In this ECG Cases blog we discover an approach to patients who present with acute chest pain through 10 cases and examine false positive STEMI, false negative STEMI as well as other causes.

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. May 2023

10 patients presented with chest pain. How would you interpret the ECG and manage the patient?

Case 1: 70 year old with acute chest pain

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Case 2: 90 year old with acute chest pain

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Case 3: 50 year old with chest pain and vomiting

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Case 4: 35 year old with exertional chest pain, now resolved

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Case 5: 75 year old previously healthy with 24 hours of chest pain

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Case 6: 35 year old with chest pain, brought by EMS as Code STEMI

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Case 7: 30 year old with chest pain

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Case 8: 30 year old with pleuritic chest pain

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Case 9: 55 year old with sudden 10/10 chest pain

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Case 10: 65 year old with acute chest pain

An Approach to ECG interpretation in patients with chest pain

The STEMI paradigm helped reorganize emergency departments to prioritize the early acquisition of ECGs in patients presenting with chest pain. But the greater challenge is correctly interpreting the ECG to identify acute coronary occlusion (whether it meets STEMI criteria or not), differentiate it from mimics, and consider other life-threatening causes of chest pain.

  1. Identify Occlusion MI, false negative STEMI and false positive STEMI

Citing the work of emergency physicians [1], the new 2022 American College of Cardiology expert consensus on the evaluation of patients with chest pain highlights the limits of STEMI criteria and evidence-based advances in ECG interpretation: “The application of STEMI ECG criteria on a standard 12-lead ECG alone will miss a significant minority of patients who have acute coronary occlusion. Therefore, the ECG should be closely examined for subtle changes that may represent initial ECG signs of vessel occlusion.” [2]

Subtle ECG findings that may indicate acute vessel occlusion:

They note that ST elevation in aVR with diffuse ST depression is a high risk but nonspecific finding, with 10% caused by OMI but others from triple vessel disease or non-cardiac shock states.

OMI often presents with acute and ongoing chest pain (or anginal equivalent), but there are other presentations to consider when correlating ECG changes to symptoms. Patients with acute but resolved chest pain and biphasic or inverted T wave (like Wellens syndrome), can indicate a spontaneously reperfused artery at risk for reocclusion. While Q waves can indicate old infarct, they can also be seen in acute or prolonged occlusion that still needs reperfusion.

All these cases of OMI, including false negative STEMI, need to be differentiated from false positive STEMI – like LVH, early repolarization, or benign T wave inversion.

  1. Consider other causes of chest pain

The ECG can also help consider other life-threatening causes of chest pain, either by the presence or absence of changes. Patients with ECG signs of acute RV strain can raise suspicion of pulmonary embolism (though PE without RV strain can present with a normal ECG), while patients with sudden and severe chest pain with nonspecific changes or just baseline LVH might raise suspicion for aortic dissection (though OMI is still more likely).

On the other hand, pericarditis is a diagnosis of exclusion – excluding more dangerous causes of chest pain, complications of pericarditis, or normal variant ST elevation.

Back to the cases

Case 1: 70 year old with acute chest pain. STEMI(-)OMI with deWinter T waves

  • Heart rate/rhythm: sinus bradycardia
  • Electrical conduction: normal conduction
  • Axis: normal axis
  • R-wave progression: loss of R waves V2-3
  • Tall/small voltages: normal voltages
  • ST/T: deWinter T waves (upsloping ST depression with hyperacute T waves) across precordium, with reciprocal inferior ST depression

Impression: STEMI(-)OMI from LAD occlusion. Cath lab activated: 99% mid LAD occlusion. First trop 15 (normal <16 in females and <26 in males) and peak 130,000 ng/L. Discharge ECG showed ongoing loss of anterior R waves, with anterolateral reperfusion T wave inversion:

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Case 2: 90 year old with acute chest pain. Posterior STEMI(-)OMI

  • H: normal sinus
  • E: incomplete RBBB
  • A: normal axis
  • R: early R wave from incomplete RBBB
  • T: normal voltages
  • S: anterior STD/TWI which is secondary to incomplete RBBB in V1-2, but primary ischemic in V3, associated with subtle inferolateral hyperacute T waves

Impression: subtle infero-postero-lateral STEMI(-)OMI. 15 lead ECG showed minimal posterior ST elevation but also less anterior ST depression and smaller infero/lateral T waves (so dynamic):

Stat cardiology consult: cath lab activation. Mid circumflex 99% occlusion, first trop 50 and peak 30,000 ng/L. Discharge ECG showed normalization of ST/T waves, Q wave in III and tall R wave in V2:

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Case 3: 50 year old with chest pain and vomiting. LBBB with posterior OMI

  • H: sinus bradycardia
  • E: LBBB
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltages
  • S: concordant ST depression V2-3

Impression: bradycardia and anterior ST depression from posterior Occlusion MI. Referred to cardiology as “non-STEMI” with troponin 8,000 ng/L. Cath lab activated: 100% RCA occlusion, peak troponin 10,000 ng/L. Discharge ECG had normalization of anterior ST segments:

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Case 4: 35 year old with exertional chest pain, now resolved. Wellens syndrome from spontaneous LAD reperfusion

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltages
  • S: biphasic T wave inversion V2-4

Impression: resolved chest pain with preserved R wave, normal voltage and primary T wave inversion in anterior leads = Wellens syndrome. First trop 70 ng/L. Admitted for angiogram: 80% LAD stenosis, peak troponin 170 ng/L. Repeat ECG had evolution of reperfusion T wave inversion:

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Case 5: 75 year old previously healthy with 24 hours of chest pain. Subacute wraparound STEMI(+)LAD occlusion

  • H: normal sinus rhythm
  • E: normal conduction
  • A: left axis from inferior Q waves
  • R: loss of R waves from anterior Q waves
  • T: normal voltages
  • S: anterior and inferior ST elevation with upright T waves

Impression: prolonged chest pain with Q waves and persisting ST elevation and upright T waves from ongoing occlusion. Cath lab activated: 99% mid LAD occlusion. First troponin 45,000 and peak 165,000 ng/L. Discharge ECG had resolution of inferior Q waves, ongoing anterior Q waves, and convex ST elevation with terminal T wave inversion:

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Case 6: 35 year old with chest pain, brought by EMS as Code STEMI. Early repolarization, false positive STEMI

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltages
  • S: mild concave ST elevation proportional to voltage, with J waves and normal T waves

Impression: early repolarization. Cath lab cancelled, troponins negative, discharged home.

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Case 7: 30 year old with chest pain. Apical hypertrophic cardiomyopathy

  • H: normal sinus rhythm
  • E: normal conductin
  • A: normal axis
  • R: normal R wave progression
  • T: tall voltages from LVH
  • S: secondary ST depression and T wave inversion, discordant and proportional to large R waves, in apical distribution

Impression: apical hypertrophic cardiomyopathy, confirmed on echo. Troponins normal.

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Case 8: 30 year old with pleuritic chest pain. Acute RV strain from PE

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltages
  • S: primary antero-inferior T wave inversion

Impression: pleuritic chest pain with acute RV strain. Troponin 800 ng/L and D-Dimer positive, CTPA showed bilateral PE.

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Case 9: 55 year old with sudden 10/10 chest pain. LVH with sudden severe chest pain from aortic dissection

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: tall voltages from LVH
  • S: secondary repolarization abnormalities

Impression: sudden severe chest pain with ECG only showing LVH. CT chest: aortic dissection

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Case 10: 65 year old with acute chest pain. STEMI(+)OMI from proximal LAD occlusion

  • H: normal sinus
  • E: normal intervals
  • A: normal axis
  • R: early R wave progression
  • T: normal voltages
  • S: anterior hyperacute T waves, anterolateral ST elevation with inferior reciprocal ST depression

Impression: proximal LAD occlusion, with hyperacute T waves and inferior reciprocal change that exclude both early repolarization and pericarditis. Initially misinterpreted as myo/pericarditis, with first troponin mildly elevated at 100ng/L. Repeat ECG done a few hours later:

Loss of precordial R waves with ongoing ST elevation and hyperacute T waves. Cath lab activated: 100% proximal LAD occlusion, peak troponin 100,000 ng/L. Post-cath ECG showed ongoing ST elevation and start of T wave inversion:

Take home points for ECG interpretation in patients with chest pain

  • STEMI criteria are limited: look for other signs of Occlusion MI including hyperacute T waves, de Winter T waves, posterior Occlusion MI, LBBB with Modified Sgarbossa Criteria
  • Correlate the ECG with symptoms including resolved chest pain with reperfusion T wave inversion, or subacute pain with new Q waves
  • Beware false positive STEMI including LVH and early repolarization
  • The ECG can sometimes identify RV strain in PE, is usually nonspecific in aortic dissection, and is a diagnosis of exclusion in pericarditis

References for ECG Cases 42: ECG interpretation in patients with chest pain

  1. Meyers HP, Bracey A, Lee D, et al. Comparison of the ST-elevation myocardial infarction (STEMI) vs NSTEMI and Occlusion MI (OMI) vs NOMI paradigms of acute MI. J Emerg Med 2021;60:273-284
  2. Kontos MC, de Lemos JA, Deitelzweig SB, et al. 2022 ACC expert consensus decision pathway on the evaluation and disposition of acute chest pain in the emergency department: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol 2022 Nov, 80(20): 1925-1960