This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Haffner, S. M. Search for Related Content PubMed PubMed Citation Articles by Haffner, S. M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CLOFIBRATE Related Collections Secondary prevention

(Circulation. 2000;102:2.)
© 2000 American Heart Association, Inc.

Editorials

Secondary Prevention of Coronary Heart Disease

The Role of Fibric Acids

Steven M. Haffner, MD

From the Department of Medicine, University of Texas Health Science Center, San Antonio, Texas.

Correspondence to Steven M. Haffner, MD, Department of Medicine, University of Texas Health Science Center, Mail Code 7873, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900. E-mail haffner@uthscsa.edu (Circulation. 2000;102:2-4.)

Key Words: Editorials • lipids • prevention • cardiovascular diseases

Areduction in low-density lipoprotein (LDL) cholesterol lowers coronary heart disease (CHD) by 24% to 31% in subjects with prevalent CHD; this reduction occurs with the use of several statins, including simvastatin¹ and pravastatin.^{2 3} Additional reductions in CHD could come from further reductions in LDL cholesterol, as was suggested by the Post Coronary Artery Bypass Graft clinical trial (POST CABG).⁴ An alternative approach is to attempt to reduce triglyceride levels and to raise levels of high-density lipoprotein (HDL) cholesterol.

The role of triglyceride levels in relation to CHD and the possible use of fibric acids in the reduction of CHD are controversial. Although initial meta-analyses challenged the possible independent role of triglycerides in relation to CHD,⁵ one recent carefully performed meta-analyses supported triglyceride levels as an independent predictor of CHD.⁶ Another potential issue is that the atherogenicity of elevated triglyceride levels may vary. Brunzell et al⁷ reported that subjects with familial hypertriglyceridemia are at a reduced risk for CHD than subjects with familial combined hyperlipidemia.⁷ In the Mevacor Atherosclerosis Regression Study (MARS),⁸ subjects with elevated levels of triglycerides rich in apoCIII had a very rapid progression of atherosclerosis. The misclassification of key variables, such as triglyceride levels, reduces the significance of relations in longitudinal studies, and it may also affect clinical trials by allowing the inclusion of subjects with, for example, elevated triglyceride levels but a low risk of CHD. The direct measurement of apoB may improve the selection of patients in clinical trials.⁹

The use of fibric acids in the . . . [Full Text of this Article]

This article has been cited by other articles:

				S. A. Malin and J. M. Nerbonne Delayed Rectifier K+ Currents, IK, Are Encoded by Kv2 alpha -Subunits and Regulate Tonic Firing in Mammalian Sympathetic Neurons J. Neurosci., December 1, 2002; 22(23): 10094 - 10105. [Abstract] [Full Text] [PDF]

				O. Olivieri, C. Stranieri, A. Bassi, B. Zaia, D. Girelli, F. Pizzolo, E. Trabetti, S. Cheng, M. A. Grow, P. F. Pignatti, et al. ApoC-III gene polymorphisms and risk of coronary artery disease J. Lipid Res., September 1, 2002; 43(9): 1450 - 1457. [Abstract] [Full Text] [PDF]

				W. B. Parsons Jr., D. Waters, and R. R. Azar Niacin After Coronary Bypass Grafting and for Coronary Disease Prevention Circulation, July 10, 2001; 104 (2): e7 - e7. [Full Text] [PDF]