Abstract:
Cardiovascular disease (CVD) have multifactorial nature, and owing to their disparate etiological roots, it is difficult to ascertain exact
determinants of CVD. In the current study, primary objective was to determine association of single nucleotide polymorphisms (SNP) in
folate pathway genes, homocysteine, antihypertensive medication, and of known risk factors in relation to CVD outcomes. The participants
numbered 477 (controls, n = 201, ischemic heart disease patients, n = 95, and myocardial infarction cases, n = 181, respectively). SNPs
that were queried for homocysteine pathway genes included, “methylene tetrahydrofolate reductase (MTHFR)” gene SNPs rs1801133 and
rs1801131, “methyltransferase (MTR)” SNP rs1805087, “paraoxonase 1 (PON1)” SNP rs662, and angiotensin-converting enzyme (ACE)
gene polymorphisms rs4646994. Medication data were collected through questionnaire, and serum-based parameters were analyzed through
commercial kits. The analysis of variance and multiple comparison scrutiny revealed that age, gender, family history, cholesterol, creatinine,
triglyceride, high density lipoproteins (HDL), homocysteine, beta-blocker, ACE inhibitors, MTHFR and PON1 SNPs related to coronary artery
disease (CAD). On regression, rs662 SNPs and C-reactive protein had nonsignificant odds ratio, whereas age, gender, creatinine, and HDL
were nonsignificant. Family history, cholesterol, homocysteine, beta blocker, and ACE inhibitors, homocysteine, rs1801133 and rs1801131
SNP maintained significance/significant odds for CAD. The current study indicates an intricate relationship between genetic variants, traditional
factors, and drug usage in etiogenesis of arterial disease. Differences in SNPs, their modulated effects in consensus with medicinal usage may
be related to ailment outcomes affecting coronary vasculature.
