Abstract
Abstract Objectives Vitamin D deficiency (VDD) is associated with coronary artery disease (CAD) directly by augmenting atherosclerosis and indirectly through cardiovascular risk factors. The present study was aimed to find an association of 25 hydroxyvitamin D (25(OH)D) with lipid profile among established CAD. Methods A cross-sectional study was conducted among 73 patients of angiographically confirmed CAD aged between 35 and 55 years of both gender. Serum 25(OH)D and lipid profile were estimated by ELISA kit and Roche autoanalyzer respectively. Atherogenic index of plasma (AIP) and sdLDL (small dense low-density lipoprotein) were calculated using the accepted formula. Results The mean 25(OH)D level was 17.95 ± 13.51. Only 15% had sufficient 25(OH)D level. There was a significant negative correlation of 25(OH)D with TC/HDL (T.cholesterol/High-density lipoprotein) ratio (p=0.022). Multivariate logistic regression analysis showed no statistically significant impact of 25(OH)D with lipid biomarkers. Conclusions We found low 25(OH)D mean value among CAD and a significant negative correlation of 25(OH)D with TC/HDL. This study suggests VDD may affect primary lipid target resulting in unfavorable outcomes in CAD.
Highlights
Vitamin D is a pro-hormone concerned with skeletal effects
Growing evidence revealed that Vitamin D deficiency (VDD) is closely associated with cardiovascular disease (CVD) directly by augmenting atherosclerosis [2] and indirectly through its association with traditional called cardiovascular risk factors, which are obesity, dyslipidemia, hypertension, diabetes mellitus (DM), metabolic syndrome, and inflammation due to the complex biological interaction between vitamin D and its receptors [3,4,5,6]
Atherogenic index of plasma (AIP) value was calculated as log[TG/High-density Lipoprotein (HDL)-C. small dense low-density lipoprotein (sdLDL) was calculated as = (0.084 × TG)+(0.281 × Total Cholesterol (TC)) − (0.251 × HDL) − 17.236
Summary
The discovery of vitamin D receptors (VDR) and the 1α-hydroxylase enzyme, which is essential to activate 25-hydroxyvitamin D [25(OH)D], to 1,25-dihydroxyvitamin D {1,25(OH)2D} in a variety of cells has sparked interest in its extra skeletal role [1]. Growing evidence revealed that VDD is closely associated with cardiovascular disease (CVD) directly by augmenting atherosclerosis [2] and indirectly through its association with traditional called cardiovascular risk factors, which are obesity, dyslipidemia, hypertension, diabetes mellitus (DM), metabolic syndrome, and inflammation due to the complex biological interaction between vitamin D and its receptors [3,4,5,6]. Apart from this, VDD has got a direct effect on the cardiovascular system through its interaction with receptors present on cardiomyocytes, vascular myocytes and vascular endothelial cells [7]. Lipoprotein lipase enzyme, which is involved in the metabolism of TG, may be regulated by the [25(OH)D] resulting in TG reduction [10] since
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