Bezafibrate and Simvastatin: Different Beneficial Effects for Different Therapeutic Aims

Alexander Tenenbaum, Enrique Z. Fisman and Michael Motro

Cardiac Rehabilitation Institute, Chaim Sheba Medical Center, Tel-Hashomet 52621, Israel

Address correspondence to: Alexander Tenenbaum, M.D., Chaim Sheba Medical Center, Cardiac Rehabilitation Institute, Tel-Hashomet 52621, Israel. E-mail: altenen{at}post.tau.ac.il.

To the editor:

We read with great interest the article by Desideri et al. (1). Significant cholesterol reductions were achieved after 6 months under either simvastatin (40 mg/d) or bezafibrate (800 mg/d) treatment in 67 highly selected hypercholesterolemic patients (e.g. without diabetes, overweight, hypertriglyceridemia, etc.). The obtained data demonstrated that hypercholesterolemia was combined with endothelial activation and lipid peroxidation, which were efficaciously counteracted by simvastatin but not by bezafibrate treatment. Desideri et al. have carefully concluded that a different vascular protection can be achieved by different lipid-lowering treatments.

However, the extent of the important question raised by the investigators seems noticeably deeper, and it needs further clarification.

1. Desideri et al. (1) have demonstrated that bezafibrate was clearly better than simvastatin in regard to high-density lipoprotein (HDL)-cholesterol level. It is now recognized that low HDL-cholesterol level is an important independent risk factor for coronary heart disease at any low-density lipoprotein-cholesterol level (2). There is also evidence that increasing HDL-cholesterol levels decreases cardiovascular risk (3).

2. The tendency for better triglyceride reduction by bezafibrate was also shown. It is likely that hypertriglyceridemia is an independent risk for coronary heart disease as well (4, 5). It was demonstrated previously that bezafibrate could achieve the highest benefits in patients with the high triglyceride level (6), whereas the patients with lipid profiles as in the study of Desideri et al. (1) were obviously expected to benefit on statin treatment.

Both HDL-cholesterol and triglyceride levels as therapeutic targets were overlooked in the Discussion.

3. Desideri et al. (1) have described glucose and insulin levels at baseline but did not report the follow-up. It would be of interest to disclose these important data. We can expect that the peroxisome proliferator activated receptors ligand bezafibrate (7, 8) may influence glucose metabolism to a greater extent than simvastatin.

4. To the best of our knowledge, the high dose of bezafibrate (800 mg/d) employed by the authors is rather unusual. Therefore, reporting any side effects (or their absence) is of overwhelming importance.

We believe that the clarification of these points will stress the impact of this important article.

Received November 24, 2003.

References

  1. Desideri G, Croce G, Tucci M, Passacquale G, Broccoletti S, Valeri L, Santucci A, Ferri C 2003 Effects of bezafibrate and simvastatin on endothelial activation and lipid peroxidation in hypercholesterolemia: evidence of different vascular protection by different lipid-lowering treatments. J Clin Endocrinol Metab 88:5341–5347[Abstract/Free Full Text]
  2. Franceschini G 2000 Epidemiologic evidence for high-density lipoprotein cholesterol as a risk factor for coronary artery disease. Am J Cardiol 88:9N–13N[CrossRef]
  3. Fruchart JC, Duriez P 2002 HDL and triglyceride as therapeutic targets. Curr Opin Lipidol 13:605–616[CrossRef][Medline]
  4. Jeppesen J, Hein HO, Suadicani P, Gyntelberg F 1998 Triglyceride concentration and ischemic heart disease: an eight-year follow-up in the Copenhagen Male Study. Circulation 97:1029–1036[Abstract/Free Full Text]
  5. Castelli WP 1986 The triglyceride issue: a view from Framingham. Am Heart J 112:432–437[Medline]
  6. 2000 Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease: the Bezafibrate Infarction Prevention (BIP) study. Circulation 102:21–27
  7. Tenenbaum A, Fisman EZ, Motro M 2003 Metabolic syndrome and type 2 diabetes mellitus: focus on peroxisome proliferator activated receptors (PPAR). Cardiovasc Diabetol 2:4[CrossRef][Medline]
  8. Berger J, Moller DE 2002 The mechanisms of action of PPARs. Annu Rev Med 53:409–435[CrossRef][Medline]




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