Lipids, clotting factors, and diabetes: endogenous risk factors for cardiovascular disease

Theories of intimal injury leading to plaque formation include platelet adhesion and production of growth factors, hypercholesterolemia, smooth muscle cell proliferation, macrophage activity, defective utilization of low-density lipoproteins via deficient receptors, and deficiency in cellular lysosomal enzymes. High levels of low-density lipoproteins and intermediate-density lipoproteins, as well as their apoproteins, are strong risk factors for cardiovascular disease. The lowering of the cholesterol level has been shown to produce significant regression of atherosclerotic lesions. Data also suggest an interaction between lipids and platelets, although the role of coagulation disorders as an independent risk factor for atherosclerosis is difficult to assess. Although much of the data are controversial, there is evidence that platelet survival time is a strong predictor of severe vessel damage. In addition, some studies have reported decreased activity of antithrombin III with coronary artery disease, and there appears to be a direct correlation between fibrinogen and cholesterol levels. Finally, diabetes mellitus (both types I and II) is a significant independent risk factor for atherosclerosis. The risk is not related to the severity or duration of diabetes, and it appears to be greater in women than in men.