Stein Evan A
Metabolic and Atherosclerosis Research Center, Cincinnati, Ohio, USA.
Am J Med. 2002 Jun 3;112 Suppl 8A:3S-9S. doi: 10.1016/s0002-9343(02)01084-7.
Low-density lipoprotein (LDL) cholesterol reduction remains the cornerstone of coronary heart disease (CHD) prevention. The most dramatic and consistent reductions in LDL cholesterol and CHD risk are achieved with statin therapy. Identification of individuals at high CHD risk is important, not only for initiating appropriate treatment and minimizing morbidity and mortality but also for optimizing the cost-effectiveness of such treatment. A simple method for identifying high-risk individuals is to identify those with preexisting atherosclerotic disease, diabetes, or familial hypercholesterolemia (FH). Treatment options for achieving LDL cholesterol goals in high-risk patients include statins, bile acid sequestrants, niacin, and plant stanols. Statin therapy should be instituted at a dose likely to result in achievement of LDL cholesterol goals based on average response; it should then be aggressively titrated if the goals are not achieved. If LDL cholesterol goals are not achieved with maximal statin therapy, combination with a bile acid sequestrant, niacin, and/or stanols should be considered. Options likely to be available in the near future include more efficacious statins with greater potential for reducing LDL cholesterol in all patients but especially in high-risk patients, such as those with FH, enabling a greater proportion to achieve LDL cholesterol goals. Other options that may soon be available as additive agents to statins to achieve greater LDL cholesterol reductions include bile acid transport inhibitors and cholesterol absorption inhibitors.
