Diabetes is characterized by impaired fibrinolysis. This phenomenon reflects augmented concentrations of plasminogen activator inhibitor type-1 in tissues and in blood. The derangement appears to depend in part on elevated concentrations of free fatty acids, triglycerides, and insulin in association with the insulin resistance syndrome. Impaired fibrinolysis may exacerbate already existing coronary artery disease and potentiate its evolution. Several measures are available to favorably modify fibrinolytic system capacity. They include inhibition of the renin angiotensin system, attenuation of dyslipidemia, and enhancement of insulin sensitivity. Accordingly, normalization of the derangement in fibrinolysis typical of diabetes is an important and achievable therapeutic objective.