A 59-year-old man presents to the emergency department because of severe chest pain that began 45 minutes ago while he was mowing his lawn. He describes crushing substernal chest pressure radiating to his left arm and jaw. The pain is associated with diaphoresis, nausea, and shortness of breath and has not improved with rest. His medical history is significant for hypertension, hyperlipidemia, and tobacco use disorder. Medications include atorvastatin and lisinopril. Temperature is 36.8°C (98.2°F), blood pressure is 148/90 mm Hg, pulse is 108/min, and respiratory rate is 22/min. He appears anxious and diaphoretic. ECG demonstrates 3-mm ST-segment elevations in leads II, III, and aVF with reciprocal ST-segment depressions in leads I and aVL. Initial high-sensitivity troponin I is mildly elevated.
Which of the following is the most likely underlying pathophysiologic mechanism of this patient’s condition?
The correct answer is:
A) Complete thrombotic occlusion of a coronary artery following plaque rupture
This patient has an acute ST-elevation myocardial infarction (STEMI). The diagnosis is supported by prolonged ischemic chest pain, autonomic symptoms such as diaphoresis and nausea, elevated cardiac biomarkers, and ST-segment elevation in contiguous leads with reciprocal ST-segment depression.
STEMI occurs when an atherosclerotic plaque ruptures, exposing thrombogenic material that triggers platelet aggregation and thrombus formation. When the thrombus completely occludes a coronary artery, blood flow to downstream myocardium is abruptly interrupted, resulting in transmural ischemia and myocardial necrosis.
The ECG findings provide important localization. ST-segment elevation in leads II, III, and aVF indicates an inferior wall myocardial infarction, most commonly involving the right coronary artery. Reciprocal ST-segment depression in leads I and aVL further supports the diagnosis.
A critical Step 2 concept is distinguishing STEMI from NSTEMI. Both conditions involve plaque rupture and myocardial necrosis, but STEMI generally results from complete coronary occlusion and produces ST-segment elevation, whereas NSTEMI usually results from incomplete occlusion and produces ST-segment depression, T-wave inversion, or a nondiagnostic ECG.
Because myocardial death progresses rapidly, STEMI requires immediate reperfusion therapy, usually with emergent percutaneous coronary intervention (PCI).
Answer choice B: Fixed coronary artery stenosis causing demand ischemia during exertion, is incorrect.
This is the mechanism of stable angina. Stable angina produces predictable exertional symptoms that resolve with rest and does not cause persistent ST-segment elevation or myocardial infarction.
Answer choice C: Inflammation of the pericardium causing epicardial irritation, is incorrect.
Acute pericarditis can cause chest pain and ST-segment elevation, but the pain is typically pleuritic and positional. Pericarditis usually causes diffuse ST-segment elevation rather than localized ST-segment elevation with reciprocal changes.
Answer choice D: Partial coronary artery occlusion causing subendocardial ischemia, is incorrect.
Partial coronary occlusion is the usual mechanism of NSTEMI and unstable angina. STEMI is generally caused by complete coronary artery occlusion producing transmural ischemia.
Answer choice E: Transient coronary vasospasm without myocardial necrosis, is incorrect.
Coronary vasospasm can cause transient ST-segment elevation during episodes of chest pain but does not typically produce the persistent symptoms, reciprocal ECG changes, and biomarker elevation seen in STEMI.
Key Learning Point
STEMI is usually caused by complete thrombotic occlusion of a coronary artery following plaque rupture. It produces transmural myocardial ischemia, ST-segment elevation on ECG, elevated cardiac biomarkers, and requires immediate reperfusion therapy.
