“This learning material is sourced from Emergency Medicine Cases and has been published here with permission as per creative commons copyright”In this ECG Cases blog we look at how awareness of STEMI and Occlusion MI complications can help identify false positive STEMI and Occlusion MI that doesn’t meet STEMI criteria, and consider specific treatments…
Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. April 2023
10 patients presented with potentially ischemic symptoms. Which had an acute coronary occlusion, STEMI or Occlusion MI, what were the complications, and how would this change management?
Case 1: 75 year old with syncope and chest discomfort. HR 140 and BP 100, other vitals normal
Case 2: 75 year old, prior Occlusion MI, with one hour of chest pain and diaphoresis, HR 200 and BP 80, other vitals normal
Case 3: 70 year old, prior Occlusion MI, with 3 hours of epigastric pain, normal vitals except bradycardia
Case 4: 65 year old with one hour of chest pain, HR 45 and BP 150, other vitals normal
Case 5: 55 year old with acute chest pain and diaphoresis
Case 6: 75 year old admitted with anterior STEMI. First ECG 5 days after admission, and then rhythm strips during episode of unresponsiveness
Case 7: 70 year old previously well, with one week shortness of breath, acutely worse. HR 150, BP 180/110, RR 32, oxygen 80%
Case 8: 80 year old, chest pain 2 days prior, presenting with right sided weakness and dysarthria
Case 9: 80 year old with a few days of shortness of breath, suddenly worse. HR 110, BP 80/50, RR 36, oxygen 87%. First ECG on arrival and repeat after intubation and inotropic support.
Case 10: 60 year old, 2 months post-CABG, with shoulder pain. Old then new ECG:
5 spheres of STEMI, Occlusion MI complicationsSTEMI is associated with a variety of electrical and mechanical complications. Some are common and may resolve without specific treatment, like some bradydysrhythmias associated with inferior STEMI, whereas some are rare and life-threatening like mechanical complications requiring surgery.[1] As the European guidelines summarize[2] these can occur at different times or co-exist, and often require specific treatment in addition to reperfusion:
These complications can often be diagnosed by ECG, complemented by POCUS, but they can also complicate the diagnosis. In the ED we see patients with undifferentiated complaints, with ECG changes that may or may not reflect acute coronary occlusion. There are many causes of ST elevation besides acute coronary occlusion (false positive STEMI), and many acutely occluded coronary arteries don’t manifest STEMI criteria (false negative STEMI).
How can we use the awareness of complications to identify false positive STEMI and Occlusion MI that doesn’t meet classic STEMI criteria, and consider specific treatment?1. Is there Occlusion Myocardial Infarction (Occlusion MI)?
ST elevation may not be caused by an acute coronary occlusion. Tachycardia is rare with Occlusion MI unless complicated by hemodynamic instability.[3] On the other hand, tachycardia from non-cardiac shock states or tachydysrhythmia (including scar-mediated monomorphic VT from old MI) are common causes of diffuse ST depression with reciprocal ST elevation in aVR.[4] Similarly, prior MI can produce LV aneurysm morphology (anterior QS waves with persisting ST elevation) that can cause false positive STEMI, but can be distinguished from acute or subacute Occlusion MI by symptom duration and T/QRS ratio: anterior T/QRS ratio > 0.36 identifies acute LAD occlusion, with lower ratios reflecting either subacute presentations or old LV aneurysm morphology [5] Pericarditis can also cause ST elevation post-MI, but this is a diagnosis of exclusion.
On the other hand, patients may have Occlusion MI without meeting STEMI criteria, i.e. STEMI(-)OMI. In these cases the presence of complications can sometimes help make the diagnosis. For example, bradycardia and AV block can raise suspicion for subtle inferior Occlusion MI because they are common complications of RCA occlusion. New RBBB +LAFB can raise suspicion of proximal LAD or left main occlusion because these can cause acute bifascicular block.[6] Polymorphic VT with a normal QT is caused by acute ischemia, and AIVR is a sign of reperfusion – both of which can indicate the need for reperfusion if not done already.
Bradycardia and AV block associated with inferior Occlusion MI involves the AV node and is often transient and atropine responsive, while bradycardia or bifascicular blocks from LAD occlusion is infranodal and requires pacing. Occlusion MI accompanied by sinus tachycardia or hypotension reflects pump failure or mechanical complications, and requires identification and treatment of the underlying cause(s). Proximal RCA occlusion can produce RV infarct that requires fluids rather than nitro, and posterolateral Occlusion MI can result in papillary muscle rupture with acute MR requiring surgery. As STEMI guidelines state, cardiogenic shock is an indication for emergent revascularization regardless of time delay from symptom onset,[7] and Non-STEMI guidelines advise urgent reperfusion for refractory ischemia or hemodynamic/electrical instability even in the absence of ECG changes.[8]
Back to the cases of STEMI/OMI complications10 patients presented with potentially ischemic symptoms. Which had an acute coronary occlusion, what were the complications, and how would this change management?
Case 1: false STEMI from tachy-arrhythmia
Impression: STE-aVR reciprocal to diffuse ST depression from tachy-arrhythmia. Code STEMI was activated by there were no obstructive lesions, and ST changes resolved after patient cardioverted:
Case 2: monomorphic VT from old occlusion MI
Impression: monomorphic VT. Cardioverted back into sinus. First post-cardioversion ECG had diffuse ST depression with reciprocal ST elevation in aVR from recent tachydysrhythmia, which resolved on repeat, along with inferior Q waves from prior Occlusion MI.
Troponin I rose to a small peak of 2,000ng/L (normal <26 in males and <16 in females) from demand ischemia, and admitted for angiogram that showed chronically occluded RCA from old Occlusion MI.
Case 3: false STEMI from old LV aneurysm morphology
Impression: acute symptoms but history of old MI with chronic LV aneurysm morphology. Cath lab activated but only chronically occluded LAD. ECG was same as prior, and troponin was negative.
Case 4: bradycardia from inferior STEMI(-)OMI, followed by AIVR post-reperfusion
Impression: bradycardia from subtle inferoposterior OMI. Repeat ECG had increasing ST depression in I and V2-3:
Cath lab activated: 100% RCA occlusion. First troponin I was normal and peak 50,000 ng/L. Post-reperfusion had transient episode of AIVR, and discharge ECG had reperfusion T wave inversion inferior/lateral and posterior (tall T waves V2-3):
Case 5: acute RBBB/LAFB from proximal LAD occlusion
Impression: tachycardic with intermittent RBBB + LAFB + anterolateral STE, reflecting proximal LAD or left main occlusion with cardiogenic shock. Cath lab activated: proximal LAD occlusion. First trop Trop 85 and peak > 50,000. Post-reperfusion ECG showed resolution of bifascicular block, with anterior Q waves but persisting ST elevation and lack of reperfusion T wave inversion suggesting ongoing microvascular ischemia (no re-flow). Subsequently developed VF arrest and could not be resuscitated.
Case 6: polymorphic VT with normal QT, from recurring ischemia
Impression: from LAD reperfusion to polymorphic VT (with normal QT) suggesting reocclusion. Treated with defibrillation and amiodarone.
Case 7: LAD occlusion with tachycardia from hemodynamic instability
Impression: anterior/inferior Q waves of undetermined age, with anterior ST elevation that could be exaggerated by severe tachycardia. But patient had no prior history and presented with flash pulmonary edema, so all ECG changes could be acute. Despite oxygenation and nitro the patient went into cardiac arrest, but was resuscitated with thrombolytics and then sent to the cath lab: triple vessel disease with 95% LAD occlusion which was stented. First trop 65 and peak 37,000, with echo showing anterolateral akinesis and inferior hypokinesis, and EF 25%. Follow up ECGs showed resolution of inferior Q waves, ongoing anterior QS waves and development anterior reperfusion T wave inversion:
Case 8: cardioembolic stroke with apical thrombus from subacute LAD occlusion
Impression: proximal LAD occlusion with subacute history but ongoing hyperacute T waves (T/QRS>0.36), presenting with stroke. POCUS showed anterior regional wall motion abnormality and apical thrombus. Cath lab activated: 100% proximal LAD occlusion, first trop 22,000 and peak 50,000. Discharge ECG had resolution of hyperacute T waves, ongoing LV aneurysm morphology:
Case 9: infero-postero-lateral STEMI(-)OMI with cardiogenic shock from papillary muscle rupture
Impression: infero-postero-lateral OMI with hemodynamic instability. POCUS showed posterior wall motion abnormality and severe MR. Cath lab activated: circumflex occlusion, first trop 2,000 and peak 90,000. Echo showed severe MR with flail of posterior leaflet from papillary muscle rupture, too high risk for surgery so transitioned to comfort measures.
Case 10: possible post-CABG pericarditis vs early repolarization
Impression: possible post-CABG pericarditis (if other causes and complications ruled out) vs early repolarization. Repeat angiogram showed patent stents, serial troponin was negative, POCUS showed no pericardial effusion.
Take home points for STEMI, Occlusion MI complications1. Is there Occlusion MI? False positive STEMI include STE-aVR from tachydysrhythmias (including scar-mediated monomorphic VT) and persisting anterior STE with small T waves from LV aneurysm, while false negative STEMI include bradycardia from subtle inferior Occlusion MI or new bifascicular block from subtle LAD occlusion 2. Is there a complication that changes management? This may include pacing for bradycardia, fluids for RV infarct, surgery for MR/VSD/rupture, and reperfusion for unstable ACS regardless of time of onset or ECG changes
References for ECG Cases 41 – STEMI/OMI complications