What initiates the pathophysiology for unstable angina and NSTEMI?

The initiation of pathophysiology for unstable angina and NSTEMI is primarily driven by atherosclerotic plaque rupture. When atherosclerotic plaques develop in the coronary arteries, they can become unstable due to various factors such as inflammation, structural changes, or stress. When the fibrous cap of the plaque ruptures, it exposes the underlying materials, including collagen and tissue factor, which trigger the coagulation cascade. This process leads to thrombosis, resulting in partial or complete obstruction of the coronary artery, thus causing decreased blood flow to the heart muscle. This reduction in blood flow can lead to ischemic symptoms associated with unstable angina and may progress to NSTEMI if myocardial injury occurs.

Other options, while relevant to cardiovascular health, do not directly initiate the pathophysiological processes for unstable angina and NSTEMI in the same way. For instance, coronary artery vasospasm can lead to transient ischemia but is less commonly associated with these specific conditions compared to plaque rupture. High levels of triglycerides and viral infections may influence overall cardiovascular risk but are not direct initiators of the acute events leading to unstable angina and NSTEMI.