For more than 50 years, it has been known that atherosclerosis begins
in childhood and progresses through adolescence and young adulthood to cause
coronary heart disease (CHD) in middle age and later.1 Although
previously considered an inevitable consequence of aging, atherosclerosis
is now thought to be caused by a number of genetic-environmental interactions.
Risk factors, including intervening variables (eg, elevated levels of low-density
lipoprotein cholesterol [LDL-C]) and environmental exposures (eg, cigarette
smoking) predict the incidence of CHD in adulthood and are associated with
advanced atherosclerotic lesions. A vast body of knowledge about the molecular
and cellular biology of atherosclerosis now provides plausible mechanisms
for a causal relationship among risk factors, atherogenesis, and clinical
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