Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease

Abstract

BackgroundMetabolic syndrome (MS) is a condition that, when associated with ischemic heart disease and cardiovascular events, can be influenced by genetic variants and determine more severe coronary atherosclerosis.ObjectivesTo examine the contribution of genetic polymorphisms to the extension and severity of coronary disease in subjects with MS and recent acute coronary syndrome (ACS).MethodsPatients (n = 116, 68% males) aged 56 (9) years, with criteria for MS, were prospectively enrolled to the study during the hospitalization period after an ACS. Clinical and laboratory parameters, high-sensitivity C-reactive protein, thiobarbituric acid reactive substances, adiponectin, endothelial function, and the Gensini score were assessed. Polymorphisms of paraoxonase-1 (PON-1), methylenotetrahydrofolate reductase (MTHFR), endothelial nitric oxide synthase (ENOS), angiotensin-converting enzyme (ACE), angiotensin II type 1 receptor (AT1R), apolipoprotein C3 (APOC3), lipoprotein lipase (LPL) were analysed by polymerase chain reaction (PCR) technique, followed by the identification of restriction fragment length polymorphisms (RFLP, and a genetic score was calculated. Parametric and non-parametric tests were used, as appropriate. Significance was set at p < 0.05.ResultsPolymorphisms of PON-1, MTHFR and ENOS were not in the Hardy-Weinberg equilibrium. The DD genotype of LPL was associated with higher severity and greater extension of coronary lesions. Genetic score tended to be higher in patients with Gensini score < P50 (13.7 ± 1.5 vs. 13.0 ± 1.6, p = 0.066), with an inverse correlation between genetic and Gensini scores (R = -0.194, p = 0.078).ConclusionsThe LPL polymorphism contributed to the severity of coronary disease in patients with MS and recent ACS. Combined polymorphisms were associated with the extension of coronary disease, and the lower the genetic score the more severe the disease.

Atorvastatin and losartan may upregulate renalase activity in hypertension but not coronary artery diseases: The role of gene polymorphism

“…The manifestation and severity of CAD and hypertension depend on inherited predisposition combined with environmental factors. 28,29 Identification of factors for genetic risk of hypertension is thus essential for risk prediction of CAD and/or hypertension. Moreover, it has been suggested that the enhanced progression of these diseases is the result of renalase activity alterations.…”

“…The manifestation and severity of CAD and hypertension depend on inherited predisposition combined with environmental factors . Identification of factors for genetic risk of hypertension is thus essential for risk prediction of CAD and/or hypertension.…”

Association between HindIII (rs320) variant in the lipoprotein lipase gene and the presence of coronary artery disease and stroke among the Saudi population

“…Genome-wide association studies have identified numerous loci for the CAD and one of the main susceptibility loci is placed at chromosome 15q26.1 which exists the single nucleotide polymorphism in the form of rs17514846 ( Yang et al, 2020 ). Several case-control and meta -analysis studies have shown the relation between LPL gene and CAD ( Xu et al, 2019 , Javorsky et al, 2007 , Daoud et al, 2013 , Fischer et al, 2018 , Ma et al, 2018 , Shahid et al, 2017 , Xie, 2017 ). The accurate genetic and molecular or any other mechanism which affects the LPL and human disease is poorly understood and LDL was interrelated towards certain heterogenous disorders which involve limited cardiovascular disorders ( Hartley et al, 2020 ).…”