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REPLY
Cost-Effectiveness Analyses
Lisa A. Prosser, PhD;
Aaron A. Stinnett, PhD;
Lee Goldman, MD, MPH; and
Milton C. Weinstein, PhD
4 September 2001 | Volume 135 Issue 5 | Pages 382-383
IN RESPONSE:
We agree with Dr. Clark that it is often relevant to differentiate between the decision to tailor therapy once treatment has been initiated and the decision to initiate treatment that we evaluated. In our cost-effectiveness analysis, we modeled dosages and lipid levels achieved by using data from observed practices in randomized clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), rather than on treatment guidelines for actual practice. For primary prevention, we used data from several large-scale trials that used a dosage of 40 mg of pravastatin per day (1-3). For secondary prevention, our analysis modeled a strategy based on the intervention evaluated in the Scandinavian Simvastatin Survival Study, in which patients initially received 20 mg of simvastatin daily and doses were titrated up or down on the basis of levels of low-density lipoprotein cholesterol. The average daily dose was 27 mg, which includes patients whose daily dose decreased to 10 mg or increased to 40 mg (4).
By demonstrating that the cost-effectiveness of initiating primary prevention with a statin varies substantially across risk factor groups, we believe our analysis shed light on a clinically relevant policy issue. There are certainly a variety of relevant issues not addressed in our analysis that affect the cost-effectiveness of strategies for cholesterol reduction. These include, for example, the implications of interventions not evaluated in our study (such as a niacin-statin combination); risk factors beyond those included in our model (such as family history); and, as Dr. Clark points outs, questions regarding how best to adjust therapy as patients' responses are observed. Because the use of pretreatment target lipid levels is common in clinical practice, we agree that information on the cost-effectiveness of these targets is an appropriate and potentially important research topic.
We hope that our results will be useful for decision makers in medicine and public health as they work toward appropriate strategies for prevention of coronary heart disease. Even more strongly, we hope that we and others will continue to provide additional information to further reduce uncertainty about how best to use our scarce resources in the pursuit of improved health and well-being for patients and populations.
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Author and Article Information
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Harvard Medical School; Boston, MA 02215 (Prosser)
University of Alabama at Birmingham; Birmingham, AL 35294 (Stinnett)
University of California, San Francisco; San Francisco, CA 94143 (Goldman)
Harvard School of Public Health; Boston, MA 02115 (Weinstein)
1. Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, MacFarlane PW, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group N Engl J Med. 1995;333:1301-7. [PMID: 7566020].[Abstract/Free Full Text]
2. Jukema JW, Bruschke AV, van Boven AJ, Reiber JH, Bal ET, Zwinderman AH, et al. Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS) Circulation. 1995;91:2528-40. [PMID: 7743614].[Abstract/Free Full Text]
3. Salonen R, Nyyssönen K, Porkkala E, Rummukainen J, Belder R, Park JS, et al. Kuopio Atherosclerosis Prevention Study (KAPS). A population-based primary preventive trial of the effect of LDL lowering on atherosclerotic progression in carotid and femoral arteries Circulation. 1995;92:1758-64. [PMID: 7671358].[Abstract/Free Full Text]
4. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) Lancet. 1994;344:1383-9. [PMID: 7968073].[Medline]
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