Abstract
Adequate vitamin D levels are necessary for good vascular health. 1,25-dihydroxycholecalciferol activates CYP3A4, an enzyme of the cytochrome P450 system, which metabolizes atorvastatin to its main metabolites. The objective of this study was to evaluate the response of cholesterol and triglycerides to atorvastatin according to vitamin D levels. Sixty-three patients with acute myocardial infarction treated with low and high doses of atorvastatin were included. Levels of total cholesterol, triglycerides, HDL cholesterol, and LDL cholesterol were measured at baseline and at 12 months of follow-up. Baseline levels of 25-hydroxyvitamin D (25-OHD) were classified as deficient (<30 nmol/L), insufficient (30–50 nmol/L), and normal (>50 nmol/L). In patients with 25-OHD <30 nmol/L, there were no significant changes in levels of total cholesterol (173 ± 47 mg/dL versus 164 ± 51 mg/dL), triglycerides (151 ± 49 mg/dL versus 177 ± 94 mg/dL), and LDL cholesterol (111 ± 48 mg/dL versus 92 45 ± mg/dL); whereas patients with insufficient (30–50 nmol/L) and normal vitamin D (>50 nmol/L) had a good response to atorvastatin. We suggest that vitamin D concentrations >30 nmol/L may be required for atorvastatin to reduce lipid levels in patients with acute myocardial infarction.
Highlights
Statins, hydro-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibiters, are effective in the primary and secondary prevention of cardiovascular disease and act principally by reducing cholesterol and triglyceride levels
We suggest that vitamin D concentrations >30 nmol/L may be required for atorvastatin to reduce lipid levels in patients with acute myocardial infarction
Baseline patient characteristics showed no significant differences between groups, 76% of patients with 25-OHD
Summary
HMG-CoA reductase inhibiters, are effective in the primary and secondary prevention of cardiovascular disease and act principally by reducing cholesterol and triglyceride levels. The relationship between high levels of plasma cholesterol and atherosclerotic vascular disease is clearly established, with a reduction in total cholesterol and LDL cholesterol to below critical levels significantly reducing the risk [1, 2]. Vitamin D deficiency may increase the risk of cardiovascular disease through three possible mechanisms. High calcitriol levels reduce plasma renin activity, leading to reduced plasma angiotensin II concentrations. This modulation of the renin-angiotensinaldosterone system, in addition to reducing blood pressure, reduces inflammation of the vascular endothelium, limiting atherosclerosis progression [7]. Adequate vitamin D levels are necessary for good vascular health
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