الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Coronary artery disease (CAD), also called Coronary heart disease (CHD), refers to the cardiovascular disease with a narrowing or blockage of the coronary arteries, which is the major cause of mortality worldwide. However, the pathogenesis of CAD remains largely unknown. The most generally accepted view is that CAD is a polygenic disease, resulting from the interplay of both genetic and environmental factors. Genetic factors are estimated to account for 30–60% of the risk of CAD. While lifestyle modification has reduced the mortality rate, the candidate gene approach has provided new insights for discovering diagnostic and therapeutic approaches. LDL-R is a transmembrane glycoprotein that plays an important role in the uptake of LDL-C from the blood circulation so that LDL-C remains at a stable level in blood. The dysfunction of LDL-R and the dysregulation of LDL-R expression can impair the regulation of lipid profile and result in atherosclerosis. LDL-R gene polymorphism rs1122608 is identified in intron 30 of SWI/SNF-related matrix-associated actin-dependent regulator of chromatin, subfamily A, member 4 (SMARCA4), which is adjacent to the LDL-R gene ,and located in chromosomal region of 19p13.2. Aim of the study: The aim of this study is to investigate LDL-R polymorphism rs1122608 as predisposing genetic marker of CAD in a cohort from the Egyptian cardiac patients. Conclusion : Significant associations were detected between the SMARCA4 rs1122608 and CAD patients compared to the controls in both the genotypic and allelic frequencies. GT and TT genotypes of rs1122608 were associated with significant higher TC, serum LDL-C and TG levels among CAD patients with low score of healthy dietary pattern. Following multivariate analysis for the confounders, BMI, hypertension, high TC, lower score of healthy and higher score of unhealthy dietary pattern, SMARCA4 rs1122608 SNP variants GT, TT, GT+TT, and T allele were related to CAD and were considered as independent risk factors for CAD.