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Curso de Atualização em Medicina Cardiovascular 2019
Reunião Anual Conjunta dos Grupos de Estudo de Cirurgia Cardíaca, Doenças Valvulares e Ecocardiografia da SPC
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01. History of Cardiology
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07. Syncope and Bradycardia
08. Ventricular Arrhythmias and Sudden Cardiac Death (SCD)
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31. Pharmacology and Pharmacotherapy
32. Cardiovascular Nursing
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34. Public Health and Health Economics
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Assessment of the additional capacity of a genetic risk score in the prediction of coronary artery disease
Session:
CO3 - Doença Coronária
Speaker:
Joel Monteiro
Congress:
CPC 2019
Topic:
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme:
12. Coronary Artery Disease (Chronic)
Subtheme:
12.2 Coronary Artery Disease – Epidemiology, Prognosis, Outcome
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Joel Ponte Monteiro; Maria Isabel Mendonça; Andreia Pereira; Joao Adriano Sousa; Flávio Mendonça; Micaela Rodrigues Neto; Ana Célia Sousa; Eva Henriques; Sónia Freitas; Sofia Borges; Graça Guerra; Ilídio Ornelas; A. Drumond de Freitas; Roberto Palma dos Reis
Abstract
<p>Predicting future coronary artery disease (CAD) in healthy adults, even using the new risk factors beyond the traditional ones, seems sometimes disappointing.</p> <p><strong>Aims:</strong> Investigate the role of 33 genetic variants emerged from GWAS apart from phenotypic and behaviour information, in prediction and discrimination of CAD.</p> <p><strong>Methods</strong><strong>:</strong> A case-control study was performed with 3050 subjects (1619 coronary patients with 53.3 ±8 years; 78.9% male and 1431 controls with 52.8 ±8 years; 76.6% male) from GENEMACOR. Traditional and new risk factors (TRF) such as smoking, dyslipidaemia, diabetes, family history, hypertension, body mass index, physical inactivity, heat rate, creatinine clearance, alcohol consumption, pulse wave velocity, homocysteine, glucose, fibrinogen, lipoprotein (a), APO B lipoprotein, CRP (as) were investigated, as well as the 33 genetic variants previously associated with CAD. A multiplicative genetic risk score (GRS) with these 33 variants was calculated. Multiple logistic regression models adjusted for potential confounders were used to estimate the OR and 95%CI, without and with GRS (5th quintile). Area under the ROC curve (AUC) of each one was compared using Delong test.</p> <p><strong>Results</strong>: In our population, the mean of GRS was 0.64±0.75 (in patients) and 0.46±0.51 (in controls) , p<0.0001. After multivariate model with all the studied risk factors, the following : alcohol consumption, pulse wave velocity, body mass index, lipoprotein (a), APO B, PCR (hs) did not remain in the equation and all others showed independency and significance for CAD. When the last quintile of GRS is added to the model, CAD risk is 1.93 (95%CI: 1.56-2.40; p<0.0001) . In the ROC curve with all risk factors, the AUC was 0.80. Adding the last quintile of GRS the AUC increased slightly to 0.81, with statistical significance (p=0.002).</p> <p><strong>Conclusions: </strong>Genetic information together with the non-genetic add a slight predictive power for CAD risk. Future knowledge about rare genetic variants and other SNPs as well as their complex interactions both with genetic and environmental factors, can provide an improved clinical utility of the GRS.</p>
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