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Plaque Rupture and Thrombosis

The rupture of the plaque's fibrous cap probably reflects an imbalance between the forces that impinge on the plaque's cap and the mechanical strength of the fibrous cap. Interstitial forms of collagen provide most of the biomechanical resistance to disruption to the fibrous cap. Hence, the metabolism of collagen probably participates in regulating the propensity of a plaque to rupture (Fig. 38-15). Factors that decrease collagen synthesis by SMCs can impair their ability to repair and maintain the plaque's fibrous cap. For example, on the one hand the T cell–derived cytokine interferon gamma potently inhibits SMC collagen synthesis. On the other hand, as already noted, certain mediators released from platelet granules during activation can increase SMC collagen synthesis, tending to reinforce the fibrous structure of the plaque. Such mediators include TGF–β and PDGF.

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In addition to reduced de novo collagen synthesis by SMCs, increased catabolism of the …