Elevated low-density lipoprotein cholesterol (LDL-C) is a major cause of coronary heart disease (CHD). The higher the LDL-C level, the greater the risk of CHD.1 While 17% to 73% of treated patients meet their target LDL-C levels, those at greatest risk rarely do.2 The Adult Treatment Panel III (ATP III) has set aggressive guidelines and goals.3
TREATMENT GOALS
The ATP III's target levels correlate with the patient's short- and long-term risk for CHD and are as follows: less than 100 mg/dL in those with CHD or CHD risk equivalents, less than 130 mg/dL in those with multiple (2+) risk factors, and less than 160 mg/dL in those with one or no risk factors.4
CHD or CHD risk equivalents In this risk group, patients are divided into 3 subcategories: LDL 130 mg/dL or higher, LDL 100 to 129 mg/dL, and LDL less than 100 mg/dL. In the 130 mg/dL or greater subgroup, therapeutic lifestyle changes (TLC) should be initiated at 100 mg/dL or greater, and LDL-lowering drugs should be started with dietary therapy. In the 100 to 129 mg/dL subcategory, TLC should generally be initiated at 100 mg/dL or greater. In the less than 100 mg/dL subgroup, TLC should be started instead of drug therapy. These recommendations also apply to patients who have a 10-year risk for CHD of greater than 20%.4
Multiple (2+) risk factors In patients who have a 10-year risk greater than 20%, TLC should be initiated at LDL levels of 100 mg/dL or greater; drug therapy is the same as in patients with CHD and CHD risk equivalents. In patients with a 10-year risk of 10% to 20%, TLC should be initiated at 130 mg/dL or greater and drug therapy should be considered at 130 mg/dL or greater. In patients with a 10-year risk less than 10%, TLC should be initiated at 130 mg/dL or greater and drug therapy should be considered at 160 mg/dL or greater.4
Zero or one risk factor TLC should be initiated at 160 mg/dL or greater and drug therapy should be considered at 190 mg/dL or greater. Most patients with 0 or 1 risk factor have a 10% or less 10-year risk for CHD. After dietary therapy, drug therapy is optional for patients who reach goal level.4
LDL-LOWERING DRUGS
The major classes of drugs used to lower LDL-C are 1) HMG CoA reductase inhibitors (statins), including lovastatin (Altocor, Altoprev, Mevacor, generics), pravastatin (Pravachol, generics), simvastatin (Zocor, generics), fluvastatin (Lescol, Lescol XL), and atorvastatin (Lipitor); 2) bile acid sequestrants, including cholestyramine, colestipol (Colestid, generics), and colesevelam (WelChol); 3) nicotinic acid, including crystalline, time-release preparations, and niacin (Niaspan, Niacor); and 4) fibric acid derivatives (fibrates), including gemfibrozil (Lopid, generics), and fenofibrate (generics).4
The ATP III recommends HMG CoA reductase inhibitors as first-line therapy when LDL-lowering drugs are indicated.5 Bile acid sequestrants can be used in persons with moderate elevations in LDL-C levels, in younger persons or women considering pregnancy with elevated LDL-C levels, for persons needing only modest reductions in their LDL-C levels, and for combination therapy with statins in patients with very high LDL-C levels.5
Nicotinic acid can be used in patients who are high risk for CHD with atherogenic dyslipidemia (AD); who have AD with no substantial increase in their LDL-C levels; and as adjunct therapy in patients with AD and elevated LDL-C levels. Nicotinic acid should be used cautiously in individuals with active liver disease, recent peptic ulcer, hyperuricemia and gout, and type 2 diabetes. Fibrates should be used to lower triglyceride levels in patients with dysbetalipoproteinemia; in patients with CHD and low levels of LDL-C and AD; and as additive therapy with statins in patients who have elevated LDL-C levels and AD.5
Abnormal blood lipids must be treated to goal, a lifelong process that includes primary and secondary prevention. Treatment to goal improves cardiovascular and cerebrovascular morbidity and mortality.5 JAAPA
Mary Hewett is an assistant professor in the PA program, Medical University of South Carolina, Charleston, and the department editor for When the Patient Asks. The author has indicated no relationships to disclose relating to the content of this article.
REFERENCES
1. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA. 1986;256(20):2823-2828.
2. Pearson TA, Laurora I, Chu H, Kafonek S. The lipid treatment assessment project (L-TAP): a multicenter survey to evaluate the percentages of dyslipidemic patients receiving lipid-lowering therapy and achieving low-density lipoprotein cholesterol goals. Arch Intern Med. 2000;160(4):459-467.
3. Davidson MH. A symposium: National Cholesterol Education Program Adult Treatment Panel III: Impact and implementation of the new guidelines. Introduction. Am J Cardiol. 2002;
89(5A):1C-2C.
4. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285(19):2486-2497.
5. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106(25):3143-3421.
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