[No authors listed]
: Recent attention has been focused on the regulation of vitamin D metabolism as modulating the cardiovascular benefits of vitamin D. The aim of the current study was to evaluate the functional impact of the genetic polymorphism rs2762939 of CYP24A1, the hydroxylase-enzyme modulating the inactivation of vitamin D, on the prevalence and extent of coronary artery disease (CAD).A consecutive cohort of patients undergoing coronary angiography in a single centre was included. Significant CAD was defined as at least one stenosis more than 50%, severe CAD as left main and/or three-vessel disease. Among 1204 patients, 673 (55.8%) carried the C allele. Baseline features showed a lower use of beta-blockers among the C-carriers (Pâ=â0.01) and higher levels of C-reactive protein (Pâ=â0.05). The prevalence of CAD and severe CAD was not conditioned by CYP24A1 genetic status [78.7%-GG vs. 81.2%-C-carriers; Pâ=â0.31; adjusted odds ratio (95% confidence interval )â=â0.71(0.20-2.56), Pâ=â0.60 and 29.1%-GG vs. 29.5%-C carriers Pâ=â0.95; adjusted odds ratio (95% confidence interval)â=â0.87 (0.73-1.04), Pâ=â0.13, respectively]. Coronary calcifications were significantly higher among GG homozygotes (Pâ=â0.005). This study showed that the polymorphisms rs2762939 of CYP24A1 is not associated with the prevalence and extent of CAD. However, the C-allele carriage significantly lowers the rate of coronary calcifications.
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