Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

Acute coronary syndrome develops due to buildup of lipid-laden atherosclerotic plaques within coronary arteries. As plaques grow, they become unstable with a lipid-rich core and thin fibrous cap. Macrophages secrete enzymes like matrix metalloproteinases that degrade the extracellular matrix, weakening the fibrous cap and triggering plaque rupture or erosion.

When the fibrous cap ruptures or erodes, the lipid core exposes to the bloodstream, triggering platelet activation and the coagulation cascade. A thrombus forms over the coronary lesion. If the clot partially occludes the artery, unstable angina develops; complete occlusion results in myocardial infarction with ischemia and cellular death.

Unstable angina occurs when plaque rupture causes partial artery occlusion, allowing some blood flow and creating a thrombus that does not completely block the vessel. Myocardial infarction results from complete coronary artery occlusion by an extensive thrombus, causing ischemia, cellular injury, and necrosis of myocardial tissue supplied by that artery.

Patients with ACS present with crushing, pressure-like chest pain radiating to the jaw, arm, shoulder, or back. Additional manifestations include dyspnea, diaphoresis, nausea, palpitations, fatigue, lightheadedness, and syncope. These symptoms result from impaired oxygen delivery, sympathetic activation, and reduced cerebral perfusion caused by coronary obstruction.

Unstable angina shows ST-segment depression or T-wave inversions without ST elevation or Q waves. Non-ST elevation myocardial infarction displays ST depression and T-wave inversions with elevated cardiac biomarkers. ST elevation myocardial infarction shows ST elevation in at least two contiguous leads, new-onset left bundle branch block, and eventual Q wave development indicating myocardial necrosis.

During myocardial infarction, an imbalance develops between myocardial oxygen supply and demand. Complete coronary artery occlusion deprives myocardial cells of oxygen, causing ischemia. This oxygen deprivation leads to cellular injury and infarction over minutes to hours, resulting in necrosis of myocardium supplied by the blocked artery.

Macrophages within atherosclerotic plaques secrete enzymes such as matrix metalloproteinases that degrade the extracellular matrix surrounding the plaque. This enzymatic degradation weakens the fibrous cap, making the plaque unstable and prone to rupture. Plaque rupture exposes the lipid core to blood, triggering thrombus formation and acute coronary events.