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Letter to the Editor |
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.
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