The pathogenesis of coronary plaques, thromboses, and hemorrhages: an evaluative review.
The initial appearance and continuous development of a coronary plaque depends on a combination of hemodynamic trauma, deposition of excess cholesterol, and accretion and incorporation of thrombogenic elements as well as fully formed mural thrombi. Plaques become life-threatening when rupture of their intimal surface due to internal necrosis and calcification leads to acute thrombosis and/or intramural hemorrhage. Although infarcts can and do occur in the absence of acute thrombi, the latter are caused not by the occurrence of infarcts, but almost always by plaque rupture. Following the occurrence of and survival from an acute occlusive coronary thrombosis, canalization of the thrombus frequently takes place, leading to the formation of a "luminal collateral vascularization." The vessels making up such complexes are prone in turn to hemorrhage and thrombosis.[1]References
- The pathogenesis of coronary plaques, thromboses, and hemorrhages: an evaluative review. Friedman, M. Circulation (1975) [Pubmed]
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