Abstract
In spite of recent advances in diagnosis and treatment, coronary artery disease and cerebral artery disease continue to be the leading causes of mortality and morbidity in the United States (Scharf and Harker, 1987; Lenfant, 1999). More than 1 million people had heart attacks last year in the U.S. and one-third of them died from their first heart attack (Lenfant, 1999). Thus there is considerable interest in the prevention of coronary and cerebral artery disease. The underlying pathogenesis of these problems is atherosclerotic vascular disease. This is marked by the chronic silent evolution of atheromas over many years, from as early as age 10 up to ages 40–50 years. Then an acute thrombotic phase appears with plaque rupture, the onset of unstable angina, and fatal or nonfatal myocardial or cerebral infarction (Scharf and Harker, 1987; Loscalzo, 1990; Ross, 1986).