Coronary atherosclerosis may lead towards thrombogenesis, usually triggered by rupture or erosion of a vulnerable epicardial coronary artery plaque. Most acute coronary syndromes are caused by ruptured atherosclerotic plaques with superimposed thrombus. Following rupture of the fibrous cap covering the atherosclerotic plaque the thrombogenic material in the core of the plaque becomes exposed to the arterial lumen. This causes platelet aggregation and the formation of thrombus. A clinical asymptomatic scenario may follow due to thrombotic sealing of the rupture. In ST-elevation myocardial infarction (STEMI) red thrombus formation often leads to acute vessel occlusion, whereas in non-ST-elevation myocardial infarction (NSTEMI) a non-occluding (mural) platelet-rich thrombus is formed.
1 Intermittent obstruction of flow may be present because the coronary thrombosis consisting of platelet aggregates is unstable and the thrombus waxes and wanes. At this point lesion site constituents may embolise into the microcirculation.
2 Formation of a fibrin network stabilises the white platelet-rich thrombus as platelet aggregation continues, sometimes leading to occlusion of the epicardial vessel lumen. Persisting alternation of flow, in combination with (partial) obstruction at the lesion site, may result in blood coagulation proximal and/or distal to the plaque rupture that may induce red thrombus formation. …
