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Relationship of raised atherosclerotic lesions to fatty streaks in coronary heart disease and hypertension

1979; Elsevier BV; Volume: 33; Issue: 1 Linguagem: Inglês

10.1016/0021-9150(79)90203-x

1879-1484

Richard E. Tracy, Jack P. Strong, Vivian Toca,

Cardiovascular Disease and Adiposity

The abdominal aortas and right coronary arteries removed during autopsies were gathered from over 18,000 subjects in 19 location-race groups. Sudanstained intimal surfaces were graded for the percent as raised lesions (R) and fatty streaks (F). The proportions of all types of lesions (ATL = F + R) that were raised (RaL = R divided by ATL) were examined. The difference between the observed RaL (in subjects having atherosclerosis-related conditions) and the expected RaL (in age-, sex-, and ATL-matched subjects without such conditions) measured the excess of RaL, which by inference indicated the tendency for an excess of raised lesions to be produced in place of fatty streaks. In cases of coronary heart disease (CHD), a large excess of RaL was found consistently on the average. The coronary arteries and aortas of hypertensive subjects, compared with those of nonhypertensives, had only a small and inconsistent excess of RaL. Both CHD and hypertension were characterized by a marked tendency for severe involvement by ATL, including extensive fatty streaks, leaving only small remnants of normal intima. Some factors (Class A) act to form fatty streaks and also to continue advancing them into raised lesions. Once the fatty streaks are formed, some new factors (Class B2) convert them into raised lesions. We concluded that hypertension is almost, if not entirely, a Class A type of atherogenic agent, and that CHD is promoted by exceptionally strong effects of both A and B2 types of causation. This conclusion exposes a biological priniciple that, if the assumptions of the model are true, is of considerable importance: Some of the more important causes of atherosclerosis (Class B causes) begin to act only after the fatty streaks have formed.