Arteriosclerosis characterized by irregularly distributed lipid deposits in the intima of large and medium-sized arteries, causing narrowing of arterial lumens and proceeding eventually to fibrosis and calcification. Lesions are usually focal and progress slowly and intermittently. Limitation of blood flow accounts for most clinical manifestations, which vary with the distribution and severity of lesions. In lower animals, atherosclerosis of swine and fowl closely resemble human atherosclerosis. Syn: nodular sclerosis.
Atherosclerosis, the most common form of arteriosclerosis, is a complex process that begins with the appearance of cholesterol-laden macrophages (foam cells) in the intima of an artery. Current theories view atherosclerosis as an inflammatory rather than a degenerative process. It is more likely to begin at areas of vascular turbulence, and biochemical mediators of inflammation are increasingly recognized as markers of atherosclerosis. Smooth muscle cells respond to the presence of lipid by proliferating, under the influence of platelet factors. Circulating monocytes and lymphocytes adhere to the intimal surface and penetrate the endothelium to mediate a local inflammatory process. A plaque forms at the site consisting of fibroblasts, leukocytes, and further deposition of lipid. In time, the plaque becomes fibrotic and may calcify. Expansion of an atherosclerotic plaque leads to gradually increasing obstruction of the artery and ischemia of tissues supplied by it. Ulceration, thrombosis, or embolization of a plaque, or intimal hemorrhage and dissection, can cause more acute and severe impairment of blood flow, with the risk of infarction. These are the principal mechanisms of coronary artery disease (arteriosclerotic heart disease with or without heart failure, angina pectoris, myocardial infarction), peripheral vascular disease (particularly occlusive disease of a lower limb causing intermittent claudication or gangrene), and stroke (cerebral infarction due to occlusion of carotid or intracranial arteries). Independent risk factors for atherosclerosis are male sex, advancing age, the postmenopausal state, a family history of atherosclerosis, cigarette smoking, hypertension, diabetes mellitus, elevated plasma LDL cholesterol, elevated plasma homocysteine, overweight, and a sedentary life style. Mounting evidence suggests that a history of infection with Chlamydia pneumoniae and elevation of plasma levels of triglycerides, fasting insulin, fibrinogen, C-reactive protein, amyloid A, interleukin-6, and lipoprotein Lp(a) are also independent risk factors. The diagnosis of atherosclerosis is usually based on history and physical examination and confirmed by angiography, Doppler ultrasonography, and other imaging techniques. Treatment is largely mechanical: balloon stretching, laser ablation, or surgical removal of plaques, and various bypass and grafting procedures. The prevention of atherosclerosis is a major objective of modern medicine. Preventive measures include regular vigorous exercise, a diet low in fat and cholesterol, maintenance of a healthful weight, avoidance of tobacco, and use of pharmacologic agents as indicated for control of hypertension, diabetes mellitus, and elevated cholesterol.
Reference: Stedman's Medical Dictionary
