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National Research Council (US) Committee on Diet and Health. Diet and Health: Implications for Reducing Chronic Disease Risk. Washington (DC): National Academies Press (US); 1989.
Atherosclerosis is the pathological process in the coronary arteries, cerebral arteries, iliac and femoral arteries, and aorta that is responsible for coronary heart disease (CHD), stroke, and peripheral arterial disease (PAD). It begins during childhood in the intima of the large elastic and muscular arteries with deposits of lipids, principally cholesterol and its esters, in macrophages and smooth muscle cells (Figure 19-1). The lesions, called fatty streaks, produce only minimal intimal thickening and cause no disturbances in blood flow during early childhood, but they rapidly become more extensive during adolescence. In young adults, more lipid is deposited at some sites, and a core of lipid and necrotic debris becomes covered by a cap of smooth muscle and fibrous tissue. These changes produce elevated lesions called fibrous plaques that project into the lumen and begin to disturb blood flow.
Natural history of atherosclerosis, showing progressive arterial occlusion and resultant health effects. From McGill et al. (1963).
The relationship between fatty streaks and fibrous plaques has been one of the most controversial aspects of the pathogenesis of atherosclerosis. The coronary arteries differ from most other arteries by having a prominent intimal layer of longitudinal smooth muscle and fibrous tissue that is apparent even in childhood. By the age of 20, the thickness of this layer is about equal to that of the media, even when it does not contain abnormal lipid (Stary, 1987a,b). This fibromuscular intimal layer occurs in all populations, even in those not predisposed to coronary atherosclerosis in adulthood (Geer et al., 1968) and is considered to be a normal anatomic structure rather than an atherosclerotic lesion.
Some evidence suggests that fibrous plaques are created by cellular proliferation and subsequent fatty degeneration without prior lipid deposition (Benditt, 1974), and some observations are not consistent with the progression of fatty streaks to fibrous plaques. For example, fatty streaks are more extensive in the thoracic aortas of children, but fibrous plaques are more extensive in the abdominal aortas of adults. Young women have more extensive fatty streaks in their coronary arteries and aortas than do young men, but among adults this pattern is reversed. (McGill, 1968).
Overall, however, evidence supports the association of fatty streaks with fibrous plaques. Lesions in the arteries of young adults have many histological and chemical characteristics of fatty streaks as well as fibrous plaques—an observation suggesting a continuous progression from one type of lesion to the other (Geer et al., 1968; Katz, 1981; Stary, 1987a,b). Furthermore, in contrast to the differences in location of fatty streaks and fibrous plaques in the aorta, the sites of fatty streaks in the coronary arteries of children are the most common sites of fibrous plaques in adults (Montenegro and Eggen, 1968). The major risk factors, hypercholesterolemia and hypertension, are closely associated 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.
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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 controlling respiration or to cerebral edema. The necrotic tissue is converted to a liquid-filled cavity. Function is usually recovered to some degree as edema subsides, but neurons do not regenerate. Neural control of muscles and sensory organs may be regained in part as other pathways are developed. If the arterial occlusion is partial or temporary, temporary functional cerebral impairment may occur for a few minutes to a few hours (transient ischemic attacks). These episodes, which are analogous to angina pectoris, indicate that the patient has a high risk of developing cerebral infarction.
Another type of stroke is cerebral hemorrhage, which includes intracerebral hemorrhage (bleeding into the brain) and subarachnoid hemorrhage (bleeding into the space between the arachnoid membrane and the surface of the brain). In an intracerebral hemorrhage, an artery within the brain ruptures and causes a large area of tissue destruction. Its clinical manifestations are similar to those of cerebral infarction, except that it is more rapid in onset and more likely to be fatal. This type of stroke is almost always associated with severe hypertension. Since hypertension augments cerebral atherosclerosis, it is a major risk factor for both cerebral infarction and intracerebral hemorrhage.
The rupture of an artery into the subarachnoid space is usually at the site of a developmental defect in the artery wall. Either the defect, or its rupture, or both may be enhanced by hypertension. The clinical manifestations of a subarachnoid hemorrhage are similar to those of other types of stroke.
Peripheral arterial disease (PAD) occurs when atherosclerosis and its complications in the abdominal aorta, iliac arteries, and femoral arteries produce temporary arterial insufficiency in the lower extremities upon exertion (intermittent claudication) or ischemic necrosis of the extremities (gangrene). In the abdominal aorta, weakening of the media underlying the atherosclerotic plaque leads to an aneurysm, which may become filled with a thrombus or rupture into the abdominal cavity.
The major risk factors associated with clinically manifest atherosclerotic diseases also are associated with the severity of atherosclerosis. In particular, LDL cholesterol levels are positively correlated with fibrous plaques and other advanced lesions, and high-density lipoprotein (HDL) cholesterol levels are inversely associated with advanced lesions (Solberg and Strong, 1983). Hypertension is more closely associated with advanced atherosclerosis in the cerebral arteries than in other arteries, a selective effect consistent with the identification of hypertension as the dominant risk factor for stroke. Cigarette smoking is associated with advanced atherosclerosis of the abdominal aorta and iliac-femoral arteries, and consequently with PAD (DHHS, 1983). Smoking also is associated with advanced coronary atherosclerosis, but the increased coronary atherosclerosis in smokers is not sufficient to account for their much greater risk of CHD; other mechanisms, particularly thrombosis, are probably involved. Diabetes mellitus also is associated with severity of atherosclerosis in all arteries. Men have more severe coronary atherosclerosis than women, just as they have a higher frequency of CHD, but there is no sex difference in the severity of atherosclerosis of the aorta or cerebral arteries.
In populations with low serum cholesterol levels, atherosclerosis is less severe in those without hypertension and diabetes. However, among the latter, the severity of the disease is less than in populations where hyperlipidemia is prevalent (Robertson and Strong, 1968). Thus, hyperlipidemia, hypertension, and diabetes are additive in their effect on atherosclerosis, just as they are additive in their effect on risk of clinical disease. There is less information about the effects of cigarette smoking among different populations, but the evidence (Keys, 1980; Robertson et al., 1977) suggests that a similar relationship exists.
CHD risk factors for which no associations with severity of atherosclerosis have been found include physical activity and obesity (Solberg and Strong, 1983). The relationship of other putative risk factors to the severity of atherosclerosis has not been determined.
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Results of animal experiments are consistent with observations in humans. LDL cholesterol and HDL cholesterol levels, and the ratio of the two lipoprotein cholesterol concentrations to one another are highly predictive of lesions in laboratory animals. High blood pressure combined with hyperlipidemia accelerates experimentally induced atherosclerosis. Despite several attempts, no effect of cigarette smoking on experimentally induced atherosclerosis has been demonstrated (Rogers et al., 1988).
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