Another serious complication is hemorrhage into the plaque. 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. These changes result in fibrous plaques that vary in their content of lipids, smooth muscle cells, connective tissue, calcium, and vessels. population, as illustrated in Figure 19-1. Regardless of their origin, fibrous plaques undergo a variety of qualitative changes in early middle age in the U.S.

For a review of this subject, see McGill (1988). 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. 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. 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). Occlusion and resultant health effects. From McGill et al. (1963).Īted with the extent of fibrous plaques in adults (Solberg and Strong, 1983). Natural history of atherosclerosis, showing progressive arterial The major risk factors, hypercholesterolemia and hypertension, are closely associ. 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). Lesions in the arteries of young adults have many histological and chemical characteristics of fatty streaks as well as fibrous plaquesan observation suggesting a continuous progression from one type of lesion to the other (Geer et al., 1968 Katz, 1981 Stary, 1987a,b). Overall, however, evidence supports the association of fatty streaks with fibrous plaques. Young women have more extensive fatty streaks in their coronary arteries and aortas than do young men, but among adults this pattern is reversed. 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. 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. 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.

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).

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. The relationship between fatty streaks and fibrous plaques has been one of the most controversial aspects of the pathogenesis of atherosclerosis. These changes produce elevated lesions called fibrous plaques that project into the lumen and begin to disturb blood flow. 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. 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. 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). 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).

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