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Letter to the Editor |
University of L’Aquila, Department of Internal Medicine and Public Health, 67100 Coppito-L’Aquila, Italy
Address correspondence to: Giovambattista Desideri, M.D., University of L’Aquila Department of Internal Medicine and Public Health, Piazza Salvatore Tommasi n.1, 67100 Coppito-L’Aquila, Italy. E-mail: giovambattista.desideri{at}cc.univaq.it.
To the editor:
We greatly appreciated the interesting letter by Tenenbaum et al. (1), commenting on our recent identification of increased endothelial activation and lipid peroxidation in hypercholesterolemic patients (2) and a possible "cholesterol-independent" benefit deriving from statin treatment. Indeed, the atherogenic activation of vascular endothelial cells and the augmented oxidative stress were counteracted by simvastatin but not bezafibrate treatment, despite the finding that significant low-density lipoprotein-cholesterol decrements were achieved by both drugs within 6 months (2).
With regard to the comments of Tenenbaum et al. (1), we are obviously aware that both low serum high-density lipoprotein (HDL)-cholesterol (3) and high serum triglyceride concentrations (4) exert a detrimental impact on life expectancy. According to this, low HDL-cholesterol levels and hypertriglyceridemia represent important therapeutic targets for cardiovascular disease prevention (5). Although we agree with Tenenbaum et al. (1) that the bezafibrate-induced improvement of the lipid pattern could manifest with cardiovascular benefits in the long run, our study was focused on pathophysiological aspects of vascular protection, and we cannot expand upon this matter. In particular, changes of the lipid pattern were slightly different between the two groups as regard serum HDL-cholesterol and triglyceride concentrations. Furthermore, we did not observe cardiovascular events in our 6-month study, because it was expected due to the peculiarity of the study population, i.e. the presence of hypercholesterolemia with no additional cardiovascular risk factors including hypertriglyceridemia (2) resulting in a low risk profile (5). Obviously, as Tenenbaum et al. (1) correctly pointed out, due to the absence of hypertriglyceridemia, such patients are expected to achieve greater benefit from statin rather than from fibrate treatments. In fact, bezafibrate is particularly effective in reducing cardiovascular morbidity and mortality in patients with high serum triglyceride levels (6).
We also agree that both treatments were substantially well-tolerated, also considering that bezafibrate was used at high doses. In this context, the randomization of patients to such an unusual dose of bezafibrate was based on the need to achieve a strong reduction of serum low-density lipoprotein-cholesterol concentrations. Indeed, we were concerned about possible differences between the two arms of the study, i.e. simvastatin vs. bezafibrate, regarding eventual "cholesterol-independent" modifications of endothelial activation and lipid peroxidation.
With regard to the interesting aspect of glucose metabolism, we did not investigate this particular aspect, and we are unable to speculate on the matter. However, our patients were selected for having no impairment of glucose tolerance. Therefore, we think it is difficult to hypothesize that changes in insulin sensitivity have been induced by 6-month treatment with either simvastatin or bezafibrate.
Received December 22, 2003.
References
This article has been cited by other articles:
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  A. Tenenbaum, M. Motro, E. Z. Fisman, D. Tanne, V. Boyko, and S. Behar Bezafibrate for the Secondary Prevention of Myocardial Infarction in Patients With Metabolic Syndrome Arch Intern Med, May 23, 2005; 165(10): 1154 - 1160. [Abstract] [Full Text] [PDF]
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 G. Desideri and C. Ferri Authors' Response: Bezafibrate and Simvastatin: Different Beneficial Effects for Different Therapeutic Aims J. Clin. Endocrinol. Metab., April 1, 2004; 89(4): 1978 - 1979. [Full Text] [PDF]
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