ated with the extent of fibrous plaques in adults (Solberg and Strong, 1983). The few relevant data indicate that there is an association between serum cholesterol and low-density lipoprotein (LDL) cholesterol concentrations with fatty streaks in childhood (Freedman et al., 1988; Newman et al., 1986). Furthermore, it seems most likely that fatty streaks in children are labile, i.e., some may regress or remain as fatty streaks whereas others progress and evolve into fibrous plaques. This later process occurs particularly in the coronary arteries and abdominal aorta, where some fatty streaks are gradually converted to fibrous plaques by continued lipid deposition and reactive chronic inflammation and repair. For a review of this subject, see McGill (1988).
Regardless of their origin, fibrous plaques undergo a variety of qualitative changes in early middle age in the U.S. population, as illustrated in Figure 19-1. These changes result in fibrous plaques that vary in their content of lipids, smooth muscle cells, connective tissue, calcium, and vessels. The most serious complication is ulceration of the connective tissue and smooth muscle cap of fibrous plaque, a change that exposes blood to the lipid-rich necrotic debris of the core and is likely to precipitate thrombosis. Another serious complication is hemorrhage into the plaque. This causes sudden swelling of the plaque and may precipitate ulceration and thrombosis.
Thrombosis overlying an advanced atherosclerotic fibrous plaque is the most common event that occludes the lumen of the coronary artery and causes ischemia. At a point, determined by such factors as blood pressure, collateral circulation, and tissue oxygen demand, the blood supply is reduced below a critical level and ischemic necrosis occurs in the tissue supplied by the affected artery.
Lesions in the coronary arteries lead to CHD, which is the most common and most serious manifestation of atherosclerotic cardiovascular diseases in middle-aged adults. The atherosclerotic process that occurs in the cerebral and peripheral arteries is similar to that which occurs in the coronary arteries, but the lesions usually develop a decade or two later than those in the coronary arteries.
In approximately one-third of all CHD cases, coronary artery occlusion causes a fatal arrhythmia within a few minutes or hours (sudden cardiac death). If the patient survives the first few hours, ischemic necrosis of the myocardium occurs (myocardial infarction). Afterward, the necrotic tissue is removed and replaced by connective tissue. The subsequent clinical outcome is determined, for the most part, by the amount and location of cardiac muscle that is lost. A few days after infarction, and before much connective tissue has formed, the heart may rupture at the site of infarction (cardiac tamponade). The patient surviving this stage may recover cardiac function as the remaining heart hypertrophies to compensate for myocardium lost by infarction. At any stage, the patient may die from failure of the heart to pump sufficient blood (congestive heart failure) or from a disturbance in the conduction system controlling the distribution of the contractile impulse (arrhythmia). Stenosis of the coronary arteries sometimes is sufficient to cause ischemic pain, but not infarction, especially on exertion (angina pectoris). This condition indicates the presence of severe lesions and high risk of myocardial infarction. All these syndromes (angina pectoris, myocardial infarction, sudden cardiac death) are included in the term coronary heart disease.
If thrombosis forms over an atherosclerotic plaque in a cerebral artery, ischemic necrosis occurs in the brain (cerebral infarct). Cerebral infarction (one type of stroke) typically causes paralysis on the contralateral side due to lack of upper motor neuron function, and disturbances of speech, vision, hearing, and memory, depending on the anatomic location of the infarct. Death may occur due to involvement of the brain centers