Smoking and the pathogenesis of atherosclerosis

Atherosclerosis begins in childhood as arterial intimal lipid deposits and progresses to occlusive arterial lesions in middle age or later. Dyslipoproteinemia, hypertension, and male sex are major risk factors for atherosclerotic disease and also contribute to atherogenesis. Tobacco smoking is well established as a contributor to atherosclerotic disease, particularly to coronary heart disease and peripheral vascular disease. Smoking augments atherosclerosis of the coronary arteries and probably also increases the risk of thrombosis independently of mural atherosclerosis. Smoking greatly augments atherosclerosis of the abdominal aorta, and is the major cause of abdominal aortic aneurysms. There are many physiologic responses of the body to tobacco smoking that may mediate its effects on atherosclerosis and atherosclerotic disease, but there is little evidence to indicate the importance of these relative to one another. We may anticipate the discovery of many smoking-genetic interactions in the future and these are likely to be helpful in resolving these questions of etiology and pathogenesis.