr. Ron Blankstein, Associate Director of the Cardiovascular Imaging Program and Director of Cardiac Computed Tomography at Brigham and Women’s Hospital. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig.

A 76-year-old man with a history of hyperlipidemia presented with one month of progressively worsening fatigue, weight loss, and dyspnea on exertion. Physical exam was notable for a 3/6 systolic murmur at the left upper sternal border, a flopping sound along the sternum heard throughout the cardiac cycle, and JVP elevated to the level of the mandible. TTE revealed a large heterogeneous echodensity in the right ventricular (RV) free wall that extended into the pericardium and into the RV myocardium with mobile components in the RV cavity and obstruction of the RV outflow tract. Nongated CT chest showed a solid nodule in the periphery of the left lower lung lobe. Gated cardiac CTA revealed a large heterogenous mass in the right atrioventricular groove that encased the proximal thoracic aorta and pulmonary artery and invaded the RV myocardium and RV outflow tract along with a large pericardial effusion. On cardiac MRI, the mass was isointense to the myocardium on T1-weighted images, hyperintense on T2-weighted images, and had heterogenous enhancement on late gadolinium enhancement images. Overall, the imaging findings were highly suspicious for cardiac lymphoma which was confirmed with biopsy of the lung nodule; pathology showed a large B cell lymphoma. The patient was treated with R-CHOP therapy (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), and TTE after 6 cycles of chemotherapy demonstrated resolution of the RV mass.

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Case Media
1. There is a large homogeneous mass in the right atrioventricular groove that extends anterior to the right ventricular outflow tract, pulmonary artery, and ascending aorta, measuring up to 9.4 x 7.1 cm (axial) x 13 cm (craniocaudal). The mass encases the proximal thoracic aorta and pulmonary artery. The mass invades the right ventricular myocardium, the right ventricular outflow tract, the pulmonary artery, and proximal main pulmonary artery. There is severe stenosis of the right ventricular outflow tract due to obstruction by the mass. The mass encases the right coronary artery, without compression of the artery. There is enhancement of this mass on delayed contrast imaging. Collectively, these findings suggest cardiac lymphoma.
2. There is a large pericardial effusion, circumferential, measuring up to 2.2 cm adjacent to the right atrium and up to 2.3 cm anterior to the intraventricular septum. There is pericardial enhancement, indicative of pericardial inflammation.
3. This study was not optimized for the assessment of the coronary arteries. However, there are severe coronary artery calcifications. There is possible severe stenosis of the mid LAD.
4. Aneurysmal dilatation of the thoracic aorta, with measurements as reported in the narrative.
1. Normal left ventricular size and function.

1. There is a large homogenous, soft-tissue intensity mass in the right atrioventricular groove infiltrating the right ventricle free wall and cranially extending anterior to the aorta and main pulmonary artery. The mass encases the main pulmonary artery, the aortic root, the right coronary artery, and the left main coronary artery. The mass invades the right ventricular outflow tract and proximal main pulmonary artery, resulting in severe luminal narrowing at the level of the RVOT/pulmonary artery valve. For the dimensions of the mass, please refer to cardiac CT from 12/1/2021. The mass is isointense to myocardium on T1-weighted images and hyperintense on T2-weighted images. The mass avidly enhances on first-pass perfusion images. There is heterogeneous enhancement of the mass on late gadolinium enhancement images.

2. There is a large circumferential pericardial effusion, measuring up to 2.3 cm.The left ventricular cavity size and wall thickness are normal. Left ventricular systolic function is normal. There are no segmental left ventricular wall motion abnormalities noted. The estimated ejection fraction is 60%. The right ventricular size is normal. Right ventricular systolic function is mildly decreased. Mildly dilated ascending aorta. Mild AI. Mild MR. There is large heterogenous echodensity in the RV free wall that extends into the parietal pericardium and also into the RV myocardium with mobile components in the RV cavity apical to the tricuspid valve and immediately adjacent to the pulmonic valve. There is obstruction of flow out of the RVOT with a peak and mean gradient of 27 and 16 mmHg respectively. There appears to be some vascularity to this structure (seen best on clips 17 and 18) and overall findings are highly suspicious for tumor. There is a small to moderate pericardial effusion. Anterior to the RV there is a larger collection that is probably pleural in etiology. Recommend cross-sectional imaging for further evaluation. There is no RV chamber collapse to suggest tamponade physiology.

3. Intensely FDG avid infiltrative mediastinal most likely high-grade lymphoma..
4. Additional discrete mediastinal and hilar nodes, and left lower lobe nodule, most likely additional areas of lymphomatous involvement. Moderate uptake along right adrenal nodule may represent additional site of lymphomatous involvement
5. Small bilateral pleural effusions and small to moderate pericardial effusion.Pearls – A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man – Brigham and Women’s Hospital1. In the diagnostic approach for cardiac masses, consider: 1) age of patient at time of presentation, 2) epidemiologic likelihood and clinical probability, 3) location of tumor, and 4) tissue characterization of the mass on CMR.
6. CMR allows for better characterization of soft tissues and can assess mass morphology, dimensions, homogeneity, and infiltration into surrounding tissues.
7. On CMR, cardiac lymphoma typically shows isointensity on T1 imaging and hyperintensity on T2 images.
8. Cardiac CT allows for high spatial and temporal resolution, and can be useful to define cardiac masses that involve the coronary arteries; compared to CMR, cardiac CT has a greater ability to assess calcifications within a mass itself.
9. Cardiac lymphomas have a predilection of right heart chambers, especially right atrium and can affect the AV groove, encasing the right coronary artery.
10. Global systolic longitudinal myocardial strain on TTE is an indicator of early anthracycline-induced cardiomyopathy before overt reduction in ejection fraction. Show Notes – A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man – Brigham and Women’s Hospital1. What is the approach to an enlarged cardiac silhouette noted on chest x-ray?
    1. Cardiothoracic ratio of greater than 50%.
    2. Two possible “buckets” of diagnoses to consider are enlargement of heart related to cardiomegaly as opposed to a pericardial process like a pericardial effusion.
    3. For cardiomegaly, it can be from dilated or hypertrophic cardiomyopathy with most common causes including coronary artery disease, hypertension, valvular heart disease, and arrythmia-induced cardiomyopathy. Other buckets to consider are inflammatory causes, either infectious or autoimmune, as well as infiltrative diseases like amyloid or sarcoid, toxins (alcohol, cocaine, medications), endocrine, and nutritional causes (like a B1 or selenium deficiency).
    4. The most sensitive sign of a pericardial effusion on chest x-ray is enlargement of cardiac silhouette with a sensitivity of around 71%, but low specificity (1).
    5. With pericardial effusion, symmetric expansion of the heart contour leads to a globular appearance which is commonly referred to as flask-shaped or the water bottle sign (1).
11. What is the approach to intracardiac masses?
    • First, consider the age of the patient at the time of presentation since certain clinical entities like rhabdomyomas and fibromas are more common in the pediatric population (2).
    • Second, consider the epidemiologic likelihood and clinical probability. In a patient with a recent anterior wall MI and akinetic ventricular apex, a cardiac mass on echo would raise concern for an intracardiac thrombus (2).
    • Third, consider the location of the tumor. If the mass is on the valves, consider thrombus or a vegetation. While masses in the chambers can still represent thrombus, would also consider myxomas, lymphomas, and metastases (2).
    • Fourth, consider the tissue characterization of the mass on further diagnostic imaging such as CMR (2).
12. What is the role of multimodality imaging in the evaluation of intracardiac masses?
13. TTE is the first modality utilized in evaluation of a cardiac mass. TEE is useful specifically when valvular lesions are suspected or in patients with atrial masses or with mobile valvular lesions. It can help to characterize size, morphology, attachment site, extension, and hemodynamic effects.
14. CMR allows for better characterization of soft tissue and can assess mass morphology, dimensions, homogeneity, infiltration in surrounding tissues. These can all help differentiate different types of masses and whether a mass is benign or malignant. Signal characteristics gathered from T1, T2, early gadolinium enhancement, and late gadolinium enhancement sequences can further assess fatty infiltration, necrosis, hemorrhage, and vascularity within a mass (3, 4).
15. Cardiac CT is another option and offers high spatial and temporal resolution, multiplanar image reconstruction capabilities, and fast acquisition times. The large field of view also allows for assessment of chest and lung tissue, vascular structures, and assessment for other masses in the chest. CT may also be more helpful in defining surgical approaches and assessing how masses may involve the coronary arteries and assess for coronary artery calcifications or obstructive coronary disease (4).
16. FDG-PET is also another valuable imaging option which offers evaluation of metabolic activity of tumors. PET imaging can also help guide biopsy location, staging, and planning for cancer therapy.
17. What are key features of Primary Cardiac Lymphoma?
    • Diffuse large B-cell lymphoma is the most common subtype, though others like Burkitt lymphoma, low grade B –cell lymphoma, and T-cell lymphoma have also been described.
    • They occur more commonly in immunocompromised individuals and in immunocompetent patients, only account for 1.3% of primary cardiac tumors
    • Presenting symptoms are usually nonspecific. They may manifest as dysrhythmias like heart block, syncopal episodes, or even restrictive cardiomyopathy.
    • Approximately 20% of patients may develop acute heart failure before other symptoms.
    • On echocardiogram, these tumors appear homogeneous, with predilection of right heart chambers, especially right atrium. The AV groove can be affected, potentially encasing the right coronary artery (5).
    • On CMR, tissue appears isointense on T1-weighted imaging. On T2-weighted imaging, lesions are mildly hyperintense due to diffuse edema (5).
18. What are risk factors associated with anthracycline toxicity and what are strategies for preventing and monitoring for cardiotoxicity when anthracycline therapy is planned?
    • Up to 35% of patients receiving anthracycline therapy develop some form of cardiotoxicity (6).
    • The risk of developing anthracycline induced cardiotoxicity is directly proportional to the dose of anthracycline received, and after studies demonstrated HF incidence of 26% with doxorubicin dose of 550mg/m2 as compared to 5% with dose of 400mg/m2, efforts have been made to limit cumulative anthracycline doses to 400 to 450mg/m2. In addition, hypertension, DM, and obesity are all associated with increased risk (6).
    • There are two primary prevention strategies: using cardioprotective agents, and aiming to reduce potency of the anthracyclines. For cardioprotection, dexrazoxane is an FDA-approved cardioprotective agent for anthracycline induced cardiotoxicity (7).
    • TTE is the most common modality used for detection and monitoring of anthracycline toxicity on the heart. While LV dysfunction is most commonly detected, recent investigations suggest that RV function is also significantly affected by anthracycline toxicity (8).
    • Global systolic longitudinal myocardial strain on TTE has also emerged as a reproducible indicator of early anthracycline-related myocardial dysfunction and future reduction in LVEF (9).
    • Enjoy Episodes 261 and 274 about CTRCD (cancer therapy related cardiac dysfunction) as part of the Cardio-Oncology Series.

References – A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man – Brigham and Women’s Hospital1. https://www.acc.org/latest-in-cardiology/articles/2019/09/09/10/46/chest-radiograph-signs-suggestive-of-pericardial-disease 2. Tyebally S, Chen D, Bhattacharyya S, Mughrabi A, Hussain Z, Manisty C, Westwood M, Ghosh AK, Guha A. Cardiac Tumors: JACC CardioOncology State-of-the-Art Review. JACC CardioOncol. 2020 Jun 16;2(2):293- 3. Motwani M, Kidambi A, Herzog BA, Uddin A, Greenwood JP, Plein S. MR imaging of cardiac tumors and masses: a review of methods and clinical applications. Radiology. 2013 Jul;268(1):26-43. 4. Lopez-Mattei JC, Lu Y. Multimodality Imaging in Cardiac Masses: To Standardize Recommendations, The Time Is Now! JACC Cardiovasc Imaging. 2020 Nov;13(11):2412-2414. 5. Jeudy J, Kirsch J, Tavora F, Burke AP, Franks TJ, Mohammed TL, Frazier AA, Galvin JR. From the radiologic pathology archives: cardiac lymphoma: radiologic-pathologic correlation. Radiographics. 2012 Sep-Oct;32(5):1369-80. 6. Henriksen PA. Anthracycline cardiotoxicity: an update on mechanisms, monitoring and prevention. Heart. 2018 Jun;104(12):971-977. 7. Vejpongsa P, Yeh ET. Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities. J Am Coll Cardiol. 2014 Sep 2;64(9):938-45 8. Liu JE. Anthracycline-Induced Cardiotoxicity: Remembering the Forgotten Ventricle. JACC CardioOncol. 2020;2(1):23-25. 9. Potter E, Marwick TH. Assessment of Left Ventricular Function by Echocardiography: The Case for Routinely Adding Global Longitudinal Strain to Ejection Fraction. JACC Cardiovasc Imaging. 2018 Feb;11(2 Pt 1):260-274.

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It’s another session of CardioNerds Rounds! In these rounds, Dr. Karan Desai (Formerly FIT at University of Maryland Medical Center and currently faculty at Johns Hopkins School of Medicine) joins Dr. Dan Burkhoff (Director of Heart Failure, Hemodynamics and MCS Research at the Cardiovascular Research Foundation) to discuss mechanical circulatory support options through the lens of pressure-volume loops! Dr. Burkhoff is the author of Harvi, an interactive simulation-based application for teaching and researching many aspects of ventricular hemodynamics. Don’t miss this wonderfully nerdy episode with a world-renowned expert in hemodynamics and MCS! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.

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Show notes – Hemodynamics and Mechanical Circulatory SupportCase Synopsis:

Case Synopsis
We focused on one case during these rounds. A man in his mid-50s presented to his local community hospital with 3 days of chest pain, nausea, and vomiting. He appeared ill in the emergency room with HR in the 150s, BP 90/70s and ECG demonstrating inferior ST elevations. He was taken emergently to the catheterization lab and received overlapping stents to his right coronary artery. Over the next 24 hours, he developed a new harsh systolic murmur heard throughout his precordium and progressed to cardiogenic shock. Echocardiogram demonstrated a large basal inferoseptum ventricular septal rupture. From this point, we discussed the hemodynamics of VSR and MCS options.

**Case Takeaways****

1. Dr. Burkhoff took us through the hemodynamics of VSR with pressure-volume loops to better understand the pathology and impact of various MCS options. Of note, there are no MCS devices specifically approved to treat acute ventricular septal rupture.
2. In regards to the acute hemodynamic effects of a VSR (an abrupt left to right shunt), there are several aspects to note. First, the effective LV afterload is reduced; however, there is less “forward flow” as well and as a consequence, decreased left-sided cardiac output (“Qs”) and blood pressure. At the same time, flow through the pulmonary artery increases (the “Qp”). Additionally, due to the abrupt shunt flow, there is increased RV “loading” with increasing central venous pressure and pulmonary artery pressure.
3. The hemodynamic priorities in treating patients with cardiogenic shock and VSR are to normalize blood pressure, cardiac output, and oxygen delivery, while attempting to minimize shunt flow to allow healing. However, medications and MCS are unlikely to completely normalize hemodynamics. For instance, if the patient was placed on peripheral VA ECMO, while total CO and BP may increase, flow across the VSR could also increase at high ECMO flows (e.g., by introducing more LV afterload).
4. In patients with persistent cardiogenic shock and VSR, short-term MCS to divert flow away from the shunt can be an effective strategy. LV-to-aorta or LA-to-arterial MCS may provide the best single-device hemodynamic profiles by decreasing shunt flow, reducing pulmonary capillary wedge pressure, and improving blood pressure.
5. Surgical and percutaneous VSD repair are the definitive treatment options. If able to stabilize patients and pursue delayed repair, it may lead to better outcomes by allowing for better tissue substrate for a more effective repair.

Enjoy this ACC.org Expert Analysis by Goyal and Menon to learn more about post-myocardial infarction ventricular septal rupture.

References 1. Pahuja M, Schrage B, Westermann D et al. Hemodynamic Effects of Mechanical Circulatory Support Devices in Ventricular Septal Defect. Circ Heart Fail. 2019 Jul;12(7):e005981. doi: 10.1161/CIRCHEARTFAILURE.119.005981. 2. TEACH Videos via Harvi.Org: https://harvi.org/book/data/00%20-%20TeachVideos/TeachVideos.html

Production TeamKaran Desai, MDNatalie Stokes, MDAmit Goyal, MDDaniel Ambinder, MD

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The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by Brigham & Women’s medicine resident and Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Shashank Sinha.

Dr. Sinha is an Assistant Professor of Medical Education at the University of Virginia School of Medicine and an advanced heart failure, MCS, and transplant cardiologist at Inova Fairfax Medical Campus. He currently serves as both the Director of the Cardiac Intensive Care Unit and Cardiovascular Critical Care Research Program at Inova Fairfax. He is also a Steering Committee member for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network and an Associate Editor for the Journal of Cardiac Failure, the official Journal of the Heart Failure Society of America.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #12

| Mr. Shock is a 65-year-old man with a history of hypertension and non-ischemic cardiomyopathy (LVEF 25%) who is admitted with acute decompensated heart failure. He is currently being diuresed with a bumetanide drip, but is only making 20 cc/hour of urine. On exam, blood pressure is 85/68 mmHg and heart rate is 110 bpm. His JVP is at 12 cm and extremities are cool with thready pulses. Bloodwork is notable for a lactate of 3.5 mmol/L and creatinine of 2.5 mg/dL (baseline Cr 1.2 mg/dL). What is the most appropriate next step? | | A | Augment diuresis with metolazone | | B | Start sodium nitroprusside | | C | Start dobutamine | | D | Start oral metoprolol | | E | None of the above |

Answer #12

| Explanation | The correct answer is C – start dobutamine.In this scenario, the patient is in cardiogenic shock given hypotension and evidence of end-organ hypoperfusion on exam and labs. The patient’s cool extremities, low urine output, elevated lactate, and elevated creatinine all point towards hypoperfusion.In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ function (Class 1, LOE B-NR). Further, in patients with cardiogenic shock whose end-organ function cannot be maintained by pharmacologic means, temporary MCS is reasonable to support cardiac function (Class 2a, LOE B-NR).The SCAI Cardiogenic Shock Criteria can be used to divide patients into stages. Stage A is a patient at risk for cardiogenic shock but currently not with any signs or symptoms, for example, a patient presenting with a myocardial infarction without present evidence of shock. Stage B is “pre-shock” – this may be a patient who has volume overload, tachycardia, and hypotension but does not have hypoperfusion based on exam and lab evaluation. Stage C is classic cardiogenic shock – the cold and wet profile. Bedside findings for Stage C shock include cool extremities, weak pulses, altered mental status, decreased urine output, and/or respiratory distress. Lab findings include impaired renal function, increased lactate, increased hepatic enzymes, and/or acidosis. Stage D is deteriorating with worsening hypotension and hypoperfusion with escalating use of pressors or mechanical circulatory support. Finally, stage E is extremis with refractory hypotension and hypoperfusion, with circulatory collapse. Our patient in the question stem is in SCAI stage C, or classic cardiogenic shock.Choice A is incorrect. Augmenting diuresis with metolazone can be useful in a patient with diuretic resistance and decompensated heart failure. However, this patient is hypotensive and fits the wet and cool profile and will benefit from inotropic support to increase end organ perfusion.Choice B is incorrect. Sodium nitroprusside can be used to increase cardiac output in cardiogenic shock and is particularly useful in patients with high systemic vascular resistance. Indeed, intravenous nitroglycerin and nitroprusside have a Class 2a indication (LOE B-NR) in patients who are admitted with decompensated HF without systemic hypotension as an adjuvant to diuretic therapy for relief of dyspnea. However, our patient is hypotensive and so vasodilators would not be appropriate at this time.Choice C is incorrect. Metoprolol, a negative inotropic agent, should not be used in this patient with cardiogenic shock.Relevant to this question is the use of invasive hemodynamic monitoring to guide therapy. The use a PA line has a Class 2b indication (LOE B-NR) in patients presenting with cardiogenic shock to define hemodynamic subsets and appropriate management strategies. Obtaining hemodynamic data via a PA line can also be particularly useful when escalating to mechanical circulatory support, when there is diagnostic uncertainty, or when a patient in shock is not responding to empiric initial shock measures. While the use of PA catheters has been controversial since the ESCAPE trial which showed no benefit in decompensated HF, the trial did not actually enroll patients with cardiogenic shock. Several observational studies have shown association between PA catheter use and improved outcomes in cardiogenic shock, particularly in conjunction with short-term MCS. PA catheters are a diagnostic tool and are best utilized when hemodynamic information can be translated into appropriate interventions, such as determining response to medical and MCS therapy, weaning off of MCS support, or uncovering right ventricular failure to guide appropriate therapy.In the case of cardiogenic shock, studies have shown benefit with multidisciplinary teams of HF and critical care specialists, interventional cardiologists, and cardiac surgeons. Such teams should also be capable of providing appropriate palliative care. There is a Class 2a (LOE B-NR) recommendation for management of patients with cardiogenic shock by an experienced multidisciplinary team. | | Main Takeaway | In summary, it is important to recognize cardiogenic shock early based on clinical criteria of hypotension and hypoperfusion and begin prompt initiation of IV inotropic agents such as dobutamine and/or MCS to optimize end-organ perfusion. When there is insufficient clinical improvement with initial measures, invasive hemodynamic assessment is recommended. | | Guideline Loc. | Section 9.5Tables 22-24 |

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The following question refers to Section 8.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by Brigham & Women’s medicine resident and Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Prateeti Khazanie.

Dr. Khazanie is an Associate Professor and Advanced Heart Failure and Transplant Cardiologist at the University of Colorado. She was an undergraduate at Duke University as a B.N. Duke Scholar. She spent two years at the NIH in the lab of Dr. Anthony Fauci and completed a dual MD-MPH program at Duke Medical School. When she started residency, she thought she was going to be an ID doctor, but she fell in love with cardiology at Stanford where she was an intern, resident, and then chief resident. She went back to Duke for her general cardiology and advanced heart failure/transplant fellowships as well as research training at the DCRI. Dr. Khazanie joined the University of Colorado in 2015 as a health services clinician researcher with a focus on improving health equity and bioethics in advanced heart failure care. She mentors medical students, residents, and fellows and is a faculty mentor for the University of Colorado Cardiology Fellows “House of Cards” mentoring group. She has research funding from the NIH/NHLBI K23, NIH Ethics Grant, and Ludeman Center for Women’s Health Research. Dr. Khazanie is an author on the 2022 ACC/AHA/HFSA HF Guidelines, the 2021 HFSA Universal Definition of Heart Failure, and multiple scientific statements.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #11

| A 64-year-old woman with a history of chronic systolic heart failure secondary to NICM (LVEF 15-20%) s/p dual chamber ICD presents for routine follow-up. She reports several months of progressive fatigue, dyspnea, and peripheral edema. She has been hospitalized twice in the past year with acute decompensated heart failure. Efforts to optimize guideline directed medical therapy have been tempered by episodes of lightheadedness and hypotension. Her exam is notable for an elevated JVP, an S3 heart sound, and a III/VI holosystolic murmur best heard at the apex with radiation to the axilla. Labs show Na 130 mmol/L, Cr 1.8 mg/dL (from 1.1 mg/dL 6 months prior), and NT-proBNP 1,200 pg/mL. ECG in clinic shows sinus rhythm and a nonspecific IVCD with QRS 116 ms. Her most recent TTE shows biventricular dilation with LVEF 15-20%, moderate functional MR, moderate functional TR and estimated RVSP of 40mmHg. What is the most appropriate next step in management? | | A | Refer to electrophysiology for upgrade to CRT-D | | B | Increase sacubitril-valsartan dose | | C | Refer for advanced therapies evaluation | | D | Start treatment with milrinone infusion |

Answer #11

| Explanation | The correct answer is C – refer for advanced therapies evaluation.Our patient has multiple signs and symptoms of advanced heart failure including NYHA Class III-IV functional status, persistently elevated natriuretic peptides, severely reduced LVEF, evidence of end organ dysfunction, multiple hospitalizations for ADHF, edema despite escalating doses of diuretics, and progressive intolerance to GDMT. Importantly, the 2018 European Society of Cardiology revised definition of advanced HF focuses on refractory symptoms rather than cardiac function and more clearly acknowledges that advanced HF can occur in patients without severely reduced LVEF, such as in those with isolated RV dysfunction, uncorrectable valvular or congenital heart disease, and in patients with preserved and mildly reduced LVEF.In such patients with advanced heart failure, when consistent with the patient’s goals of care, timely referral for HF specialty care is recommended to review HF management and assess suitability for advanced HF therapies (eg, LVAD, cardiac transplantation, palliative care, and palliative inotropes) (Class I, LOE C-LD).Clinical indicators of advanced heart failure should prompt a possible referral to an advanced HF specialist and can be remembered by the INEEDHELP acronym:· I – IV inotropes· N – NYHA IIIb-VI or persistently elevated natriuretic peptides· E – End-organ dysfunction· E – EF ≤ 35%· D – Defibrillator shocks· H – Hospitalizations > 1 in past year· E – Edema despite escalating diuretics· L – Low systolic blood pressure (≤90) or high heart rate· P – Prognostic medication; progressive intolerance or down-titration of GDMTIt would not be appropriate to refer to EP for CRT-D upgrade as this is a Class 3 recommendation (LOE B-R) in patients with QRS duration <120 ms for no benefit.Increasing the dose of sacubitril-valsartan would not be appropriate in this setting as the patient would be likely unable to tolerate a higher dose given her complaints of lightheadedness and episodes of hypotension.Initiating treatment with IV inotropes would not be appropriate in this setting. Although the use of IV inotropes is given a Class 1 recommendation (LOE B-NR) for the treatment of cardiogenic shock, the patient described in the question stem does not meet clinical criteria for cardiogenic shock. | | Main Takeaway | Clinical indicators for advanced heart failure can be remembered by the I-Need-Help acronym, and there is a Class 1, LOE C recommendation for these patients to be referred to HF specialists for further management and assessment for advanced therapies, when consistent with the patient’s goals of care. | | Guideline Loc. | Section 8.1Tables 16-18 |

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The following question refers to Section 7.7 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by St. George’s University medical student and CardioNerds Intern Chelsea Tweneboah, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Michelle Kittleson.

Dr. Kittleson is Director of Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute, Cedars-Sinai. She is Deputy Editor of the Journal of Heart and Lung Transplantation, on Guideline Writing Committees for the American College of Cardiology (ACC)/American Heart Association, is the Co Editor-in-Chief for the ACC Heart Failure Self-Assessment Program, and on the Board of Directors for the Heart Failure Society of America. Her Clinician’s Guide to the 2022 Heart Failure guidelines, published in the Journal of Cardiac Failure, are a must-read for everyone!

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #10

| Ms. Heffpefner is a 54-year-old woman who comes to your office for a routine visit. She does report increased fatigue and dyspnea on exertion without new orthopnea or extremity edema. She was previously diagnosed with type 2 diabetes, morbid obesity, obstructive sleep apnea, and TIA. She is currently prescribed metformin 1000mg twice daily, aspirin 81mg daily, rosuvastatin 40mg nightly, and furosemide 40mg daily. In clinic, her BP is 140/85 mmHg, HR is 110/min (rhythm irregularly irregular, found to be atrial fibrillation on ECG), and BMI is 43 kg/m2. Transthoracic echo shows an LVEF of 60%, moderate LV hypertrophy, moderate LA enlargement, and grade 2 diastolic dysfunction with no significant valvulopathy. What is the best next step? | | A | Provide reassurance | | B | Refer for gastric bypass | | C | Refer for atrial fibrillation ablation | | D | Start metoprolol and apixaban |

Answer #10

| Explanation | The correct answer is D – start metoprolol and apixaban.Ms. Hefpeffner has a new diagnosis of atrial fibrillation (AF) and has a significantly elevated risk for embolic stroke based on her CHA2DS2-VASc score of 6 (hypertension, diabetes, heart failure, prior TIA, and female sex). The relationship between AF and HF is complex and they the presence of either worsens the status of the other. Managing AF in patients with HFpEF can lead to symptom improvement (Class 2a, LOR C-EO). However, large, randomized trial data are unavailable to specifically guide therapy in patients with AF and HFpEF.Generally, management of AF involves stroke prevention, rate and/or rhythm control, and lifestyle / risk-factor modification. With regards to stroke prevention, patients with chronic HF with permanent-persistent-paroxysmal AF and a CHA2DS2-VASc score of ≥2 (for men) and ≥3 (for women) should receive chronic anticoagulant therapy (Class 1, LOE A). When anticoagulation is used in chronic HF patients with AF, DOAC is recommended over warfarin in eligible patients (Class 1, LOE A).The decision for rate versus rhythm control should be individualized and reflects both patient symptoms and the likelihood of better ventricular function with sinus rhythm. For patients with HF and symptoms caused by AF, AF ablation is reasonable to improve symptoms and QOL (Class 2a, LOE B-R). However, referring for catheter ablation would be premature before first attempting rate control and instituting anticoagulation therapy.Traditionally, beta-blockers and nondihydropyridine calcium channel blockers are used as first-line agents for rate control in AF. Interestingly, a small open-label trial, RATE-AF in elderly patients with AF and symptoms of HF (mostly with preserved LVEF), compared bisoprolol to digoxin. Although the primary endpoint of quality of life at 6 months was similar between the 2 groups, several secondary QOL endpoints, functional capacity, and reduction in NT-proBNP favored digoxin at 12 months, with similar rate reductions in both groups. More side effects (such as dizziness, lethargy, and hypotension) were seen with bisoprolol than with digoxin. However, digoxin has a narrow therapeutic window and needs to be monitored more closely.Option A (provide reassurance) is inappropriate as this patient has heart failure with preserved EF, defined by signs and symptoms of HF in patients with an LVEF of 50% or more. Echocardiogram hints in this case include LV hypertrophy and diastolic dysfunction. Our patient also has comorbidities frequently associated with HFpEF such as hypertension, diabetes, OSA, and obesity. Other common comorbidities include CAD, CKD, and atrial arrhythmias. When diagnosing HFpEF, care must be taken to rule out mimicking conditions such as pulmonary hypertension or amyloidosis. A large portion of the management of HFpEF includes managing comorbid conditions such as hypertension, OSA, and atrial fibrillation. At this time, she is symptomatic with atrial fibrillation and rapid ventricular response, and warrants both rate control and stroke prophylaxis.Although gastric bypass should be considered for patients with a BMI >35 kg/m2 with comorbidities (such as HTN or diabetes) and patients with a BMI > 40 kg/m2 independent of comorbid conditions, this is not the best next step at this time. First, she should receive anticoagulation to reduce the risk of stroke and achieve better control of her HR and BP.Patients with HFpEF and hypertension should have medication titrated to attain blood pressure targets in accordance with published clinical practice guidelines to prevent morbidity (Class 1, LOE C-LD). Although the optimal BP goal and antihypertensive regimen in patient with HFpEF is not known, HFpEF trials so far have shown that RAAS antagonists including ACEi, ARB, MRA and possibly ARNi could be first-line agents to treat HTN in patients with HFpEF. Beta blockers may be used to treat hypertension in patients with a history ofMI, symptomatic CAD, or AF with rapid ventricular response. These effects need to be balanced with the potential contribution of chronotropic incompetence to exercise intolerance in some patients. | | Main Takeaway | In patients with HFpEF, the diagnosis and management of comorbidities are very important, especially the treatment of HTN (Class 1, LOE C-LD) and AF (Class 2a, LOE C-EO). | | Expert Suggestions | · What is your current framework of diagnosis and workup when you encounter a patient with HFpEF? Are there any signs and symptoms you specifically look for or any studies you usually order?· What are your thoughts on the use of digoxin for rate control of AF in patients with heart failure? | | Guideline Loc. | Section 7.7.1, Figure 12Section 10.2 |

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The following question refers to Section 7.6 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by premedical student and CardioNerds Intern Pacey Wetstein, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Nancy Sweitzer.

Dr. Sweitzer is Professor of Medicine, Vice Chair of Clinical Research for the Department of Medicine, and Director of Clinical Research for the Division of Cardiology at Washington University School of Medicine. She is the editor-in-chief of Circulation: Heart Failure. Dr. Sweitzer is a faculty mentor for this Decipher the HF Guidelines series.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #9

| Mr. Flo Zin is a 64-year-old man who comes to discuss persistent lower extremity edema and dyspnea with mild exertion. He takes amlodipine for hypertension but has no other known comorbidities. In the clinic, his heart rate is 52 bpm and blood pressure is 120/70 mmHg. Physical exam reveals mildly elevated jugular venous pulsations and 1+ bilateral lower extremity edema. Labs show an unremarkable CBC, normal renal function and electrolytes, a Hb A1c of 6.1%, and an NT-proBNP of 750 (no prior baseline available). On echocardiogram, his LVEF is 44% and nuclear stress testing was negative for inducible ischemia. What is the best next step in management? | | A | Add furosemide BID and daily metolazone | | B | Start empagliflozin and furosemide as needed | | C | Start metoprolol succinate | | D | No change to medical therapy |

Answer #9

| Explanation | The correct answer is B – start empagliflozin and furosemide as needed.The patient described here has heart failure with mildly reduced EF (HFmrEF), given LVEF in the range of 41-49%.In patients with HF who have fluid retention, diuretics are recommended to relieve congestion, improve symptoms, and prevent worsening HF (Class 1, LOE B-NR). For patients with HF and congestive symptoms, addition of a thiazide (eg, metolazone) to treatment with a loop diuretic should be reserved for patients who do not respond to moderate or high-dose loop diuretics to minimize electrolyte abnormalities (Class 1, LOE B-NR). Therefore, option A is not correct as he is only mildly congested on examination, and likely would not require such aggressive decongestive therapy, particularly with normal renal function. Adding a thiazide diuretic without first optimizing loop diuretic dosing would be premature.The EMPEROR-Preserved trial showed a significant benefit of the SGLT2i, empagliflozin, in patients with symptomatic HF, with LVEF >40% and elevated natriuretic peptides. The 21% reduction in the primary composite endpoint of time to HF hospitalization or cardiovascular death was driven mostly by a significant 29% reduction in time to HF hospitalization, with no benefit on all-cause mortality. Empagliflozin also resulted in a significant reduction in total HF hospitalizations, decrease in the slope of the eGFR decline, and a modest improvement in QOL at 52 weeks. Of note, the benefit was similar irrespective of the presence or absence of diabetes at baseline. In a subgroup of 1983 patients with LVEF 41% to 49% in EMPEROR-Preserved, empagliflozin, an SGLT2i, reduced the risk of the primary composite endpoint of cardiovascular death or hospitalization for HF. Therefore, in patients with HFmrEF, SGLT2i can be beneficial in decreasing HF hospitalizations and cardiovascular mortality (Class 2a, LOE B-R). Furthermore, by inhibiting glucose reabsorption in the kidney, they have a diuretic effect which may help ease congestion and limit loop diuretic dosing. SGLT2i are beneficial to the vast majority of cardiovascular patients but are contraindicated in patients with type 1 diabetes or prior episodes of diabetic ketoacidosis as they may cause euglycemic DKA.Option C is incorrect. Among patients with current or previous symptomatic HFmrEF (LVEF, 41%–49%), use of evidence-based beta blockers for HFrEF, ARNi, ACEi, or ARB, and MRAs may be considered to reduce the risk of HF hospitalization and cardiovascular mortality, particularly among patients with LVEF on the lower end of this spectrum (Class 2b, LOE B-NR). However, the patient’s heart rate is already low and so initiating a beta blocker would be inappropriate. Switching his calcium channel blocker to ARNi may be considered.Option D is not correct as we can help counsel him on lifestyle and medication changes which can relieve his symptoms and reduce his risk of HF hospitalizations and mortality. | | Main Takeaway | In patients with HFmrEF, diuretics are useful for decongestion and symptomatic improvement (Class 1) and there is a role for GDMT including SGLT2i (Class 2a) and BB, ARNI, ACEi/ARB, MRA (Class 2b). | | Guideline Loc. | Section 7.6.1, Figure 11 |

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The following question refers to Section 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by MedStar Washington Hospital Center cardiology hospitalist & CardioNerds Academy Graduate Dr. Luis Calderon, and then by expert faculty Dr. Gregg Fonarow.

Dr. Fonarow is the Professor of Medicine and Interim Chief of UCLA’s Division of Cardiology, Director of the Ahmanson-UCLA Cardiomyopathy Center, and Co-director of UCLA’s Preventative Cardiology Program.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #8

| Ms. Flo Zinn is a 60-year-old woman seen in cardiology clinic for follow up of her chronic HFrEF management. She has a history of stable coronary artery disease, hypertension, hypothyroidism, and recurrent urinary tract infections. She does not have a history of diabetes and recent hemoglobin A1c is 5.0%. Her current medications include carvedilol, sacubitril-valsartan, eplerenone, and atorvastatin. Her friend was recently placed on an SGLT2 inhibitor and asks if she should be considered for one as well. Which of the following is the most important consideration when deciding to start this patient on an SGLT2 inhibitor? | | A | The patient does not have a history of type 2 diabetes and so does not qualify for SGLT2 inhibitor therapy | | B | While SGLT2 inhibitors improve hospitalization rates for HFrEF, there is no evidence that they improve cardiovascular mortality | | C | Patients taking SGLT2 inhibitors tend to suffer a more rapid decline in renal function than patients not taking SGLT2 inhibitor therapy | | D | Patients may be at a higher risk for genitourinary infections if an SGLT2 inhibitor is started |

Answer #8

| Explanation | The correct answer is D – SGLT2 inhibitors have been associated with increased risk of genitourinary infections.Sodium-glucose co-transporter protein 2 (SGLT2) inhibitors have gathered a lot of press recently as the new kid on the block with respect to heart failure management. While they were initially developed as antihyperglycemic medications for treating diabetes, early cardiovascular outcomes trials showed reduced rates of heart failure hospitalization amongst study participants independent of glucose-lowering effects and irrespective of baseline heart failure status – only 10-14% of patients carried a heart failure diagnosis at baseline. This prompted trials to study the effects of SGLT2 inhibitors in patients with symptomatic chronic HFrEF who were already on guideline directed medical therapy irrespective of the presence of type 2 diabetes mellitus. The DAPA-HF and EMPEROR-Reduced trials showed that dapagliflozin and empagliflozin, respectively, both conferred statistically significant improvements in a composite of heart failure hospitalizations and cardiovascular death (Option B). Most interestingly, these effects were seen irrespective of diabetes history. In light of these findings, the 2022 HF guidelines recommend SGLT2 inhibitors in patients with chronic, symptomatic HFrEF with or without diabetes to reduce hospitalization for HF and cardiovascular mortality (Class I, LOE A).The benefits of SGLT2 inhibitors extend beyond cardiovascular health. Analyses of the DAPA-HF and EMPEROR-Reduced trials showed that patients receiving SGLT2 inhibitor therapy had fewer serious renal outcomes and slower rates of decline in eGFR than patients in the control groups.As with all medications, though, SGLT2 inhibitors must be used with an awareness of some potentially serious side effects. SGLT2 inhibitors have been associated with higher rates of genitourinary infections, potentially related to the increased glycosuria associated with sodium-glucose co-transporter 2 inhibition. Trials have shown a 2 to 4-fold increased risk of vulvovaginal candidiasis for patients on SGLT2is compared to placebo. SGLT2 inhibitor use has also been associated with bacterial urinary tract infections, Fournier’s gangrene, and euglycemic ketoacidosis. | | Main Takeaway | SGLT2 inhibitors are now a class I recommendation for patients with chronic symptomatic HFrEF regardless of whether or not they have diabetes. Although SGLT2i increased risk for genital infections, they were otherwise well tolerated in the trials. | | Guideline Loc. | Section 7.3.4 |

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The following question refers to Section 7.3.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by MedStar Washington Hospital Center cardiology hospitalist & CardioNerds Academy Graduate Dr. Luis Calderon, and then by expert faculty Dr. Robert Mentz.

Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz is a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very 2022 heart failure Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22. Welcome Dr. Mentz!

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #7

| Ms. Valarie Sartan is a 55-year-old woman with a history of HFrEF (EF 35%) and well controlled, non-insulin dependent diabetes mellitus who presents to heart failure clinic for routine follow up. She is currently being treated with metoprolol succinate 200mg daily, lisinopril 10mg daily, empagliflozin 10mg daily, and spironolactone 50mg daily. She notes stable dyspnea with moderate exertion, making it difficult to do her yardwork. On exam she is well appearing, and blood pressure is 115/70 mmHg with normal jugular venous pulsations and trace bilateral lower extremity edema. On labs, her potassium is 4.0 mmol/L and creatinine is 0.7 mg/dL with an eGFR > 60 mL/min/1.73m2. Which of the following options would be the most appropriate next step in heart failure therapy? | | A | Increase lisinopril to 40mg daily | | B | Increase spironolactone to 100mg daily | | C | Add sacubitril-valsartan to her regimen | | D | Discontinue lisinopril and start sacubitril-valsartan in 36 hours | | E | No change |

Answer #7

| Explanation | The correct answer is D – transitioning from an ACEi to an ARNi is the most appropriate next step in management. The renin-angiotensin aldosterone system (RAAS) is upregulated in patients with chronic heart failure with reduced ejection fraction (HFrEF). Blockade of the RAAS system with ACE inhibitors (ACEi), angiotensin receptor blockers (ARB), or angiotensin receptor neprilysin inhibitors (ARNi) have proven mortality benefit in these patients. The PARADIGM-HF trial compared sacubitril-valsartan (an ARNi) with enalapril in symptomatic patients with HFrEF. Patients receiving ARNi incurred a 20% relative risk reduction in the composite primary endpoint of cardiovascular death or heart failure hospitalization. Based on these results, the 2022 heart failure guidelines recommend replacing an ACEi or ARB for an ARNi in patients with chronic symptomatic HFrEF with NYHA class II or III symptoms to further reduce morbidity and mortality (Option D). This is a class I recommendation with level of evidence of B-R and is also of high economic value. Making no changes at this time would be inappropriate (Option E). While it would be reasonable to increase the dose of lisinopril to 40mg (Option A), this should be pursued only if ARNi therapy is not tolerated. Mineralocorticoid receptor antagonists (MRAs) have a class I (LOE A) recommendation in patients with HFrEF and NYHA class II to IV to reduce morbidity and mortality, provided that eGFR is >30 mL/min/1.73 m2 and serum potassium is <5.0 mEq/L, and there is careful monitoring of potassium, renal function, and diuretic dosing. However, the starting dose of spironolactone (or eplerenone) is 25 mg orally daily, increased to 50 mg daily orally after a month. Higher doses may be appropriate for other indications but are not advocated for HFrEF as the sole indication and so option B is incorrect. Guidance on starting an ARNi While switching from an ACEi to an ARNi, note that ARNi should not be administered concomitantly with ACEi or within 36 hours of the last dose of an ACEi (Class 3 for Harm, LOE B-R). This recommendation comes largely from studies of omapatrilat—a combination ACEi/neprilysin inhibitor. Patients receiving omapatrilat suffered significantly increased risk of angioedema thought secondary to dual suppression of both ACE and neprilysin leading to high concentrations of bradykinin. The current guidelines therefore recommend a washout period of at least 36 hours between the last ACEi dose and the first ARNi dose. If this patient were being transitioned from an ARB such as valsartan, then the first dose of ARNi could simply be given in lieu of the next anticipated dose of ARB. When initiating sacubitril-valsartan, it is important to monitor for signs of hypotension. With this patient’s blood pressure of 115/70 mmHg in clinic, she should have enough blood pressure room to tolerate the new medication; both PARADIGM-HF (ARNi vs ACEi in stable chronic HFrEF) and PIONEER-HF (ARNi vs ACEi in hospitalized patients with ADHF) excluded patients with SBP < 100 mmHg. That said, every patient responds differently, and anticipatory guidance should be given to anybody starting a new drug. In particular, Ms. H.F. should be counseled on symptoms that could reflect low blood pressure, such as lightheadedness or orthostatic syncope, asked to call her provider should she experience anything concerning. Laboratory follow-up should include renal function and potassium levels. ARNis should not be initiated on any patient with a history of angioedema (Class III for Harm, LOE C-LD). While this patient likely does not have this history since she is tolerating and ACEi, it is an important part of any CardioNerd’s checklist when reaching for RAAS inhibitors. | | Main Takeaway | Patients with symptomatic HFrEF who are tolerating ACEi or ARB therapy should be transitioned to ARNi therapy to further reduce morbidity and mortality. | | Expert Suggestions | * Offer tips & tricks for initiating and monitoring ARNis in the outpatient setting. * Discuss PIONEER-HF & initiation in the inpatient setting. * Discuss ACEi & ARB combination therapy. | | Guideline Loc. | Section 7.3.1 |

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CardioNerds co-founder Daniel Ambinder joins Dr. Essa Hariri, Dr. Anna Scandinaro, Dr. Beka Bekhdatze, and Dr. Ashley Kasper (Cleveland Clinic cardiology fellows) as well as Dr. Craig Parris from Ohio State University Medical Center for a walk at Edgewater Park in Cleveland, Ohio. Dr. Andrew Higgins (Crtitical Care Cardiology and Advanced HF / Transplant Cardiology at Cleveland Clinic) provides the ECPR for this episode. They discuss the following case involving a rare cause of non-ischemic cardiomyopathy. A young African American male was admitted for cardiogenic shock following an admission a month earlier for treatment resistant psychosis. He was diagnosed with medication-induced non-ischemic cardiomyopathy, which resolved with a remarkable recovery of his systolic function after discontinuation of the culprit medication, Clozapine. Episode notes were drafted by Dr. Essa Hariri. Audio editing by CardioNerds Academy Intern, student doctor Shivani Reddy.

Enjoy this case report co-published in US Cardiology Review: Clozapine-induced Cardiomyopathy: A Case Report

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Pearls – An Unusual Case of Non-ischemic Cardiomyopathy1. The diagnosis of drug-induced non-ischemic cardiomyopathy is usually one of exclusion. High clinical suspicion is needed to diagnose drug-induced cardiomyopathy. 2. Missing the culprit medication causing drug-induced cardiomyopathy could be detrimental as there is a high probability of reversing a systolic dysfunction after stopping the offending medication. 3. Clozapine is an effective medication for the treatment-resistant schizophrenia and is associated with reduced suicide risk. 4. Clozapine is reported to cause drug-induced cardiomyopathy and is more common with rapid drug titration. Clozapine is more commonly associated with myocarditis. 5. Close monitoring and vigilance are critical to preventing cardiac complications associated with initiating clozapine. 6. The management of clozapine-associated cardiomyopathy includes clozapine cessation and heart failure guideline-directed medical therapy. Show Notes – An Unusual Case of Non-ischemic CardiomyopathyWe treated a case of clozapine-associated cardiomyopathy presenting in cardiogenic shock. Drug-induced cardiomyopathy is a common yet under-recognized etiology of non-ischemic cardiomyopathy. Clozapine is an FDA-approved atypical antipsychotic medication frequently prescribed for treatment-resistant schizophrenia and the only antipsychotic agent that has been proven to significantly reduce suicide among this patient population.

However, Clozapine is reported to be associated with several forms of cardiotoxicity, including myocarditis (most common), subclinical clozapine associated cardiotoxicity, and least commonly, drug-induced cardiomyopathy. Clozapine-associated cardiomyopathy should be considered as a differential diagnosis in schizophrenic patients presenting with signs of acute heart failure.

Rapid titration of clozapine is a risk factor for clozapine-associated cardiomyopathy and clozapine-associated myocarditis. To date, there is no evidence or consensus supporting preemptive screening.According to the American Psychiatric Association, whenever clozapine-induced myocarditis or cardiomyopathy is suspected, a cardiology consult is warranted. Experts recommend, when initiating clozapine, to obtain baseline troponin, CRP, and echocardiography upon drug initiation. This is followed by daily symptom assessment and a hemodynamic assessment on every other day. A biochemical assessment of CRP and troponin levels is warranted every 7 days. The authors recommend clozapine caseation if troponin rises above twice the upper normal limit or if CRP levels exceeds 100 mg/L. Because clozapine is a highly effective medication in treating schizophrenia, close monitoring and vigilance is critical to prevent deleterious complications associated with drug cardiotoxicity. Several mechanisms have been proposed to explain the cardiotoxicities reported with clozapine. Most patients with clozapine-associated cardiotoxicity remain asymptomatic, while others may present with typical acute congestive heart failure. The most common presenting symptom was shortness of breath (60%) followed by palpitations (36%), and the main echocardiographic finding in all patients with this disease is systolic dysfunction with reduced ejection fraction.

The management of clozapine-associated cardiomyopathy includes clozapine cessation and heart failure guideline-directed medical therapy. Clozapine suspension along with conventional heart failure management have led to a significant improvement in left ventricular function. Decisions regarding resuming clozapine therapy are highly individualized and should consider weighing in the risks and benefits of treatment. Whenever clozapine is rechallenged, very close monitoring and frequent echocardiography may be warranted to prevent subsequent cardiotoxicity.

References – An Unusual Case of Non-ischemic Cardiomyopathy1. Tsao CW, Aday AW, Almarzooq ZI, et al. Heart Disease and Stroke Statistics-2022 Update: A Report from the American Heart Association. Circulation. 2022;145(8). doi:10.1161/CIR.0000000000001052

1. Heidenreich PA, Albert NM, Allen LA, et al. Forecasting the impact of heart failure in the united states a policy statement from the american heart association. Circ Heart Fail. 2013;6(3). doi:10.1161/HHF.0b013e318291329a

2. VanDyck TJ, Pinsky MR. Hemodynamic monitoring in cardiogenic shock. Curr Opin Crit Care. 2021;27(4). doi:10.1097/MCC.0000000000000838

3. Keepers GA, Fochtmann LJ, Anzia JM, et al. The American psychiatric association practice guideline for the treatment of patients with schizophrenia. American Journal of Psychiatry. 2020;177(9). doi:10.1176/appi.ajp.2020.177901

4. Hennen J, Baldessarini RJ. Suicidal risk during treatment with clozapine: A meta-analysis. Schizophr Res. 2005;73(2-3). doi:10.1016/j.schres.2004.05.015

5. Taipale H, Tanskanen A, Mehtälä J, Vattulainen P, Correll CU, Tiihonen J. 20-year follow-up study of physical morbidity and mortality in relationship to antipsychotic treatment in a nationwide cohort of 62,250 patients with schizophrenia (FIN20). World Psychiatry. 2020;19(1):61-68. doi:10.1002/wps.20699

6. Citrome L, McEvoy JP, Saklad SR. A guide to the management of clozapine-related tolerability and safety concerns. Clin Schizophr Relat Psychoses. 2016;10(3). doi:10.3371/1935-1232.10.3.163

7. Knoph KN, Morgan RJ, Palmer BA, et al. Clozapine-induced cardiomyopathy and myocarditis monitoring: A systematic review. Schizophr Res. 2018;199. doi:10.1016/j.schres.2018.03.006

8. Kanniah G, Kumar S. Clozapine associated cardiotoxicity: Issues, challenges and way forward. Asian J Psychiatr. 2020;50. doi:10.1016/j.ajp.2020.101950

9. Curto M, Girardi N, Lionetto L, Ciavarella GM, Ferracuti S, Baldessarini RJ. Systematic Review of Clozapine Cardiotoxicity. Curr Psychiatry Rep. 2016;18(7). doi:10.1007/s11920-016-0704-3

10. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019. Catheterization and Cardiovascular Interventions. 2019;94(1). doi:10.1002/ccd.28329

11. Alawami M, Wasywich C, Cicovic A, Kenedi C. A systematic review of clozapine induced cardiomyopathy. Int J Cardiol. 2014;176(2). doi:10.1016/j.ijcard.2014.07.103

12. Arzuk E, Karakuş F, Orhan H. Bioactivation of clozapine by mitochondria of the murine heart: Possible cause of cardiotoxicity. Toxicology. 2021;447. doi:10.1016/j.tox.2020.152628

13. Vaddadi KS, Soosai E, Vaddadi G. Low blood selenium concentrations in schizophrenic patients on clozapine. Br J Clin Pharmacol. 2003;55(3). doi:10.1046/j.1365-2125.2003.01773.x

14. Yost BL, Gleich GJ, Fryer AD. Ozone-induced hyperresponsiveness and blockade of M2 muscarinic receptors by eosinophil major basic protein. J Appl Physiol. 1999;87(4). doi:10.1152/jappl.1999.87.4.1272

15. Yuen JWY, Kim DD, Procyshyn RM, White RF, Honer WG, Barr AM. Clozapine-induced cardiovascular side effects and autonomic dysfunction: A systematic review. Front Neurosci. 2018;12(APR). doi:10.3389/fnins.2018.00203

16. Ronaldson KJ, Taylor AJ, Fitzgerald PB, Topliss DJ, Elsik M, McNeil JJ. Diagnostic characteristics of clozapine-induced myocarditis identified by an analysis of 38 cases and 47 controls. Journal of Clinical Psychiatry. 2010;71(8). doi:10.4088/JCP.09m05024yel

17. de Leon J, Tang YL, Baptista T, Cohen D, Schulte PFJ. Titrating clozapine amidst recommendations proposing high myocarditis risk and rapid titrations. Acta Psychiatr Scand. 2015;132(4). doi:10.1111/acps.12421

18. Ronaldson KJ, Fitzgerald PB, Taylor AJ, Topliss DJ, Wolfe R, McNeil JJ. Rapid clozapine dose titration and concomitant sodium valproate increase the risk of myocarditis with clozapine: A case-control study. Schizophr Res. 2012;141(2-3). doi:10.1016/j.schres.2012.08.018

19. Ronaldson KJ, Fitzgerald PB, Taylor AJ, Topliss DJ, McNeil JJ. A new monitoring protocol for clozapine-induced myocarditis based on an analysis of 75 cases and 94 controls. Australian and New Zealand Journal of Psychiatry. 2011;45(6). doi:10.3109/00048674.2011.572852

20. Patel RK, Moore AM, Piper S, et al. Clozapine and cardiotoxicity – A guide for psychiatrists written by cardiologists. Psychiatry Res. 2019;282. doi:10.1016/j.psychres.2019.112491

21. Cook SC, Ferguson BA, Cotes RO, Heinrich TW, Schwartz AC. Clozapine-Induced Myocarditis: Prevention and Considerations in Rechallenge. Psychosomatics. 2015;56(6). doi:10.1016/j.psym.2015.07.002

22. de Leon J, Schoretsanitis G, Smith RL, et al. An International Adult Guideline for Making Clozapine Titration Safer by Using Six Ancestry-Based Personalized Dosing Titrations, CRP, and Clozapine Levels [published correction appears in Pharmacopsychiatry. 2022 Jan 20;:]. Pharmacopsychiatry. 2022;55(2):73-86. doi:10.1055/a-1625-6388

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The following question refers to Section 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by New York Medical College medical student and CardioNerds Intern Akiva Rosenzveig, answered first by Cornell cardiology fellow and CardioNerds Ambassador Dr. Jaya Kanduri, and then by expert faculty Dr. Randall Starling.

Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #6

| Mr. D is a 50-year-old man who presented two months ago with palpations and new onset bilateral lower extremity swelling. Review of systems was negative for prior syncope. On transthoracic echocardiogram, he had an LVEF of 40% with moderate RV dilation and dysfunction. EKG showed inverted T-waves and low-amplitude signals just after the QRS in leads V1-V3. Ambulatory monitor revealed several episodes non-sustained ventricular tachycardia with a LBBB morphology.He was initiated on GDMT and underwent genetic testing that revealed 2 desmosomal gene variants associated with arrhythmogenic right ventricular cardiomyopathy (ARVC).Is the following statement true or false?“ICD implantation is inappropriate at this time because his LVEF is >35%” | | True | | False |

Answer #6

| Explanation | This statement is False. ICD implantation is reasonable to decrease sudden death in patients with genetic arrhythmogenic cardiomyopathy with high-risk features of sudden death who have an LVEF ≤45% (Class 2a, LOE B-NR).While the HF guidelines do not define high-risk features of sudden death, the 2019 HRS expert consensus statement on evaluation, risk stratification, and management of arrhythmogenic cardiomyopathy identify major and minor risk factors for ventricular arrhythmias as follows:* Major criteria: NSVT, inducibility of VT during EPS, LVEF ≤ 49%. * Minor criteria: male sex, >1000 premature ventricular contractions (PVCs)/24 hours, RV dysfunction, proband status, 2 or more desmosomal variants.

According to the HRS statement, high risk is defined as having either three major, two major and two minor, or one major and four minor risk factors for a class 2a recommendation for primary prevention ICD in this population (LOE B-NR).Based on these criteria, our patient has 2 major risk factors (NSVT & LVEF ≤ 49%), and 3 minor risk factors (male sex, RV dysfunction, and 2 desmosomal variants) for ventricular arrhythmias. Therefore, ICD implantation for primary prevention of sudden cardiac death is reasonable.Decisions around ICD implantation for primary prevention remain challenging and depend on estimated risk for SCD, co-morbidities, and patient preferences, and so should be guided by shared decision making weighing the possible benefits against the risks, especially in younger patients. | | Main Takeaway | In patients with genetic arrhythmogenic cardiomyopathy with high-risk features of sudden death with LVEF ≤ 45%, implantation of ICD is reasonable. | | Guideline Loc. | Section 7.4Also: Section 3.10 from “Towbin, J. A., McKenna, W. J., Abrams, D. J., Ackerman, M. J., Calkins, H., Darrieux, F. C. C., Daubert, J. P., de Chillou, C., DePasquale, E. C., Desai, M. Y., Estes, N. A. M., Hua, W., Indik, J. H., Ingles, J., James, C. A., John, R. M., Judge, D. P., Keegan, R., Krahn, A. D., … Zareba, W. (2019). 2019 HRS expert consensus statement on evaluation, risk stratification, and management of arrhythmogenic cardiomyopathy. Heart Rhythm, 16(11), e301–e372. https://doi.org/10.1016/j.hrthm.2019.05.007” |

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The following question refers to Section 7.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by New York Medical College medical student and CardioNerds Intern Akiva Rosenzveig, answered first by Cornell cardiology fellow and CardioNerds Ambassador Dr. Jaya Kanduri, and then by expert faculty Dr. Clyde Yancy.

Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the AHA/ACC/HFSA Heart Failure Guideline Writing Committee.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #5

| Ms. L is a 65-year-old woman with nonischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 35%, hypertension, and type 2 diabetes mellitus. She has been admitted to the hospital with decompensated heart failure (HF) twice in the last six months and admits that she struggles to understand how to take her medications and adjust her sodium intake to prevent this. Which of the following interventions has the potential to decrease the risk of rehospitalization and/or improve mortality? | | A | Access to a multidisciplinary team (physicians, nurses, pharmacists, social workers, care managers, etc) to assist with management of her HF | | B | Engaging in a mobile app aimed at improving HF self-care | | C | Vaccination against respiratory illnesses | | D | A & C |

Answer #5

| The correct answer is D – both A (access to a multidisciplinary team) and C (vaccination against respiratory illness).Choice A is correct. Multidisciplinary teams involving physicians, nurses, pharmacists, social workers, care managers, dieticians, and others, have been shown in multiple RCTs, metanalyses, and Cochrane reviews to both reduce hospital admissions and all-cause mortality. As such, it is a class I recommendation (LOE A) that patients with HF should receive care from multidisciplinary teams to facilitate the implementation of GDMT, address potential barriers to self-care, reduce the risk of subsequent rehospitalization for HF, and improve survival.Choice B is incorrect. Self-care in HF comprises treatment adherence and health maintenance behaviors. Patients with HF should learn to take medications as prescribed, restrict sodium intake, stay physically active, and get vaccinations. They also should understand how to monitor for signs and symptoms of worsening HF, and what to do in response to symptoms when they occur. Interventions focused on improving the self-care of HF patients significantly reduce hospitalizations and all-cause mortality as well as improve quality of life. Therefore, patients with HF should receive specific education and support to facilitate HF self-care in a multidisciplinary manner (Class I, LOE B-R). However, the method of delivery and education matters. Reinforcement with structured telephone support has been shown to be effective. In contrast the efficacy of mobile health-delivered educational interventions in improve self-care in patients with HF remains uncertain.Choice C is correct. In patients with HF, vaccinating against respiratory illnesses is reasonable to reduce mortality (Class 2a, LOE B-NR). For example, administration of the influenza vaccine in HF patients has been shown to reduce all-cause mortality and hospitalizations. | | Main Takeaway | Implementation of multidisciplinary care teams has been proven to reduce rehospitalization and mortality in HF patients. While education on self-care of HF patients is important, not all delivery methods have been shown to be effective. | | Guideline Loc. | Section 7.1 |

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The following question refers to Section 4.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Baylor University cardiology fellow and CardioNerds FIT Trialist Dr. Shiva Patlolla, and then by expert faculty Dr. Eldrin Lewis.

Dr. Lewis is an Advanced Heart Failure and Transplant Cardiologist, Professor of Medicine and Chief of the Division of Cardiovascular Medicine at Stanford University.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #4

| Mr. Stevens is a 55-year-old man who presents with progressively worsening dyspnea on exertion for the past 2 weeks. He has associated paroxysmal nocturnal dyspnea, intermittent exertional chest pressure, and bilateral lower extremity edema. Otherwise, Mr. Stevens does not have any medical history and does not take any medications. Which of the following will be helpful for diagnosis at this time? | | A | Detailed history and physical examination | | B | Chest x-ray | | C | Blood workup including CBC, CMP, NT proBNP | | D | 12-lead ECG | | E | All of the above |

Answer #4

| The correct answer is E – All of the above. Mr. Stevens presents with signs and symptoms of volume overload concerning for new onset heart failure. The history and physical exam remain the cornerstone in the assessment of patients with HF. Not only is the H&P valuable for identifying the presence of heart failure but also may provide hints about the degree of congestion, underlying etiology, and alternative diagnoses. As such H&P earns a Class 1 indication for a variety of reasons in patients with heart failure:1. Vital signs and evidence of clinical congestion should be assessed at each encounter to guide overall management, including adjustment of diuretics and other medications (Class 1, LOE B-NR)2. Clinical factors indicating the presence of advanced HF should be sought via the history and physical examination (Class 1, LOE B-NR)3. A 3-generation family history should be obtained or updated when assessing the cause of the cardiomyopathy to identify possible inherited disease (Class 1, LOE B-NR)4. A thorough history and physical examination should direct diagnostic strategies to uncover specific causes that may warrant disease-specific management (Class 1, LOE B-NR)5. A thorough history and physical examination should be obtained and performed to identify cardiac and noncardiac disorders, lifestyle and behavioral factors, and social determinants of health that might cause or accelerate the development or progression of HF (Class 1, LOE C-EO)Building on the H&P, laboratory evaluation provides important information about comorbidities, suitability for and adverse effects of treatments, potential causes or confounders of HF, severity and prognosis of HF, and more. As such, for patients who are diagnosed with HF, laboratory evaluation should include complete blood count, urinalysis, serum electrolytes, blood urea nitrogen, serum creatinine, glucose, lipid profile, liver function tests, iron studies, and thyroid-stimulating hormone to optimize management (Class 1, LOE C-EO). In addition, the specific cause of HF should be explored using additional laboratory testing for appropriate management (LOE 1, LOE B-NR). In patients presenting with dyspnea such as Mr. Stevens, measurement of B-type natriuretic peptide (BNP) or N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) is useful to support a diagnosis or exclusion of HF (Class 1, LOE A); and in those with chronic HF, measurements of BNP or NT-proBNP levels are recommended for risk stratification (Class 1, LOE A).In addition to bloodwork, electrocardiography is part of the routine evaluation of a patient with HF and provides important information on rhythm, heart rate, QRS morphology and duration, cause, and prognosis of HF. So for all patients with HF, a 12-lead ECG should be performed at the initial encounter to optimize management (Class 1, LOE C-EO).Imaging is essential in the diagnosis and management of heart failure. In patients with suspected or new-onset HF, or those presenting with acute decompensatedHF, a chest x-ray should be performed to assess heart size and pulmonary congestion and to detect alternative cardiac, pulmonary, and other diseases that may cause or contribute to the patient’s symptoms (Class 1, LOE C-LD). Additionally, in those with suspected or newly diagnosed HF, transthoracic echocardiography (TTE) should be performed during the initial evaluation to assess cardiac structure and function (Class 1, LOE C-LD); and when echocardiography is inadequate, alternative imaging (e.g., cardiacmagnetic resonance [CMR], cardiac computed tomography [CT], radionuclide imaging) is recommended for assessment of LVEF (Class 1, LOE C-LD). | | Main Takeaway | In patients who present with signs and symptoms of volume overload concerning for new-onset heart failure, it is essential to rule out non-cardiac causes and assess for specific underlying causes of heart failure by using detailed history and physical examination. Once heart failure diagnosis is established, further workup with laboratory testing, ECG, and non-invasive cardiac imaging is warranted to investigate the etiology of heart failure and guide further management. Special attention should be given to detection of signs and symptoms suggesting an advanced stage of disease. | | Guideline Loc. | Section 4.1 |

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The following question refers to Section 3.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by expert faculty Dr. Shelley Zieroth.

Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She is a steering committee member for PARAGLIE-HF and a PI Mentor for the CardioNerds Clinical Trials Program.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #3

| Which of the following is/are true about heart failure epidemiology?

| A | Although the absolute number of patients with HF has partly grown, the incidence of HF has decreased | | B | Non-Hispanic Black patients have the highest death rate per capita resulting from HF | | C | In patients with established HF, non-Hispanic Black patients have a higher HF hospitalization rate compared with non-Hispanic White patients | | D | In patients with established HF, non-Hispanic Black patients have a lower death rate compared with non-Hispanic White patients | | E | All of the above |

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Answer #3

| Explanation | The correct answer is “E – all of the above.”Although the absolute number of patients with HF has partly grown as a result of the increasing number of older adults, the incidence of HF has decreased. There is decreasing incidence of HFrEF and increasing incidence of HFpEF. The health and socioeconomic burden of HF is growing. Beginning in 2012, the age-adjusted death-rate per capita for HF increased for the first time in the US. HF hospitalizations have also been increasing in the US. In 2017, there were 1.2 million HF hospitalizations in the US among 924,000 patients with HF, a 26% increase compared with 2013.Non-Hispanic Black patients have the highest death rate per capita. A report examining the US population found the age-adjusted mortality rate for HF to be 92 per 100,000 individuals for non-Hispanic Black patients, 87 per 100,000 for non-Hispanic White patients, and 53 per 100,000 for Hispanic patients.Among patients with established HF, non-Hispanic Black patients experienced a higher rate of HF hospitalization and a lower rate of death than non-Hispanic White patients with HF.Hispanic patients with HF have been found to have similar or higher HF hospitalization rates and similar or lower mortality rates compared with non-Hispanic White patients.Asian/Pacific Islander patients with HF have had a similar rate of hospitalization as non-Hispanic White patients but a lower death rate.These racial and ethnic disparities warrant studies and health policy changes to address health inequity. | | Main Takeaway | Racial and ethnic disparities in death resulting from HF persist, with non-Hispanic Black patients having the highest death rate per capita, and a higher rate of HF hospitalization. Further clinical studies and health policy changes are needed to address these inequalities. | | Guideline Loc. | Section 3.1 |

Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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The following question refers to Section 6.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Mount Sinai Hospital cardiology fellow and CardioNerds FIT Trialist Dr. Jason Feinman, and then by expert faculty Dr. Mark Drazner.

Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #2A 67-year-old man with a past medical history of type 2 diabetes mellitus, hypertension, and active tobacco smoking presents to the emergency room with substernal chest pain for the past 5 hours. An electrocardiogram reveals ST segment elevations in the anterior precordial leads and he is transferred emergently to the catheterization laboratory. Coronary angiography reveals 100% occlusion of the proximal left anterior descending artery, and he is successfully treated with a drug eluting stent resulting in TIMI 3 coronary flow. Following his procedure, a transthoracic echocardiogram is performed which reveals a left ventricular ejection fraction of 35% with a hypokinetic anterior wall. Which of the following medications would be the best choice to prevent the incidence of heart failure and reduce mortality?

| A | Lisinopril | | B | Diltiazem | | C | Carvedilol | | D | Sacubitril-valsartan | | E | Both A and C |

Answer #2The correct answer is E – both lisinopril and carvedilol are appropriate to reduce the incidence of heart failure and mortality.

Evidence-based beta-blockers and ACE inhibitors both have Class 1 recommendations in patients with a recent myocardial infarction and left ventricular ejection fraction ≤ 40% to reduce the incidence of heart failure and to reduce mortality. Multiple randomized controlled trials have investigated both medications in the post myocardial infarction setting and demonstrated improved ventricular remodeling as well as benefits for mortality and development of incident heart failure.

At this time, there is not sufficient evidence to recommend ARNi over ACEi for patients with reduced LVEF following acute MI. The PARADISE-MI trial randomized a total of 5,661 patients with myocardial infarction complicated by a reduced LVEF, pulmonary congestion, or both to receive either sacubitril-valsartan (97-103mg twice daily) or ramipril (5mg twice daily). After a median follow up time of 22 months, there was no statistically significant difference in the primary outcome of cardiovascular death or incident heart failure. At this time, ARNi have not been included in the guidelines for this specific population.

Diltiazem is a non-dihydropyridine calcium channel blocker, a family of drugs with negative inotropic effects and which may be harmful in patients with depressed LVEF (Class 3: Harm, LOE C-LD).

Main Takeaway:

For patients with recent myocardial infarction and reduced left ventricular function both beta blockers and ACEi have Class 1 recommendations to reduce the incidence of heart failure and decrease mortality.

Guideline Location:

Section 6.1

Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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The CardioNerds Cardiovascular Genomics Series continues! In this episode Dr. Dan Ambinder (CardioNerds Cofounder and Interventional Cardiologist), Dr. Anjali Wagle (FIT Ambassador at Johns Hopkins) and Dr. James Sampognaro (medicine resident at Johns Hopkins Osler Medicine Residency) learn from Dr. Allison Hays (Associate Professor of Medicine, Division of Cardiology, Johns Hopkins CMR researcher and Medical […]

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