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Endothelial dysfunction warrants continued mechanistic study in atherosclerosis; leaves open targeted interventions pending higher-level evidence.
Cardiovascular disease accounts for considerable mortality and morbidity in Western countries. Most of the common forms of cardiovascular disease, such as atherosclerosis, are caused by functional and structural changes in the blood-vessel wall. These changes include abnormal vasoconstriction, enhanced interaction of blood cells with the vessel wall, activation of coagulation mechanisms, and migration and proliferation of vascular smooth-muscle cells13. Depending on the stage and location of the disease, one or more of these factors predominate. These vascular abnormalities have an important role in the pathogenesis of angina pectoris, myocardial infarction, stroke, and vascular forms of renal failure.A . . .
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Thomas F. Lüscher (1994) studied this question.
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