scholarly journals 959Coronary artery disease risk according to genetic risk score deciles, Age and cardiovascular risk factors

2017 ◽  
Vol 38 (suppl_1) ◽  
Author(s):  
A. Pereira ◽  
M. Neto ◽  
R. Rodrigues ◽  
J. Monteiro ◽  
A.C. Sousa ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Risk Score ◽  
Genetic Risk ◽  
Disease Risk ◽  
Genetic Risk Score ◽  
Artery Disease

P4455The controversial role of genetics behind premature CAD: a plausible excuse for the young?

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Sousa ◽  
M Mendonca ◽  
A Pereira ◽  
F Mendonca ◽  
M Neto ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Risk Score ◽  
Genetic Risk ◽  
Genetic Risk Score ◽  
Young Patients ◽  
Premature Cad ◽  
Artery Disease ◽  
Group B

Abstract Introduction The complex interaction between genes and environmental factors contribute to individual-level risk of coronary artery disease (CAD), often resulting in premature CAD. The role for genetic risk scores in premature CAD is still controversial. Objective To evaluate the importance of conventional risk factors and of a genetic risk score in younger and older patients with coronary artery disease Methods From a group of 1619 pts with angiographic documented CAD from the GENEMACOR study, we selected 1276 pts admitted for ACS and analysed them in 2 groups (group A: ≤50 years, n=491 pts, 87.2% male, mean age 44±4.9 and group B: >50 years, n=785 pts, 75.2% male, mean age 57±4.2). Univariate analysis was used to characterize the traits of each group and we used ROC curves and respective AUCs to evaluate the power of genetics in the prediction of CAD, through a Genetic Risk Score (GRS). Results 99.3% of the young patients had at least one modifiable risk factor, 18.4% had 2 modifiable risk factors and 75.2% had 3 or more modifiable risk factors. The pattern of risk factors contributing to CAD were different among groups: family history (A: 27.5%, B: 21.4%, p=0.015) and smoking habits (A: 64.8%, B: 42.9%, p<0.001) were more frequent among patients under 50, and traditional age-linked factors like hypertension (A: 58%, B: 75.7%, p<0.001), diabetes (A: 21.6%, B: 38.6%, p<0.001) were more common in the older group. Acute ST-elevation myocardial infarction was more frequent among the young (A: 55.4%, B: 47.4%, p=0.006), as non-ST clinical presentation was higher among elder patients. Regarding angiographic presentation, single vessel CAD was higher in group A (A: 50.3%, B: 40.9%, p<0.001), while multivessel diasease was higher in group B (A: 33.3%, B: 53.9%, p<0.001). At a mean follow-up of 5 years, older patients had a worst prognosis, registering a higher rate of cardiovascular death (A: 4.1%, B: 8.6%, p=0.002) and higher MACE (A: 26.8%, B: 31%, p=0.128),. Adding the genetic risk score (GRS), we achieved only a slight improvement in the AUC for predicting CAD (0.796->0.805, p=0.0178 and 0.748->0.761, p=0.0007 in patients under and over 50, respectively). Conclusion Coronary artery disease is not all the same, as premature CAD shares a unique and specific pattern of risk factors, clinical presentation, angiographic severity and prognosis. Genetics should not be used as an excuse to justify premature CAD, as there is frequently more than one potentially reversible risk factor present even in young patients and the additive predictive value of GRS is modest.

scholarly journals A Journey through Genetic Architecture and Predisposition of Coronary Artery Disease

2020 ◽  
Vol 21 (5) ◽  
pp. 382-398
Author(s):  
Robert Roberts ◽  
Chih Chao Chang
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Primary Prevention ◽  
Risk Score ◽  
Genetic Risk ◽  
Genetic Risk Score ◽  
Cardiac Events ◽  
Artery Disease ◽  
Conventional Risk Factors

Introduction: To halt the spread of coronary artery disease (CAD), the number one killer in the world, requires primary prevention. Fifty percent of all Americans are expected to experience a cardiac event; the challenge is identifying those at risk. 40 to 60% of predisposition to CAD is genetic. The first genetic risk variant, 9p21, was discovered in 2007. Genome-Wide Association Studies has since discovered hundreds of genetic risk variants. The genetic burden for CAD can be expressed as a single number, Genetic Risk Score (GRS). Assessment of GRS to risk stratify for CAD was superior to conventional risk factors in several large clinical trials assessing statin therapy, and more recently in a population of nearly 500,000 (UK Biobank). Studies were performed based on prospective genetic risk stratification for CAD. These studies showed that a favorable lifestyle was associated with a 46% reduction in cardiac events and programmed exercise, a 50% reduction in cardiac events. Genetic risk score is superior to conventional risk factors, and is markedly attenuated by lifestyle changes and drug therapy. Genetic risk can be determined at birth or any time thereafter. Conclusion: Utilizing the GRS to risk stratify young, asymptomatic individuals could provide a paradigm shift in the primary prevention of CAD and significantly halt its spread.

scholarly journals P6214Genetic risk score, family history of coronary artery disease and cardiovascular risk factors

2017 ◽  
Vol 38 (suppl_1) ◽  
Author(s):  
A. Pereira ◽  
R. Palma Dos Reis ◽  
M. Neto ◽  
R. Rodrigues ◽  
J. Monteiro ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Cardiovascular Risk ◽  
Coronary Artery ◽  
Family History ◽  
Cardiovascular Risk Factors ◽  
Risk Score ◽  
History Of ◽  
Artery Disease

HIV may indirectly accelerate coronary artery disease through enhancing the effects of conventional and non-conventional cardiovascular risk factors

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Kolossvary ◽  
E.K Fishman ◽  
G Gerstenblith ◽  
D.A Bluemke ◽  
R.N Mandler ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Hiv Infection ◽  
Cardiovascular Risk Factors ◽  
Agatston Score ◽  
Funding Source ◽  
Significant Difference ◽  
Ascvd Risk ◽  
Artery Disease

Abstract Background/Introduction Cross-sectional studies are inconsistent on the potential independent adverse effects of human immunodeficiency virus (HIV)-infection on coronary artery disease (CAD). Furthermore, there is no information on the potential effects of HIV-infection on plaque volumes. Also, only the independent effects of HIV-infection on CAD have been investigated. Purpose In a prospective longitudinal observational cohort, we wished to assess whether HIV-infection accelerates CAD independently, or by acting in synergistic fashion with conventional and nonconventional cardiovascular risk factors to accelerate disease progression as assessed by clinical and volumetric parameters of CAD on coronary CT angiography (CCTA). Methods Overall, 300 asymptomatic individuals without cardiovascular symptoms but with CCTA-confirmed coronary plaques (210 males, age: 48.0±7.2 years) with or without HIV (226 HIV-infected) prospectively underwent CCTA at two time points (mean follow-up: 4.0±2.3 years). Agatston-score, number of coronary plaques, segment stenosis score were calculated, and we also segmented the coronary plaques to enumerate total, noncalcified (−100–350HU) and calcified (≥351HU) plaque volumes. Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use and high-sensitivity C-reactive protein on CCTA markers of CAD. Results In univariate analysis, there was no significant difference in CAD characteristics between HIV-infected and -uninfected, neither at baseline nor at follow-up (p&gt;0.05 for all). Furthermore, there was no significant difference in annual progression rates between the two groups (p&gt;0.05 for all). By multivariate analysis, HIV was not associated with any CAD parameter (p&gt;0.05 for all). However, among HIV-infected individuals, each year of cocaine use significantly increased all CAD parameters (p&lt;0.05 for all), while ASCVD risk score was significantly associated with CAD parameters except for Agatston-score (p&lt;0.05). These associations were only present among HIV-infected individuals. Conclusion(s) Instead of directly worsening CAD, HIV may promote CAD through increased susceptibility to conventional and nonconventional cardiovascular risk factors. Therefore, aggressive management of both conventional and nonconventional cardiovascular risk factors is needed to reduce cardiovascular burden of HIV-infection. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Institutes of Health, National Institute on Drug Abuse

scholarly journals Cardiovascular Risk Factors and Diabetes in Medical Students: Observational Study, Experience in Colombia

2018 ◽  
Vol 6 (2) ◽  
pp. 61-65 ◽  
Author(s):  
Diego Mauricio Bados Enriquez ◽  
Karoll Vanessa Ladino Oyola ◽  
Juan Esteban Yucuma Ruiz
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Medical Students ◽  
Cardiovascular Risk Factors ◽  
Risk Score ◽  
Low Risk ◽  
Early Interventions ◽  
Moderate Risk

Background: Cardiovascular Disease is a leading cause of preventable death. Cardiovascular risk factors’ identification is the cornerstone for effective and early interventions decreasing the frequency of acute health-threatening events. Since adolescence and youth are very vulnerable stages to develop risky habits, we decided to run this study in the Multidisciplinary Universitary Camp for Research and Service. Methods: A descriptive cross-sectional study was performed in the Multidisciplinary Universitary Camp for Research and Service in which 450 medical students from Colombia were assessed. After a probabilistic random simple sampling (n=50), we applied the World Health Organization test and Finnish Risk Score to calculate Cardiovascular and Diabetes Mellitus risk, respectively. We characterized the population by sociodemographic variables and anthropometric measurements. Results: The study shows that from 18 participating universities (n=50), the mean age of the participants was 21.14 years (SD 7.3) of whom 40% were male and 60% were female. Overall, 92% have a low risk of cardiovascular disease, 6% are at moderate risk and 2% are at high risk. 92% have low risk of diabetes mellitus and 8% are at moderate risk of having diabetes mellitus in the long term. Conclusion: The early identification of and intervention on risk factors could decrease significantly the onset of acute health-threatening cardiovascular pathologies. As medical students, adolescents and young adults are at risk of developing unhealthy habits which increase the incidence of cardiovascular disorders. The use of anthropometric measures and validated risk score scales is an appropriate way to get evidence for starting early interventions.

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