What is the primary pathophysiological mechanism involved in Acute Coronary Syndrome (ACS)?

The primary pathophysiological mechanism involved in Acute Coronary Syndrome (ACS) is the disruption of coronary artery plaque leading to thrombosis and reduced blood flow. This process typically begins with the rupture of an atherosclerotic plaque within a coronary artery, causing the contents of the plaque to come into contact with the bloodstream. This triggers the coagulation cascade, resulting in the formation of a thrombus (clot) at the site of the rupture.

As the thrombus develops, it can significantly obstruct the coronary artery, leading to reduced perfusion of the heart muscle (myocardium). This reduced blood flow can result in ischemia, causing chest pain and other symptoms associated with ACS, such as shortness of breath and diaphoresis. If the blockage persists, it can lead to myocardial infarction, or heart attack, where portions of the heart muscle become necrotic due to lack of oxygen.

In contrast, while increased heart rate due to stress and anxiety can occur in patients with ACS, it is more of a compensatory response rather than a primary mechanism. Inflammation of the heart muscle is related to conditions such as myocarditis rather than being a direct cause of ACS. Lastly, spasms of coronary arteries may cause temporary