Vitamin D status was not associated with ‘one-year’ progression of coronary artery disease, assessed by coronary angiography in statin-treated patients

• Published in: European journal of preventive cardiology 2015-05, Vol.22 (5), p.594-602
• Main Authors: Degerud, Eirik, Løland, Kjetil H, Nygård, Ottar, Midttun, Øivind, Ueland, Per M, Seifert, Reinhard, Strand, Elin, Bleie, Øivind, Dierkes, Jutta
• Format: Article
• Language: English
• Subjects: Aged; Calcifediol - blood; Chromatography, Liquid; Coronary Angiography - methods; Coronary Artery Disease - blood; Coronary Artery Disease - diagnosis; Coronary Artery Disease - drug therapy; Disease Progression; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Male; Middle Aged; Tandem Mass Spectrometry; Vitamins - blood
• ISSN: 2047-4873; 2047-4881
• DOI: 10.1177/2047487314522137

Background Low vitamin D status is associated with increased risk of cardiovascular disease and may be involved in atherosclerosis. Our aim was to assess the association between vitamin D status and the progression of coronary artery disease (CAD). Methods and Results We measured 25-hydroxyvitamin D3 (25OHD3) by liquid chromatography tandem mass spectrometry (LC-MS/MS) in plasma from 348 participants with established CAD (84% males, mean ± standard deviation (SD) age 60 ± 10 years) of the Western Norway B-vitamin Intervention Trial (WENBIT, 1999–2006). The patients underwent invasive coronary angiography (CA) and percutaneous coronary intervention at baseline and a second CA after 302 ± 79 days of follow-up. From the angiograms, minimal lumen diameter (MLD) and diameter stenosis (DS) of atherosclerotic lesions were obtained. Significant CAD in non-intervened vessels was found in 309 coronary arteries from 183 participants either at baseline and/or at follow-up. To assess the association between levels of 25OHD3 and CAD progression in non-intervened vessels, we applied a linear quantile fitted mixed effects model with MLD or DS measured at follow-up as a function of continuous 25OHD3 concentrations. There were no statistically significant associations between plasma 25OHD3 concentrations (median: 63.9, 95% confidence interval (CI): 48.1–78.5 nmol/l) measured at baseline and the follow-up measures of either MLD (estimated effect per 10 nmol/l increase of 25OHD3 and 95% CI: –0.015 (−0.032–0.002) mm, p = 0.088) or DS (0.225 (−0.354–0.804) percentage points, p = 0.444). Multivariate adjustment did not alter these results. Conclusion Plasma 25OHD3 levels were not associated with ‘one-year’ progression of CAD, assessed by CA in statin-treated patients.