Debate over the role of hyperlipidemia in causing coronary heart disease has dominated discussion of this disease since it emerged on an epidemic scale in industrialized countries after World War II. Although many questions remain about how, the question about whether hyperlipidemia causes atherosclerosis and its sequelae (the so-called lipid hypothesis) has been settled: it does. Nearly two decades of clinical trials have confirmed predictions derived from observational epidemiology and animal experimentation that control of hyperlipidemia reduces the frequency of coronary heart disease and causes regression of coronary atherosclerosis. This knowledge is now modifying public health and clinical medical practice.1
See also p 289.
However, continued investigation discloses new aspects of this disease. A few years ago, lipoprotein (a) was a laboratory curiosity of uncertain significance; now, its similarity to plasminogen suggests that it may predispose to coronary heart disease by augmenting thrombosis.2 The discovery of oxidized low-density