Atherosclerosis Là Gì

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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.quý khách đã xem: Atherosclerosis là gì

National Research Council (US) Committee on Diet và Health. Diet and Health: Implications for Reducing Chronic Disease Risk. Washington (DC): National Academies Press (US); 1989.


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Atherosclerosis is the pathological process in the coronary arteries, cerebral arteries, iliac & femoral arteries, và aorta that is responsible for coronary heart disease (CHD), stroke, và peripheral arterial disease (PAD). It begins during childhood in the intima of the large elastic and muscular arteries with deposits of lipids, principally cholesterol và its esters, in macrophages & smooth muscle cells (Figure 19-1). The lesions, called fatty streaks, produce only minimal intimal thickening và cause no disturbances in blood flow during early childhood, but they rapidly become more extensive sầu during adolescence. In young adults, more lipid is deposited at some sites, và 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 lớn the lumen & begin khổng lồ disturb blood flow.

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FIGURE 19-1

Natural history of atherosclerosis, showing progressive sầu arterial occlusion và resultant health effects. From McGill et al. (1963).

The relationship between fatty streaks & 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 và 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 lớn 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 khổng lồ fibrous plaques. For example, fatty streaks are more extensive sầu in the thoracic aortas of children, but fibrous plaques are more extensive sầu in the abdominal aortas of adults. Young women have sầu more extensive fatty streaks in their coronary arteries và aortas than vì chưng young men, but among mỏi 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 & chemical characteristics of fatty streaks as well as fibrous plaques—an observation suggesting a continuous progression from one type of lesion lớn the other (Geer et al., 1968; Katz, 1981; Stary, 1987a,b). Furthermore, in contrast to lớn the differences in location of fatty streaks và fibrous plaques in the aorta, the sites of fatty streaks in the coronary arteries of children are the most comtháng sites of fibrous plaques in adults (Montenegro and Eggene, 1968). The major risk factors, hypercholesterolemia and hypertension, are closely associated with the extent of fibrous plaques in adults (Solberg & 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 sầu into fibrous plaques. This later process occurs particularly in the coronary arteries and abdominal aorta, where some fatty streaks are gradually converted lớn fibrous plaques by continued lipid deposition and reactive sầu 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 nội dung of lipids, smooth muscle cells, connective sầu tissue, calcium, và vessels. The most serious complication is ulceration of the connective tissue và smooth muscle cap of fibrous plaque, a change that exposes blood to lớn the lipid-rich necrotic debris of the core & is likely to lớn precipitate thrombosis. Another serious complication is hemorrhage inkhổng lồ the plaque. This causes sudden swelling of the plaque và may precipitate ulceration & thrombosis.

Thrombosis overlying an advanced atherosclerotic fibrous plaque is the most comtháng sự kiện that occludes the lumen of the coronary artery & causes ischemia. At a point, determined by such factors as blood pressure, collateral circulation, & tissue oxygen demvà, the blood supply is reduced below a critical cấp độ & ischemic necrosis occurs in the tissue supplied by the affected artery.

Lesions in the coronary arteries lead lớn CHD, which is the most common và most serious manifestation of atherosclerotic cardiovascular diseases in middle-aged adults. The atherosclerotic process that occurs in the cerebral & peripheral arteries is similar to lớn that which occurs in the coronary arteries, but the lesions usually develop a decade or two later than those in the coronary arteries.

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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 laông xã of upper motor neuron function, và disturbances of speech, vision, hearing, and memory, depending on the anatomic location of the infarct. Death may occur due to lớn involvement of the brain centers controlling respiration or to lớn cerebral edema. The necrotic tissue is converted to lớn a liquid-filled cavity. Function is usually recovered khổng lồ some degree as edema subsides, but neurons bởi not regenerate. Neural control of muscles & 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 khổng lồ 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 lớn the brain) & subarachnoid hemorrhage (bleeding into lớn the space between the arachnoid membrane và 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 lớn those of cerebral infarction, except that it is more rapid in onphối và more likely to lớn 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 lớn those of other types of stroke.

Peripheral arterial disease (PAD) occurs when atherosclerosis and its complications in the abdominal aorta, iliac arteries, và 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 lớn 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 & other advanced lesions, & high-density lipoprotein (HDL) cholesterol levels are inversely associated with advanced lesions (Solberg & Strong, 1983). Hypertension is more closely associated with advanced atherosclerosis in the cerebral arteries than in other arteries, a selective sầu 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, và consequently with PAD (DHHS, 1983). Smoking also is associated with advanced coronary atherosclerosis, but the increased coronary atherosclerosis in smokers is not sufficient to lớn tài khoản 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 và diabetes. However, ahy vọng the latter, the severity of the disease is less than in populations where hyperlipidemia is prevalent (Robertson and Strong, 1968). Thus, hyperlipidemia, hypertension, & diabetes are additive sầu 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 aý muốn different populations, but the evidence (Keys, 1980; Robertson et al., 1977) suggests that a similar relationship exists.

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Results of animal experiments are consistent with observations in humans. LDL cholesterol và HDL cholesterol levels, & the ratio of the two lipoprotein cholesterol concentrations khổng lồ 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).