Pediatric hyperlipidemia: the Cleveland Clinic experience 1979–1981

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In the United States, a middle-aged male Caucasian now has a one in five chance of developing clinical coronary heart disease before his 60th birthday,1 and a one in three chance of dying during the initial coronary attack. This is one of the highest incidences in the world.

Coronary disease may actually begin very early in life. Fatty streaks are commonly found in the intima of children the world over, even in countries with a low incidence of coronary artery disease. Progression from fatty streak to fibrous plaque has not been convincingly documented, but cross-sectional studies suggest that some fatty streaks do progress to fibrous plaques and that these changes occur in the same vessels.2 This progression suggests that atherosclerosis is a pediatric problem.

Many environmental as well as genetic factors play a role in the development of atherosclerotic lesions. Genetic predisposition to coronary heart disease, hyperlipidemia, hypertension, and smoking are the major primary risk factors.1 Secondary factors are sedentary living habits, obesity, psychosocial tension, diabetes mellitus, gout, and long-term maintenance hemodialysis for renal failure. Atherosclerotic lesions seem to be related to serum cholesterol and dietary fat when comparing populations, but this association cannot be confirmed on an individual basis.3 Since the extent of coronary atherosclerosis varies among individuals of similar race, sex, geographic location, disease, and smoking habits, other important factors must be involved.

However, if the occlusive complications leading to clinical disease can be prevented, it seems reasonable to initiate programs of prevention as early as the first . . .



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