Constituents of the Arterial Wall and Atherosclerotic Plaque: An Introduction to Atherosclerosis

Coronary heart disease is the leading cause of mortality and morbidity in most industrialized countries. 1–3 The conditions known as angina, ischemic heart disease, myocardial infarction, and sudden (ischemic) cardiac death are all late and overlapping manifestations of the same underlying disease process — atherosclerosis of the coronary arteries. Put simply, atherosclerosis is the process by which portions of the inner layer of an artery become thickened with fibromuscular material and lipid, ultimately causing narrowing or occlusion of the vessel lumen. 4–6 The earlier stages of this disease process are silent, clinical symptoms usually only becoming apparent after decades of lesion progression. When advanced, atherosclerotic lesions (plaques) in the coronary artery restrict blood supply to the portion of heart muscle served by the diseased vessel, causing transient ischemic episodes that are commonly experienced as angina. Though this condition is associated with increased risk of myocardial infarction, it may, if the lesions involved are predominantly fibromuscular, persist in stable form for many years. Atherosclerotic plaques are, however, prone to fissure or rupture, especially when a soft deformable core of lipid is present, and this can precipitate thrombosis in the vessel lumen — an acute, life-threatening event that can result in unstable angina, myocardial infarction, and ventricular fibrillation. 7–9 Al though atherosclerosis is particularly prevalent in coronary arteries, it also commonly affects the aorta (especially the abdominal segment) and the carotid, cerebral, iliac, and femoral arteries, forming the underlying pathology for aneurysm and dissection of the aorta, stroke, and intermittent claudication. However, not all arteries are equally prone to disease; the renal, brachial, and pulmonary arteries, for example, are seldom seriously affected.