Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

Acute Coronary Syndrome, or ACS, develops due to the buildup of lipid-laden atherosclerotic plaques within the coronary arteries.

As the atherosclerotic plaque grows, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap.

Macrophages within the plaque secrete enzymes such as matrix metalloproteinases, which degrade the extracellular matrix and weaken the fibrous cap.

When the fibrous cap ruptures or the plaque erodes, the lipid core is exposed to the bloodstream, triggering the formation of a thrombus over the coronary lesion.

Initially, the artery may remain partially open, leading to unstable angina.

Although, if the thrombus expands and completely occludes the artery, it results in myocardial infarction. This blockage leads to ischemia, cellular injury, and eventual infarction or cell death.

Patients may present with chest pain, dyspnea, nausea, epigastric discomfort, diaphoresis, lightheadedness, fatigue, and palpitations.