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A better understanding of coronary artery disease molecular biology through an intermediate phenotype
Session:
Comunicações Orais - Sessão 17 -Síndromes Coronárias Crónicas
Speaker:
Ana Débora Câmara de Sá
Congress:
CPC 2023
Topic:
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme:
12. Coronary Artery Disease (Chronic)
Subtheme:
12.8 Coronary Artery Disease - Other
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Ana Débora Câmara De Sá; Maria Isabel Mendonça; Marina Santos; Margarida Temtem; Francisco Sousa; Sónia Freitas; Mariana Rodrigues; Eva Henriques; Sofia Borges; Graça Guerra; Ilídio Ornelas; António Drumond; Ana Célia Sousa; Roberto Palma Dos Reis
Abstract
<p style="text-align:justify"><span style="font-family:Calibri"><span style="font-size:medium"><span style="color:#000000">Coronary Artery Disease (CAD) remains a common cause of death worldwide; over half of these deaths are asymptomatic until the first fatal presentation.</span><span style="background-color:white"><span style="color:#212121"> Previous studies have often compared coronary artery calcification (CAC) with coronary stenosis or its sequelae. </span></span><span style="color:#000000"> However, the genetic contribution to CAC in sub-clinical atherosclerosis is controversial. </span></span></span></p> <p style="text-align:justify"><span style="font-family:Calibri"><span style="font-size:medium"><span style="color:#000000"><strong>Purpose:</strong> This study intended to assess the relationship between a set of single nucleotide polymorphisms associated with CAD (GWAS) and CAC score in an asymptomatic population. </span></span></span></p> <p style="text-align:justify"><span style="font-family:Calibri"><span style="font-size:medium"><span style="color:#000000"><strong>Methods:</strong> Prospective study performed in an asymptomatic cohort from GENEMACOR population-based sample of 1207 subjects aged 51.7±8.3, 73.8 male, without apparent prior CAD. CAC score was performed by cardiac computed tomography and reported as Agatston units according to the Hoff nomogram (Low, Moderate and High-risk categories). For the present work, we considered two groups: Group 1 (0≤CAC<100 and Percentile<50) and Group 2 (CAC≥100 or Percentile≥50). We genotyped thirty-three single nucleotide polymorphisms (SNP) associated with CAD by TaqMan real-time PCR. Anthropometric, conventional, and biochemical risk factors were assessed. The association of these SNPs with CAC score groups were evaluated by bivariate and multivariate logistic regression analysis, and the dominant genetic model was considered for comparison. </span></span></span></p> <p style="text-align:justify"><span style="font-family:Calibri"><span style="font-size:medium"><span style="color:#000000"><strong>Results:</strong> After bivariate analysis, only PHACTR1 rs1332844 C>T (CT+TT genetic model) showed a significative association with CAC score (OR=1.45; 95%CI 1.09-1.94; p=0.011). Multivariate logistic regression analysis, adjusted to traditional risk factors, genetic model and CAC score showed that PHACTR1 rs1332844 remained in the equation as significantly associated to CAC score (P=0.009) together with age (0.0001), hypertension (0.006), Diabetes (0.0001), smoking (0.001) and obesity (0.028).</span></span></span></p> <p style="text-align:justify"><span style="font-family:Calibri"><span style="font-size:medium"><span style="color:#000000"><strong>Conclusion:</strong> PHACTR1 genetic variant is known to contribute to atherosclerosis and plaque formation. In the present study it showed a significant association with plaque calcium. More research in this field is critical to understanding the genetic basis of CAD through an intermediate phenotype, plaque calcification. We highlight this point since it can be crucial for the prognosis and therapy of the asymptomatic population.</span></span></span></p>
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