Improvement in Current Approaches to Lipid Lowering
Am Fam Physician. 2002 Mar 1;65(5):783-787.
The National Cholesterol Education Program (NCEP) has updated its recommendations for cholesterol screening and therapeutic strategies based on coronary risk assessment.1 In this issue of American Family Physician, Safeer and Ugalat2 review the changes in the new NCEP Adult Treatment Panel III (ATP III) guidelines, which include more intensive low-density lipoprotein (LDL) cholesterol control in patients with multiple coronary risk factors, diabetes mellitus, and low levels of high-density lipoprotein (HDL) cholesterol.
These recommendations follow the recognition that a large number of persons have hyperlipidemia that warrants treatment even according to the less aggressive NCEP–ATP II goals. Last year, it was estimated that 10.4 million Americans required pharmacologic lipid modification based on the ATP II guidelines.
This number rises to 28.4 million when we include persons covered by the NCEP “clinical judgment” criteria3 and climbs to 35.6 million when we apply the new ATP III guidelines. Yet only a small minority of these persons—4.5 million—is receiving such therapy. Of particular concern is the revelation from a recent nationwide study that only 32 percent of patients hospitalized with acute myocardial infarction were discharged on cholesterol medication.4
For many patients who are prescribed lipid-lowering therapy, the treatment they are given is inadequate. For example, the Lipid Treatment Assessment Project (L-TAP)5 found that only 38 percent of patients being treated for hyperlipidemia are at NCEP LDL cholesterol target levels. The patients who were most likely to benefit were the least likely to achieve their target levels: only 37 percent of high-risk patients and 18 percent of patients with coronary heart disease reached target LDL cholesterol levels.5
The basis for this treatment gap is multifactorial and includes physician, pharmacologic, and patient factors. Lipid-lowering treatment may be inadequate because of an inappropriate choice of agent or dosage, drug intolerance, or lack of patient adherence.
To close this treatment gap, physicians need to improve their strategies for recognizing and managing the risks associated with dyslipidemia. Chart reminders, hospital discharge protocols, and the involvement of non-physician health care professionals improve the rate of effective lipid therapy.
In the next several years, the introduction of agents with novel lipid-modifying effects should also allow for further improvement in treatment rates. Although current statins have a safe and effective track record as mono-therapy, they frequently require combination with other agents to control severe or combined dyslipidemias. An agent now in development, pitivastatin, is reported to have brought 86 percent of dyslipidemic patients to NCEP LDL cholesterol target levels.6 Another agent, rosuvastatin, was reported to have a significant effect on LDL cholesterol, lowering levels by up to 65 percent; among hypercholesterolemic patients, a higher fraction of those taking this agent (87 percent) achieved ATP II target LDL cholesterol levels, compared with those taking pravastatin (53 percent) or simvastatin (64 percent).7
Other drugs in development that modify lipid levels through novel mechanisms may prove useful as mono- or adjunctive therapy. These include bile acid transport inhibitors, acyl-CoA cholesterol acyl-transferase (ACAT) inhibitors, and peroxisome proliferator-activated receptor (PPAR) agonists. The potential for additional coronary risk reduction with these agents exists, but further clinical study is needed before their use will affect treatment recommendations.
The ATP III guidelines advise that we take a more aggressive posture in identifying and treating dyslipidemia to prevent cardiovascular diseases in our patients. These recommendations must be followed through continued educational efforts, practice improvements, and pharmaceutical development to help patients achieve the new target levels.
Benjamin J. Ansell, M.D., is director of the UCLA Center for Primary Care-Based Cardiovascular Disease Prevention in the Department of Medicine at the University of California, Los Angeles, School of Medicine.
Address correspondence to Benjamin J. Ansell, M.D., UCLA Dept. of Medicine, Div. of General Internal Medicine and Health Services Research, 200 UCLA Medical Plaza, Suite 370, Los Angeles, CA 90095 (e-mail: firstname.lastname@example.org).
1. 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;285:2486–97.
2. Safeer RS, Ugalat PS. Cholesterol treatment guidelines update. Am Fam Physician. 2002;65:871–80.
3. Jacobson TA, Griffiths GG, Varas C, Gause D, Sung JC, Ballantyne CM. Impact of evidence-based “clinical judgment” on the number of American adults requiring lipid-lowering therapy based on updated NHANES III data. National Health and Nutrition Examination Survey. Arch Intern Med. 2000;160:1361–9.
4. Fonarow GC, French WJ, Parsons LS, Sun H, Malmgren JA. Use of lipid-lowering medications at discharge in patients with acute myocardial infarction: data from the National Registry of Myocardial Infarction 3. Circulation. 2001;103:38–44.
5. 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;160:459–67.
6. Kajinami K, Koizumi J, Ueda K, Miyamoto S, Takegoshi T, Mabuchi H. Effects of NK-104, a new hydroxymethylglutaryl-coenzyme reductase inhibitor, on low-density lipoprotein cholesterol in heterozygous familial hypercholesterolemia. Hokuriku NK-104 Study Group. Am J Cardiol. 2000;85:178–83.
7. Olsson AG. Statin therapy and reductions in low-density lipoprotein cholesterol: initial clinical data on the potent new statin Rosuvastatin. Am J Cardiol. 2001;87:33B–36B.
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