ECG Cases 41 – STEMI, Occlusion MI Complications

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 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 complications

STEMI 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:

1. Myocardial dysfunction (acute or subacute):
   • LV dysfunction, including LV aneurysm and LV thrombus requiring anticoagulation
   • RV infarct with inferior STEMI, requiring fluids rather than nitro
2. Heart failure (acute or subacute)
   • Pulmonary congestion requiring oxygen, diuretics, +/- nitro
   • Cardiogenic shock requiring inotropes and treatment of underlying cause(s)
3. Dysrhythmias and conduction disturbances (acute)
   • Bradycardia/block: inferior STEMI can cause AV block that responds to atropine, anterior STEMI can cause infranodal block requiring pacing
   • Tachycardia: atrial fibrillation which may or may not require treatment, or VF/VT (often polymorphic) requiring defibrillation
4. Mechanical complications (subacute) requiring emergency surgery
   • Including free wall rupture with tamponade
   • Ventricular septal rupture
   • Papillary muscle rupture with acute mitral regurgitation, associated with posterolateral STEMI
5. Pericarditis (early or late) and pericardial effusion

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.

2. If there’s Occlusion MI, is there a complication that changes management?

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 complications

10 patients presented with potentially ischemic symptoms. Which had an acute coronary occlusion, 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. False STEMI from tachy-arrhythmia

• Heart rate/rhythm: atrial fibrillation with rapid ventricular response
• Electrical conduction: incomplete RBBB
• Axis: borderline right axis
• R-wave progression: normal R wave progression
• Tall/small voltages: normal voltages
• ST/T changes: diffuse ST depression with reciprocal STE-aVR

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 3: 70 year old, prior Occlusion MI, with 3 hours of epigastric pain, normal vitals except bradycardia. False STEMI from old LV aneurysm morphology

• H: sinus bradycardia
• E: normal conduction
• A: right axis from lateral Q
• R: poor R wave progression, anterior QS waves
• T: normal voltages
• S: anterolateral mild convex ST elevation with shallow and inverted T waves

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: 65 year old with one hour of chest pain, HR 45 and BP 150, other vitals normal Bradycardia from inferior STEMI(-)OMI, followed by AIVR post-reperfusion

• Heart rate/rhythm: sinus bradycardia
• Electrical conduction: normal intervals
• Axis: normal
• R-wave progression: normal
• Tall/small voltages: normal
• ST/T: mild straight ST elevation in III with reciprocal TWI in aVL and ST depression in V2

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: 55 year old with acute chest pain and diaphoresis. Acute RBBB/LAFB from proximal LAD occlusion

• H: sinus tachycardia (biphasic P waves in V1)
• E: intermittent RBBB
• A: left axis from LAFB
• R: anterior Q waves
• T: normal voltages
• S: massive anterolateral ST elevation (concordant to RBBB in the anterior leads) and inferior reciprocal ST depression

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: 75 year old admitted with anterior STEMI. First ECG 5 days after admission, and then rhythm strips during episode of unresponsiveness. Polymorphic VT with normal QT, from recurring ischemia

• H: first ECG normal sinus, next developed polymorphic VT
• E: normal conduction including normal QT
• A: normal axis
• R: loss of R waves from anterior infarct
• T: low limb lead voltages
• S: first ECG convex ST and shall inverted T waves, but pseudonormalized prior to VT

Impression: from LAD reperfusion to polymorphic VT (with normal QT) suggesting reocclusion. Treated with defibrillation and amiodarone.

Case 7: 70 year old previously well, with one week shortness of breath, acutely worse. HR 150, BP 180/110, RR 32, oxygen 80%. LAD occlusion with tachycardia from hemodynamic instability

• H: sinus tach
• E: normal conduction
• A: left axis from inferior Q waves
• R: poor R wave progression, anterior QS waves
• T: normal voltages
• S: mild anterior ST elevation and upright T waves

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: 80 year old, chest pain 2 days prior, presenting with right sided weakness and dysarthria. Cardioembolic stroke with apical thrombus from subacute LAD occlusion

• H: normal sinus
• E: normal conduction
• A: normal axis
• R: loss of anterior R waves, anterior QS waves
  
• T: normal voltages
• S: anterolateral ST elevation and hyperacute T wave, with inferior reciprocal ST depression

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: 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. Infero-postero-lateral STEMI(-)OMI with cardiogenic shock from papillary muscle rupture

• H: initial sinus tach
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: normal voltages
• S: subtle inferior ST elevation with reciprocal STD/TWI in I/aVL, STD V2-4, and STE in V6

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: 60 year old, 2 months post-CABG, with shoulder pain. Old then new ECG. Possible post-CABG pericarditis vs early repolarization

• H: normal sinus
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: normal voltages
• S: mild new inferolateral concave STE without reciprocal change in aVL (making inferior OMI less likely), but also with more prominent J waves

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 complications

1. 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

1. Damluji AA, van Dipen S, Katz JN, et al. Mechanical complications of acute myocardial infarction: a scientific statement from the American Heart Association
2. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018 Jan 7;39(2): 119-177
3. Trostel S, Meyers HP, McLaren J, et al. Sinus tachycardia is rare among hemodynamically stable patients with Occlusion Myocardial Infarction. Ann Emerg Med 2022 Oct;80(4):S115-116
4. Harhash AA, Huang JJ, Reddy S, et al. aVR ST segment elevation: acute STEMI or not? Incidence of an acute coronary occlusion. Am J Med 2019, 132(5):622-630
5. Klein LR, Shroff GR, Beeman W, et al. Electrocardiographic criteria to differentiate acute anterior ST-elevation myocardial infarction from left ventricular aneurysm. Am J Emerg Med 2015;33:786-790
6. Widimsky P, ROhac F, Stasek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J 2012 Jan;33(1):86-95
7. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:e362-e425
8. Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA Guidelines for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction: Executive Summary and Recommendations. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). Circ 2000;102:1193-1209