Acceleration of atherosclerosis by abnormalities in thrombosis and fibrinolysis associated with diabetes mellitus

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Abstract

A high prevalence and rapid progression of atherosclerosis are seen in patients with diabetes mellitus and are likely related, in part, to disorders of thrombosis and fibrinolysis. Increased propensity for thrombosis and impaired fibrinolysis may accelerate atherosclerosis by favoring exuberant thrombosis in response to atherosclerotic plaque rupture. Vessel wall expression of plasminogen activators and their inhibitor, plasminogen activator inhibitor type 1 (PAl-1), may potentiate atherosclerotic plaque rupture, migration of smooth muscle cells and macrophages, and accumulation of extracellular matrix. Blood from patients with diabetes is prothrombotic because of increased platelet reactivity and increased concentrations of fibrinogen and von Willebrand factor. Hypofibrinolysis is secondary to overexpression of PAI-1 by hepatic, arterial, and adipose tissue in response to hyperinsulinemia associated also with hypertriglyceridernia. Therapy that reduces insulin resistance and hence the concentration of insulin in blood improves fibrinolytic capacity by reducing PAI-1.

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