Paraoxonase-1 and Simvastatin Treatment in Patients with Stable Coronary Artery Disease
Background. Paraoxonase-1 (PON1) is the crucial antioxidant marker of high-density lipoproteins. The present study is aimed at assessing the effect of simvastatin treatment on PON1 activity and its relationship to Q192R and M55L polymorphisms in subjects with stable coronary artery disease (CAD). Me...
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| Main Author: | |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2016-01-01
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| Series: | International Journal of Vascular Medicine |
| Online Access: | http://dx.doi.org/10.1155/2016/6312478 |
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| Summary: | Background. Paraoxonase-1 (PON1) is the crucial antioxidant marker of high-density lipoproteins. The present study is aimed at assessing the effect of simvastatin treatment on PON1 activity and its relationship to Q192R and M55L polymorphisms in subjects with stable coronary artery disease (CAD). Methods. The patient group was composed of 53 individuals with stable CAD, and the control group included 53 sex-matched police officers without CAD. CAD patients were treated with simvastatin 40mg/day for 12 months. Respectively, flow mediated dilatation (FMD), serum hs-CRP and TNF-α levels, urinary 8-iso-PGF2α concentrations, and PON1 activity were evaluated in definitive intervals. Results. There was no effect of simvastatin treatment on urinary 8-iso-PGF2α. Simvastatin treatment significantly increased FMD value, decreased CRP and TNF-α concentration. After adjusting for PON1 genotypes, significantly higher PON1 activity was noted in the 192R allele carriers, in both groups. Regardless of genotype, PON1 activity remained stable after simvastatin treatment. Conclusions. The present study confirms a positive effect of simvastatin therapy on endothelial function and inflammatory markers in secondary prevention. Simvastatin treatment shows no effects on PON1 activity and 8-isoprostanes level. The effect of simvastatin therapy on PON1 activity is not modulated by Q192R and M55L polymorphisms. |
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| ISSN: | 2090-2824 2090-2832 |