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 CHD.