The results of the World Health Organization Cooperative Trial, the Coronary
Drug Project, the Coronary Primary Prevention Trial and the Helsinki Heart Study indicate that clinical expression of
coronary artery disease can be delayed with pharmacologic modification of plasma
lipoproteins. Change in
coronary artery disease can be semiquantitated by repeat arteriograms. Three randomized clinical trials indicate that rate of progression of
atherosclerosis, as defined by arteriography, can be reduced, and existing lumen obstruction decreased. Tendon
xanthomas occur in
hypercholesterolemia, and reduction in
xanthoma size with
drug therapy suggests an improved atherosclerotic disease state. The clinician has a variety of pharmacologic
therapies available. The role of
bile acid-binding resins,
fibric acid derivatives, hydroxymethylglutaryl
coenzyme A reductase inhibitors,
nicotinic acid and
antioxidants is each unique. Understanding the role of
lipoproteins in
atherosclerosis will help in selecting the most appropriate
therapy for each individual patient. Medications not designed for their
lipoprotein effects can significantly alter
lipoproteins. Medications, such as nonselective beta blockers, can alter
low-density lipoprotein (
LDL) subclass distribution with no change in
LDL cholesterol content. Such changes may eradicate part of the beneficial cardiovascular effect of beta blockade
therapy. In the future, therapeutic choices may depend in part on
lipoprotein abnormalities such as
lipoprotein (a),
apolipoprotein E
isoforms, hyperapobetalipoproteinemia,
LDL.