A 58-year-old man with diabetes and hypertension presents to the emergency department with acute severe substernal chest pain and diaphoresis. His blood pressure is 88/54 mmHg, heart rate 112/min, and respiratory rate 28/min. Physical examination reveals an S3 gallop and bilateral crackles at the lung bases. The 12-lead ECG shows the pattern marked **C** in the diagram: ST-segment elevation in lead aVR (2 mm) and lead V1 (1.5 mm), with diffuse ST-segment depression in leads I, II, III, V4, V5, and V6. Troponin I is markedly elevated at 4.2 ng/mL. Which of the following coronary pathologies is MOST likely to produce this ECG pattern and clinical presentation?
A. Isolated proximal left anterior descending artery occlusion with preserved left main flow
B. Acute right ventricular infarction secondary to right coronary artery occlusion
C. Acute pericarditis with fibrinous inflammation and diffuse epicardial injury
D. Left main coronary artery occlusion or critical stenosis causing global subendocardial ischemia
Explanation
Why "Left main coronary artery occlusion or critical stenosis causing global subendocardial ischemia" is right
The ECG pattern marked C — ST-segment elevation in lead aVR (and V1) with diffuse ST-segment depression in 6 or more leads (I, II, III, V4–V6) — is the hallmark of left main coronary artery (LMCA) occlusion or critical stenosis, or severe three-vessel disease. The mechanism is global subendocardial ischemia: the widespread subendocardial injury current produces ST depression in the lateral and inferior leads, and the reciprocal vector (pointing toward the right shoulder) generates ST elevation in aVR. The magnitude of aVR ST elevation (≥1 mm) correlates with severity and strongly favors LMCA/3VD. This pattern is now classified as a "STEMI equivalent" by the 2021 ACC/AHA guidelines and mandates emergent coronary angiography. The clinical context — hemodynamic shock, S3 gallop, pulmonary edema, and markedly elevated troponin — is consistent with acute LMCA/3VD occlusion causing cardiogenic shock and global myocardial ischemia (Harrison 21e Ch 269; 2021 ACC/AHA Chest Pain Guidelines).
Why each distractor is wrong
Isolated proximal left anterior descending artery occlusion with preserved left main flow: Proximal LAD occlusion produces ST elevation in the anterior and lateral leads (V1–V4, I, aVL) with reciprocal ST depression in the inferior leads (II, III, aVF), but does NOT typically produce the diffuse, global pattern of ST depression across 6+ leads or the characteristic aVR ST elevation > V1 ST elevation. When V1 ST elevation exceeds aVR ST elevation, LAD occlusion is favored, but the reverse pattern (aVR > V1) points to LMCA.
Acute right ventricular infarction secondary to right coronary artery occlusion: RV infarction produces ST elevation in the right precordial leads (V3R, V4R) and inferior leads (II, III, aVF) with reciprocal ST depression in V1–V2 and I, aVL. It does NOT produce the diffuse, global ST depression pattern across lateral and anterior leads, nor does it characteristically elevate ST in aVR. The hemodynamic picture (hypotension with elevated JVP and clear lungs) also differs from LMCA shock.
Acute pericarditis with fibrinous inflammation and diffuse epicardial injury: Pericarditis (pattern D) produces diffuse, concave ST-segment elevation across multiple leads (I, II, III, aVL, aVF, V2–V6) WITHOUT reciprocal ST depression in aVR. The PR segment is typically depressed. Pericarditis presents with pleuritic chest pain, pericardial friction rub, and normal or mildly elevated troponin, not the acute hemodynamic collapse and markedly elevated troponin seen in LMCA occlusion.
High-YieldNEET PG
aVR ST elevation ≥1 mm + diffuse ST depression in ≥6 leads = LMCA/3VD until proven otherwise; emergent cath-lab activation required.
Harrison 21e Ch 269; 2021 ACC/AHA Chest Pain Guidelines
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