Abstract

The accelerated development of atherothrombotic cardiovascular disease in type 2 diabetes mellitus may be enhanced by the presence of a prothrombotic state. This prothrombotic state includes a diminished fibrinolytic capacity and an increased coagulability. Impaired fibrinolytic capacity appears to be a hallmark of the metabolic syndrome of type 2 diabetes and can be a direct consequence of visceral obesity. In addition, a chronic low inflammatory state with hyperinsulinemia and dyslipidemia may further influence the hemostatic balance. The characteristic dyslipidemia of type 2 diabetes, coined the atherogenic lipoprotein profile, with raised plasma levels of fasting and postprandial triglyceride lipoproteins, atherogenic low-density lipoproteins, and low high-density lipoproteins, is involved in promoting a hypercoagulable state. Lifestyle and pharmacologic interventions that reduce cardiovascular risk in the general population and that may improve the metabolic syndrome may also reduce the prothrombotic state.

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