The burden of atherosclerotic coronary heart disease (CHD) is tremendous—both genes and environment contribute to this problem. From a clinical perspective, physicians are well aware of the importance of genetic lipid abnormalities in the causation of CHD.1 The best studied genetic lipid abnormality is familial hypercholesterolemia (FH), which can cause clinical findings such as xanthomas, early atherosclerosis, and premature CHD. Approximately 1 out of 500 of the population are FH heterozygotes and 1 out of 1 000 000 are homozgotes.2 It has been estimated that FH accounts for approximately 6% of CHD on a population basis.3
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