How Epicardial Coronary Artery Occlusion Causes ST-Segment Elevation Myocardial Infarction
Acute and complete occlusion of an epicardial coronary artery by a thrombus superimposed on a disrupted atherosclerotic plaque creates transmural myocardial ischemia that, when prolonged, produces ST-segment elevation on the ECG and leads to myocardial necrosis. 1
The Pathophysiologic Sequence
Plaque Disruption and Thrombotic Occlusion
The mechanism begins with rupture or erosion of an atherosclerotic plaque in the epicardial coronary artery, which triggers platelet aggregation and formation of a platelet-rich thrombus. 1 This "plaque + superimposed thrombus complex" completely occludes the coronary artery, distinguishing STEMI from NSTEMI where the thrombus is typically nonocclusive. 1
The underlying plaque vulnerability results from arterial inflammation driven by oxidized lipids and possibly infectious stimuli. 1 Activated macrophages and T lymphocytes at the plaque shoulder increase expression of metalloproteinases that thin and destabilize the fibrous cap, leading to rupture or erosion and subsequent thrombogenesis. 1
Acute Myocardial Oxygen Supply-Demand Imbalance
Complete coronary occlusion creates an acute imbalance between myocardial oxygen supply and demand. 1 Blood flow to the myocardium supplied by that epicardial vessel ceases abruptly, while oxygen demand continues. 2
Myocardial necrosis begins within 15-30 minutes of complete coronary occlusion when there is no forward or collateral flow. 3 The infarction progresses in a "wave-front phenomenon" from subendocardium to subepicardium in a time-dependent manner. 3
The Electrocardiographic Manifestation: ST-Segment Elevation
The complete occlusion produces transmural ischemia—ischemia affecting the full thickness of the myocardial wall. 2, 4 This transmural ischemia generates injury currents that manifest as ST-segment elevation on the ECG. 1
ST-segment elevation appears in leads whose positive poles are located over the ischemic region, with reciprocal ST depression in leads whose positive poles are oriented in the opposite direction. 1 This is not merely a surface phenomenon but reflects the underlying transmural nature of the ischemic injury. 1
The ECG changes are anatomically reasonable: leads should be identified by their original nomenclature (I, II, III, aVR, aVL, aVF, V1-V6) rather than labeled as "anterior" or "inferior," though reference to the anatomic location of the ischemic region based on which leads show ST-segment changes remains appropriate. 1
Critical Distinction: STEMI vs. NSTEMI
The key differentiator is the completeness of occlusion:
STEMI: Acute and complete occlusion of the epicardial coronary artery results in transmural ischemia and persistent ST-elevation on ECG (or STEMI equivalents such as hyperacute T-waves, true posterior MI, or multilead ST depression with ST-elevation in aVR). 1, 5
NSTEMI: Severely obstructive but incompletely occlusive coronary lesions produce subendocardial ischemia, characterized by absence of persistent ST elevation but rather ST depression, T-wave inversion, or nonspecific changes. 1
An important caveat: an occlusive thrombus can occasionally cause NSTEMI rather than STEMI if extensive collateral blood supply exists. 1 Recruitment of existing collaterals can occur rapidly (within hours) during acute occlusion, potentially extending the time window for myocardial salvage. 3
Clinical Implications
The time-dependent nature of myocardial necrosis makes immediate reperfusion the most effective way to limit myocardial ischemia and infarct size. 2 Primary percutaneous coronary intervention should be performed as soon as possible, ideally within 90-120 minutes of first medical contact. 5
In approximately 25-30% of patients undergoing primary PCI, the infarct-related artery is patent on initial angiography, which may reflect spontaneous lysis or collateral-supported flow. 3 This dynamic nature of thrombosis and clot lysis during acute coronary syndrome, along with collateral recruitment, contributes to variability in clinical presentations and outcomes. 3
The diagnosis requires both persistent ST-segment elevation meeting specific criteria (≥1 mm in most leads, ≥2 mm in V2-V3 for men ≥40 years, ≥2.5 mm for men <40 years, ≥1.5 mm for women in V2-V3) and cardiac biomarker elevation above the 99th percentile upper reference limit. 5