A. Rupture of the Plaque
Uneven thinning and fracture or fissuring of the plaque’s fibrous cap leads to rupture. The porridge-like substances exposed to the flowing blood are highly thrombogenic and trigger thrombosis that blocks the lumen of the artery. This is the main underlying cause of a myocardial infarct (see Fig. 2). Fracture of the fibrous cap occurs often at the shoulders of a lipid-rich plaque where macrophages enter. The processes and mechanisms that underlie thin¬ning fracture and rupture of plaques are unclear, and they are presently a subject of extensive research.
The provision of durable collagenous tissue processed by smooth muscle cells is important in maintaining the existence of the plaque’s fibrous cap. Collagen provides most of the biomechanical resistance to disruption of the fibrous cap. Substances found in degranulating platelets appear to increase smooth muscle cell collagen synthesis that may reinforce the strength and viability of the fibrous cap. Additionally, in some lesions there is a marked decrease in the presence of smooth muscle cells or increased smooth muscle cell death within the plaque occurs, and this reduces collagen production. It is possible that the new capillaries and vessels within the plaque may be important for the survival of smooth muscle cells. Thus, angiogenesis may be hazardous.

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