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Gene-gene and Gene-environment interaction in Coronary Artery Disease risk
Session:
Sessão de Posters 20 - Doença coronária - marcadores de prognóstico
Speaker:
Francisco Homem de Gouveia e Sousa
Congress:
CPC 2024
Topic:
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme:
13. Acute Coronary Syndromes
Subtheme:
13.1 Acute Coronary Syndromes – Pathophysiology and Mechanisms
Session Type:
Cartazes
FP Number:
---
Authors:
Francisco Sousa; M.I. Mendonça; D. Sá; E. Henriques; M. Rodrigues; S. Freitas; S. Borges; G. Guerra; G. Abreu; A. Drumond; A.C. Sousa; R. Palma Dos Reis
Abstract
<p style="text-align:justify"><strong><span style="font-size:11.0pt"><span style="font-family:"Calibri",sans-serif">Background: </span></span></strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#212121">Coronary Artery Disease (CAD) is a lethal illness that kills millions of individuals each year worldwide. This disorder is multifactorial, resulting in the complex interplay of genetic, epigenetic, and environmental factors. Exploring gene-gene and gene-environment interactions is essential to understanding the aetiology of common complex diseases like CAD.</span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><span style="color:#212121">Aim:</span></strong><span style="color:#212121"> We proposed investigating the interaction between two genetic variants robustly associated with CAD by GWAS (</span>MTHFR rs1801133 and APOE<span style="color:black"> rs7412/rs429358) in cardiovascular susceptibility. After that, consider whether there was a new interaction between this genetic association and </span><span style="color:black">and environment (hypertension, dyslipidemia and smoking).</span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><span style="color:black">Methods</span></strong><span style="color:black">: A case-control study enrolled 3,157 individuals, 1,721 coronary patients</span> (with at least 70% stenosis of one or more major coronary arteries or its primary branches on the coronary angiography) and 1,436 controls without CAD.<span style="color:#212121"> Traditional risk factors were investigated, and the two polymorphisms were performed</span> by TaqMan real-time PCR. Bivariate analysis was used to study genotypic proportions between CAD and non-CAD patients with respective odds ratios (OR). Logistic regression analysis displayed the interaction between the two genetic variants each other and with some important environmental risk factors.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Results</strong>: In bivariate analysis, the genetic models were studied for both genes, being the dominant model the one which showed significance for CAD. In MTHFR, 57.8% of the patients and 53.4% of the controls presented the CT+TT genotype (OR=1.20; p=0.013). In APOE, 26.5% of the patients and 22.3% of the controls had E2E4;E3E4+E4E4 (OR=1.26; p=0.006). <span style="color:#212121">The first multivariate logistic regression showed a synergistic interaction between the two genetic variants (OR=1.50; p=0.001).</span> After adjusting for conventional risk factors, the logistic regression analysis entered the MTHFR rs1801133 and APOE rs7412/rs429358, showing a combined interaction effect between those genes and smoking status with an OR of 3.44 (p<0.0001), with hypertension (OR=1.55; p=0.002) and with dyslipidemia (OR=1.71; p<0.0001).</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Conclusion: </strong>According to our results, the genetic interaction between APOE and MTHFR synergistically affected the susceptibility to CAD. This interaction, linked to conventional risk factors, consistently increased the risk of CAD in our population, particularly in the group of genetic carriers who did not quit smoking.</span></span></p>
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