Four diverse mechanisms cause acute coronary syndromes

(A) Plaque rupture, also referred to as fissure, traditionally considered the dominant substrate for ACS, usually associates with both local inflammation, as depicted by the blue monocytes, and systemic inflammation, as indicated by the gauge showing an increase in blood C-reactive protein (CRP; measured with a high-sensitivity [hsCRP] assay).
(B) In some cases, plaque rupture complicates atheromata that do not harbor large collections of intimal macrophages, as identified by optical coherence tomography criteria, and do not associate with elevations in circulating CRP. Plaque rupture usually provokes the formation of fibrin-rich red thrombi.
(C) Plaque erosion appears to account for a growing portion of ACS, often provoking non-ST-segment-elevation myocardial infarction. The thrombi overlying patches of intimal erosion generally exhibit characteristics of white platelet-rich structures.
(D) Vasospasm can also cause ACS, long recognized as a phenomenon in the epicardial arteries but also affecting coronary microcirculation.