Abstract
OVER THE LAST 30 years, several epidemiological studies have reported a direct relationship between total plasma cholesterol and low-density lipoprotein cholesterol (LDL-C) concentrations and the risk of coronary artery disease (CAD),1,2 and elevated total plasma cholesterol levels are considered by many to be the main cause of coronary atherosclerosis. However, the ability to adequately identify individuals at high risk for the development of CAD solely on the basis of total cholesterol or LDL-C concentration has recently been challenged by evidence suggesting that a considerable proportion of patients with CAD may have cholesterol levels in the normal range (Genest et al3 reported the proportion to be as high as 50%).4 There are also data to suggest that a notable proportion of patients undergoing cholesterol-lowering therapy and who achieve significant LDL-C reduction may still develop CAD.5 These observations have emphasized the need to find additional markers of risk that would allow a more refined identification of individuals at high risk for CAD.