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, meanstandard deviation (SD) age 6010 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 30279 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 statintreated patients.
CITATION STYLE
Degerud, E., Løland, K. H., Nygård, O., Midttun, Ø., Ueland, P. M., Seifert, R., … Dierkes, J. (2015). Vitamin D status was not associated with “one-year” progression of coronary artery disease, assessed by coronary angiography in statin-treated patients. European Journal of Preventive Cardiology, 22(5), 594–602. https://doi.org/10.1177/2047487314522137
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