Figure 7.

Complex lesions and thrombosis. Vulnerable plaques with thin fibrous caps result from degradation of matrix by various proteinases such as collagenases, gelatinases, stromolysin and cathepsins and by inhibition of matrix secretion. Among various factors that may destabilize plaques and promote thrombosis are infection, which may have systemic effects such as induction of acute phase proteins and local effects such as increased expression of tissue factor and decreased expression of plasminogen activator (PA). The calcification of lesions appears to be an active, regulated process involving the secretion by pericyte-like cells in the intima of a scaffold for calcium phosphate deposition. The formation of a thrombus, consisting of adherent platelets and fibrin crosslinks, usually results from plaque rupture, exposing tissue factor in the necrotic core.