Background:Coronary artery disease (CAD) is a major cause of death and disability in developed countries. Chronic stable angina is the initial manifestation of CAD in approximately 50% of the patients. Recent evidence suggests that vitamin D is crucial for cardiovascular health. The prevalence of vitamin D deficiency in our region is 83%. A low level of vitamin D is associated with chronic stable angina.Aim:This study was aimed at supporting or refuting this hypothesis in our population.Materials and Methods:The study was a prospective case-control study. We studied 100 cases of chronic stable angina and compared them with 100 matched controls. Vitamin D deficiency was defined as <20 ng/mL, vitamin D insufficiency as 20-30 ng/mL and normal vitamin D level as 31-150 ng/mL.Results:The prevalence of vitamin D deficiency among cases and controls was 75% and 10%, respectively. 75% of the cases were vitamin D-deficient (<20 ng/mL); 12% were vitamin D-insufficient (20-30 ng/mL), and 13% had normal vitamin D levels (31-150 ng/mL). None had a toxic level of vitamin D. Among the controls, 10% were vitamin D-deficient, 33% were vitamin D-insufficient, and 57% had normal vitamin D levels. The mean vitamin level among cases and controls was 15.53 ng/mL and 40.95 ng/mL, respectively, with the difference being statistically significant (P ≤ 0.0001). There was no statistically significant relation between the disease severities, i.e., on coronary angiography (CAG) with vitamin D level. Among the cases, we found that an increasing age was inversely related to vitamin D levels (P = 0.027).Conclusion:Our study indicates a correlation between vitamin D deficiency and chronic stable angina. Low levels may be an independent, potentially modifiable cardiovascular risk factor.

Coronary artery disease (CAD) is a clinical manifestation of atherosclerosis in the arteries supplying myocardium. Inflammation is the cornerstone in the development and progression of atherosclerosis. Amongst the various biomolecules tumour necrosis factor-a (TNF-a), interleukin-18 (IL-18) and interleukin-1b (IL-1b) build an inflammatory bionetwork in developing the disease. In this study we investigated the association of TNF-a SNPs [-308G/A (rs1800629), À1031T/C (rs1799964), À863C/A (rs1800630)]; IL-18 [-137G/C (rs187238)] and IL-1b SNPs [+3954C/T (rs1143634), À31C/T (rs1143627), and À511C/T (rs16944)] with coronary artery disease risk in Kashmiri population. A total of 200 cases and 260 controls were recruited in the study. Logistic regression analysis was done to investigate the association between SNPs and CAD risk. In case of TNF-a, the À308G/A-A/A and À863A/A showed an association with disease while À1031T/C was found to have an inverse relation. The IL-18-137G/C showed no statistically significant difference between controls and cases. For IL-1b the +3954C/T and À31C/T SNP variants showed no disease association while À511T/T showed significant association. Haplotypic analysis revealed the haplotype ATCGCC and GTACCTC to be associated with CAD risk and GTCGTTT, in particular, showing a profound association. Overall, our study suggests that TNF-a and IL-1b promoter polymorphisms may act as genetic risk factors in developing the coronary artery disease.