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‘Late STEMI’ – How acute is the coronary occlusion? | ECG Cases

10 patients presented with potentially ischemic symptoms. Which had a coronary occlusion, and how acute were they?

Case 1: 70yo with a prior MI, presents with 3 hours epigastric pain. Normal vitals

Case 2: 70yo, no prior MI, with two days of back pain and vomiting. Normal vitals.

Case 3: 50yo with 2 days intermittent chest pain, currently mild. Normal vitals

Case 4: 80yo with chest pain 5 days ago, ongoing weakness, then syncopal episode. HR 110 BP 100/60

Case 5: 75yo history COPD presenting with one month shortness of breath on exertion worse over one week. Currently asymptomatic with normal vitals. Old then new ECG:

Case 6: 70yo one week on/off chest pain, sent for stress test and found to have ST elevation. EMS treated with ASA and nitro took to cath lab, painfree on arrival. ECG from stress test and cath lab:

Case 7: 70yo no history of MI, with one hour of constant chest pain, shortness of breath and nausea. Old then new ECG.

Case 8: 65yo, no prior MI, with one week on/off chest pain, currently symptomatic. Normal vitals. Old then new ECG

Case 9: 80yo with chest pain 3 days ago and ongoing weakness. Normal vitals. Old then new ECG:

Case 10: 80yo no prior MI with 2 days of progressive shortness of breath at rest. Normal vitals. Old then new ECG:

Coronary occlusion acuity

Time is myocardium, but how can we tell the acuity of a coronary occlusion and which patients require emergent reperfusion? Traditionally the duration of occlusion is based on patient history, and reperfusion has been targeted to those meeting STEMI criteria and presenting within 12 hours of symptom onset. But symptom onset is a poor predictor of onset and extent of infarction, trials and guidelines have gone beyond the 12 hour mark, and the ECG can help determine the acuity of occlusion MI.

First of all, symptom onset does not necessarily correlate with the duration or extent of infarction: patients may present with fluctuating symptoms that make it difficult to assess onset (including ischemic equivalents like weakness, dyspnea or nausea), symptoms can be attenuated or masked by medication, an occluded artery can spontaneously reperfuse and re-occlude, and the presence of collateral circulation can help maintain perfusion. Unfortunately, the assumption that acute coronary occlusion presents with acute chest pain and without Q waves can lead to the denial of reperfusion. Even among Occlusion MIs that meet classic STEMI criteria (STEMI(+)OMI), a quarter do not receive emergent reperfusion—with the main reasons being anginal equivalents, prolonged chest pain or intermittent chest pain over days, resolved chest pain despite ongoing ECG signs of occlusion, or Q waves that are assumed to represent a completed infarct.[1-2] This doesn’t include STEMI(-)OMI who are denied reperfusion because they don’t meet STEMI criteria.

Secondly, reperfusion is still beneficial in those with resolved ischemic symptoms but ongoing ECG signs 12-48 hours after symptom onset [3] and in those with persisting symptoms up to three days (in whom duration from symptom onset does not correlate well with myocardial salvage). [4] The Occluded Artery Trial found no benefit for PCI for totally occluded arteries 3 to 28 days after symptom onset, but median time to PCI was 8 days and the trial excluded those with ongoing pain or cardiogenic shock. [5]

American guidelines call for PCI for STEMI patients <12 hours of symptom onset, 12-24 hours after symptoms onset if there is clinical and/or ECG evidence of ongoing ischemia, and in those with cardiogenic shock or acute severe heart failure regardless of time delay. [6] European guidelines do not make reference to any time cut off for PCI if there is ongoing ECG or clinical evidence of ischemia: “There is general agreement that a primary PCI strategy should also be followed for patients with symptoms lasting >12h in the presence of: 1) ECG evidence of ongoing ischemia; 2) ongoing or recurrent pain and dynamic ECG changes; and 3) ongoing or recurring pain, symptoms, and signs of heart failure, shock, or malignant arrhythmias. However, there is no consensus as to whether PCI is also beneficial in patients presenting >12h from symptom onset in the absence of clinical and/or electrocardiographic evidence of ongoing ischemia.” [7]

Thirdly, the ECG can help determine acuity. Acute coronary occlusion, in the absence of reperfusion, typically produces sequential ECG changes: hyperacute T waves, then ST elevation, then Q waves, then T wave inversion, and finally resolution of ST elevation. But Q waves can indicate early ischemia or late infarction, and T waves inversion can happen early from spontaneous reperfusion or late from prolonged infarction. The Anderson-Wilkins acuteness score combines the presence or absence of hyperacute T waves and Q waves to identify features of decreasing acuity—from hyperacute T waves without Q waves, to Q waves without hyperacute T waves. This has been found to be superior to duration of symptom onset for predicting benefit of reperfusion, in both early and late presenters.[8,9] Hyperacute T waves (relative to the preceding QRS) can also help to differentiate anterior Q waves from old MI from anterior Q waves with acute MI—in order to avoid unnecessary cath lab activation for those with old MIs with persisting ST elevation (LV aneurysm morphology), and avoid delayed cath lab activation for those with acute MIs with Q waves. If one lead in V1-4 has a ratio of T wave amplitude to QRS amplitude of >0.36, this predicts acute anterior MI. If it is less than 0.36 it is either old, or a subacute MI whose hyperacute T waves have diminished over time. [10,11]

Back to the cases

Case 1: acute symptoms but ECG evidence of old LV aneurysm morphology, false positive

  • Heart rate/rhythm: sinus bradycardia
  • Electrical conduction: normal
  • Axis: right axis from lateral Q waves
  • R-wave progression: late from anterior Q waves
  • Tall/small voltages: normal voltages
  • ST/T changes: mild anterior T waves with proportionally small and inverted T waves, with T/QRS< 0.36

Impression: acute symptoms with old LV aneurysm morphology. Had the cath lab activated but ECG was similar to prior, troponin was negative and there were no occlusive lesions on angiography.

Case 2: subacute symptoms with late STEMI(-)OMI, delayed diagnosis

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: late R wave progression from anterior Q waves
  • T: normal voltages
  • S: anterolateral convex ST segments with T wave inversion

Impression: subacute symptoms with subacute MI which has progressed to Q waves + T wave inversion. When Trop I returned at 29,000 (normal <26), patient was given aspirin/heparin and referred to cardiology as NSTEMI. Cardiology activated the cath lab: 100% proximal LAD occlusion. Door-to-balloon time of 3 hours, peak trop 50,000. Discharge ECG had ongoing anterior QS wave and deeper anterior T wave inversion:

Case 3: intermittent symptoms with Q waves but still acute, STEMI(+)OMI, early diagnosis

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: late R wave-progression from anterior Q wave
  • T: normal voltage
  • S: anterior ST elevation with hyperacute T waves

Impression: STEMI(+)OMI with Q waves but still significant ST elevation and hyperacute T waves. Treated with aspirin/ticagrelor/heparin and cath lab activated, with ECG-to-Activation time of 20 minutes. Repeat ECG before cath showed terminal T wave inversion from the start of reperfusion:

Cath: 95% mid LAD occlusion. First trop I was 6,000 and peak 50,000. Discharge ECG had ongoing QS waves with persisting ST elevation but now deep reperfusion T wave inversions:

Case 4: subacute symptoms with subacute STEMI(+)OMI, rapid diagnosis

  • H: sinus tach
  • E: normal conduction
  • A: left axis from LAFB
  • R: late R wave progression from anterior Q waves
  • T: normal voltages
  • S: anterolateral ST elevation with hyperacute T waves, T/QRS>0.36 in V3

Impression: subacute anterolateral STEMI(+)OMI with Q waves but also ongoing hyperacute T waves, and tachycardia concerning for cardiogenic shock. Direct from EMS to cath lab: 99% proximal LAD occlusion, Trop I rise from 17,000 to 46,000. EF 25%. Next day T waves diminished (below), ongoing tachycardia from cardiogenic shock, then cardiac arrest.

Case 5: subacute symptoms with reperfused occlusion, STEMI(-)NOMI

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltage
  • S: anterolateral T wave inversion

Impression: resolved symptoms, no Q waves, and anterolateral T wave inversion (i.e. Wellens’ syndrome). First trop 100. Treated with aspirin and referred to cardiology as reperfused occlusion, but given subacute presentation without chest pain and history of COPD was referred to Medicine as noncardiac shortness of breath. Eventually had angiogram showing 90% proximal LAD occlusion. Discharge ECG was the same.

Case 6: STEMI (+)OMI, transiently reperfused, with rapid diagnosis

  • H: borderline sinus brady
  • E: normal conduction
  • A: left axis with inferior Q
  • R: poor R wave progression with acute loss of lateral R waves
  • T: normal voltage
  • S: first ECG inferolateral ST elevation and anterior ST depression, second ECG resolution of ST segments with new inferolateral loss of R waves and T wave inversion

Impression: inferoposterolateral STEMI(+)OMI with reperfusion but not before loss of R waves. 99% circumflex occlusion, first trop 30,000. Discharge ECG had ongoing inferior Q waves.

Case 7: acute symptoms but subacute STEMI(+)OMI on ECG, delayed diagnosis

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltage
  • S: inferior Q + convex ST + T wave inversion, with reciprocal ST depression in aVL

Impression: acute ongoing symptoms but ECG suggesting subacute MI. Delayed diagnosis with ECG-to-Activation time of 60 minutes: 100% RCA occlusion, first trop 50,000.

Case 8: subacute symptoms with acute findings of STEMI(-)OMI, rapid diagnosis

  • H: sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltage
  • S: mild concave ST elevation with hyperacute T and terminal T wave inversion in III/aVF, with reciprcocal ST depression and T wave inversion in aVL, and anterior ST depression in V2; Q wave in III

Impression: inferoposterior STEMI(-)OMI. Treated with ASA/ticagrelor/heparin and cath lab activated, with ECG-to-Activation time of 6 minutes. Terminal T wave inversion suggests partial reperfusion at the time of the ECG, but by the time of angiography there was 100% RCA occlusion. First Trop I was 1,500 and peak 19,000. Discharge ECG had resolution of ST segment and full T wave inversion:

Case 9: resolved chest pain but ongoing ECG evidence of STEMI(+)OMI

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: tall R waves in V1
  • T: normal voltage
  • S: inferior Q + STE + hyperacute T wave, with reciprocal ST depression and T wave inversion in aVL

Impression: resolved symptoms but ongoing inferoposterior STEMI(+)OMI ECG. Treated with ASA/ticagrelor/heparin and cath lab activated: 100% circumflex occlusion. Trop I rise from 32,000 to 40,000. Discharge ECG had ongoing inferoposterior Q waves and normalization of T waves:

Case 10: subacute symptoms and subacute STEMI(+)OMI on ECG, delayed diagnosis and reperfusion

  • H: normal sinus
  • E: normal conduction
  • A: left axis from interior Q wave
  • R: tall R wave in V1-2
  • T: normal voltage
  • S: inferolateral Q +STE + hyperacute T waves, and anterior tall R + ST depression

Impression: subacute inferoposterolateral STEMI(+)OMI with ongoing symptoms and ongoing hyperacute T waves. Initially not thought to be acute coronary occlusion because of lack of chest pain. When trop I returned at 6,500, patients was treated with aspirin/Plavix/heparin and referred to cardiology. Admitted as “missed STEMI” based on Q waves. Next day patient had ongoing symptoms and dynamic ECG changes, with increased lateral ST elevation and anterior ST depression, with troponin rise to 8,500:

Cath lab activated: 100% circumflex occlusion. Discharge ECG had ongoing inferoposterolateral Q+ STE, but with T wave inversion:

Take home points for Late STEMI: how acute is the coronary occlusion?

  1. Refractory ischemia, ongoing ECG signs of acute coronary occlusion, or cardiogenic shock are indications for reperfusion regardless of the onset of symptoms
  2. Q waves can be acute, especially with ST elevation and hyperacute T waves, and the T/QRS ratio can differentiate between old and acute anterior MI
  3. T wave inversion can be a sign of reperfusion (resolved symptoms) or refractory ischemia (ongoing symptoms)

References for “ECG Cases 25: ‘Late STEMI’: how acute is the coronary occlusion?”

  1. Tricomi AJ, Magid D, Rumsfeld JS, et al. Missed opportunities for reperfusion therapy for ST-segment elevation myocardial infarction: results of the Emergency Department Quality in Myocardial Infarction (EDQMI) study. Am Heart J 2008 Mar;155(3):471-7.
  2. Welsh RC, Deckert-Sookram J, Sookram S, et al. Evaluating clinical reason and rationale for not delivering reperfusion therapy in ST elevation myocardial infarction patients: insights from a comprehensive cohort. Int J Cardiol 2016 Aug 1;216:99-103.
  3. Schömig A, Mehilli J, Antoniucci D, et al. Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom onset: a randomized controlled trial. JAMA 2005 June 15;293(23):2865-2872.
  4. Busk M, Kaltoft A, Nielsen S, et al. Infarct size and myocardial salvage after primary angioplasty in patients presenting with symptoms for <12 h vs. 12-72 h. Eur Heart J 2009 June;30(11):1322-1330.
  5. Hochman JS, Gervasio L, Buller CE, et al. Coronary intervention for persistent occlusion after myocardial infarction. NEJM 2006;355:2395-2407
  6. 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 Jan 29;127(4):e362-425.
  7. 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 8;39(2):119-177.
  8. Sejersten M, Ripa RS, Maynard C, et al. Timing of ischemic onset estimated from the electrocardriogram is better than historical timing for predicting outcome after reperfusion therapy for acute anterior myocardial infarction: A DANish trial in Acute Myocardial Infarction 2 (DANAMI-2) substudy. Am Heart J 20070;154:61.e1-61.e.8.
  9. Kahhri Y, Busk M, Schoos MM, et al. Evaluation of acute ischemia in pre-procedure ECG predicts myocardial salvage after primary PCI in STEMI patients with symptoms > 12 hours. J of Electrocardiol 2016;49:278-283.
  10. Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J of Emerg Med 2005;23:279-287.
  11. 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.

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