Effect of treatment with pravastatin or ezetimibe on endothelial function in patients with moderate hypercholesterolemia.
Summary of "Effect of treatment with pravastatin or ezetimibe on endothelial function in patients with moderate hypercholesterolemia."
BACKGROUND/
AIM:
Statin treatment improves endothelial function. It is matter of debate, however, if this effect of statins is due to their action on low-density lipoprotein cholesterol (LDL-C) or to other non-lipidic (pleiotropic) effects. The aim of this study was to evaluate whether the effect of pravastatin on endothelial function is mediated by pleiotropic effects. We therefore compared the effect of pravastatin and ezetimibe, a cholesterol absorption inhibitor, at doses yielding similar reductions in LDL-C and examined the effect of the two treatments on flow-mediated dilation (FMD) in hypercholesterolemic subjects.
METHODS:
A total of 33 moderately hypercholesterolemic patients were randomized into three treatment groups to receive ezetimibe 10 mg/day (n = 10), pravastatin 10 mg/day (n = 13) or no treatment (control, n = 10) for 6 weeks. To assess endothelial function, we determined FMD of the brachial artery non-invasively by high-resolution ultrasound before and after treatment.
RESULTS:
Ezetimibe and pravastatin treatment reduced LDL-C (mean ± standard error) to a similar extent (-20.6 ± 4.1 vs. -24.1 ± 4.0 %, respectively; P = 0.4771), while no decrease was observed in the control group. FMD increased significantly after treatment with ezetimibe (from 11.4 ± 5.7 to 16.8 ± 3.6 %; P = 0.022) and with pravastatin (from 13.7 ± 4.9 to 17.5 ± 4.4 %; P = 0.0466), but not in the control group. There were no differences in the endothelial function changes between the two treatment groups.
CONCLUSIONS:
In this study, two treatments that lower cholesterol via different mechanisms improved endothelial function to a similar extent, suggesting that the observed effect can be explained by the reduction of cholesterol levels.
Affiliation
Center for the Study of Atherosclerosis-SISA Lombardia, Bassini Hospital, Via Gorki 50, 20092, Cinisello Balsamo, Milan, Italy.
Journal Details
This article was published in the following journal.
Name: European journal of clinical pharmacology
ISSN: 1432-1041
Pages:
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22777149
- DOI: http://dx.doi.org/10.1007/s00228-012-1345-z
Medical and Biotech [MESH] Definitions
Enprostil
A synthetic PGE2 analog that has an inhibitory effect on gastric acid secretion, a mucoprotective effect, and a postprandial lowering effect on gastrin. It has been shown to be efficient and safe in the treatment of gastroduodenal ulcers.
Placebo Effect
An effect usually, but not necessarily, beneficial that is attributable to an expectation that the regimen will have an effect, i.e., the effect is due to the power of suggestion.
Vascular Endothelial Growth Factor Receptor-2
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Vascular Endothelial Growth Factor D
A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR C in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.
Vascular Endothelial Growth Factor C
A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR D in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.
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