PEDIATRIC GENESIS OF ATHEROSCLEROSIS
Atherosclerosis results from a variety of pathophysiologic disturbances, some currently recognized, and many undoubtedly not yet recognized, which in aggregate are identified as risk factors. Genetic and environmental influences conjointly affect the incidence and the severity of these risk factors and, thus, coronary heart disease (CHD) risk. Prophylaxis should be designed to prevent or retard the development of arterial plaques. This suggests that diagnostic and preventive efforts should begin in childhood. Eating habits are also probably established in childhood, allowing their early modification.
The atherosclerotic plaque appears to have its genesis in childhood. The data from wartime autopsies confirm the presence of mature atherosclerotic lesions by the end of the second decade and emphasize the importance of primary atherosclerosis prevention beginning in the first and second decades.
While there are clearly genetic factors in CHD, variation in rates in differing geographic areas appears less likely to be related to genetic than to environmental differences. Marked differences in plasma cholesterol levels are found in children in different geographic areas, generally paralleling pediatric cholesterol and saturated fat intake and the incidence of adult coronary heart disease. The relationships of elevated total plasma cholesterol levels to the incidence of coronary heart disease are clearly established in adults.
Pravastatin reduces total mortality in patients with coronary heart disease and average cholesterol levels: relationship of baseline cholesterol and treatment effects in the LIPID trial
