ABSTRACT
Lipids are essential for a normally functioning body. Cholesterol is necessary for cell wall formation and is a precursor for the formation of steroids and bile acids, while triglycerides are the body’s major energy source (1). However, lipid and lipoprotein abnormalities are also firmly linked to the development of coronary heart disease (CHD). Research studies conducted over the last 40 years have consistently demonstrated that high levels of blood cholesterol are associated with both the development and the progression of CHD. In a recent primary prevention trial, lowering cholesterol resulted in a 29% decrease in coronary events and 33% reduction in coronary deaths (2). Benefit was also evident in the AFCAPS/TexCAPS primary prevention trial. Numerous secondary prevention studies have shown that lowering blood cholesterol reduces angiographic progression of CHD, and results in a 25 to 41% decrease in coronary event rates (3) and a 27 to 54% reduction in coronary and all-cause mortality (4). In the past decade, much has also been learned about the cellular and biological effects of elevated cholesterol. High blood cholesterol alters the normal vasodilator responses of the endothelium, resulting in inappropriate vasoconstriction, enhanced platelet adhesion, and increased cell growth and proliferation (5). These cellular effects result in increased cardiac symptoms such as angina, increased plaque growth, plaque rupture, and catastrophic coronary events. The increased knowledge about the effects of elevated blood cholesterol levels has led to the conclusion that blood cholesterol is a primary and modifiable coronary risk factor.
