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      Association of traditional cardiovascular risk factors in adults younger than 55 years with coronary heart disease. Case-control study

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          Abstract

          Objectives:

          The traditional cardiovascular risk factors associated with coronary artery disease in individuals younger than 55 years old was determined in this study.

          Methods:

          A retrospective, paired case–control study comprised of patients younger than 55 years old who were admitted to the hospital due to acute coronary syndrome with coronary artery disease from 2011 to 2016. There were two controls per case, paired by age, gender, admission date, and health insurance. Data from patients were collected, such as sociodemographic information, cardiovascular risk factors, and drug therapy information. A conditional logistic regression model was created to evaluate the association between traditional cardiovascular risk factors and coronary artery disease.

          Results:

          There were 171 cases and 342 controls included in the study. The median age was 49 years, with a predominance of male gender (80.12%). Nearly 66% of cases had at least one traditional cardiovascular risk factor. The most common risk factors were obesity (57.31%), arterial hypertension (45.62%), and smoking (28.97%). Independent risk factors of coronary artery disease in patients younger than 55 years were arterial hypertension (odds ratio, 2.52; 95% confidence interval, 1.48–4.20; p = 0.001) and smoking (odds ratio, 7.15; 95% confidence interval, 3.19–15.99; p = 0.00). No significant association between diabetes mellitus and coronary heart disease in the global group (odds ratio, 2.04; 95% confidence innterval, 0.91–4.58; p = 0.083) was found.

          Conclusion:

          For patients younger than 55 years, with a theoretically lower risk of coronary artery disease due to their age, having one or several traditional risk factors (smoking, arterial hypertension, dyslipidemia, or diabetes mellitus) confers an increased risk of coronary artery disease regardless of age.

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          Most cited references18

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          Explaining how "high-grade" systemic inflammation accelerates vascular risk in rheumatoid arthritis.

          There is intense interest in mechanisms whereby low-grade inflammation could interact with conventional and novel vascular risk factors to promote the atheromatous lesion. Patients with rheumatoid arthritis (RA), who by definition manifest persistent high levels of inflammation, are at greater risk of developing cardiovascular disease. Mechanisms mediating this enhanced risk are ill defined. On the basis of available evidence, we argue here that the systemic inflammatory response in RA is critical to accelerated atherogenesis operating via accentuation of established and novel risk factor pathways. By implication, long-term suppression of the systemic inflammatory response in RA should be effective in reducing risk of coronary heart disease. Early epidemiological observational and clinical studies are commensurate with this hypothesis. By contrast, risk factor modulation with conventional agents, such as statins, may provide unpredictable clinical benefit in the context of uncontrolled systemic inflammatory parameters. Unraveling such complex relationships in which exaggerated inflammation-risk factor interactions are prevalent may elicit novel insights to effector mechanisms in vascular disease generally.
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            Sex Differences in Cardiac Risk Factors, Perceived Risk, and Health Care Provider Discussion of Risk and Risk Modification Among Young Patients With Acute Myocardial Infarction: The VIRGO Study.

            Differences between sexes in cardiac risk factors, perceptions of cardiac risk, and health care provider discussions about risk among young patients with acute myocardial infarction (AMI) are not well studied.
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              • Article: not found

              Parental history is an independent risk factor for coronary artery disease: the Framingham Study.

              Family history of CAD, defined as parental death by CAD, was found to be a significant independent predictor of CAD in a logistic regression model controlling for standard risk factors and length of follow-up among the 5209 participants in the Framingham Study. Persons with a positive parental history have a 29% increased risk of CAD, and the strength of the association between parental history and CAD is similar to that found for other standard risk factors such as systolic blood pressure, cholesterol level, and cigarette smoking. No evidence was found that persons with a family history of CAD have a decreased capacity to cope with the deleterious effects of known risk factors; that is, no significant interaction was found between any of the risk factors and parental history of CAD. Among men with low risk for CAD by risk-factor profile (i.e., nonsmoking, thin, nonhypertensive persons), more than two thirds of those who experience CAD have a positive parental history. This study suggests that CAD among persons who are predicted to be at low risk by standard risk factors may have a substantial genetic component and that the risk associated with parental history may not be reduced by modification of these factors. Nevertheless, among persons with a positive family history, those with a favorable risk profile are at substantially less risk for CAD than those with an unfavorable risk profile.
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                Author and article information

                Journal
                SAGE Open Med
                SAGE Open Med
                SMO
                spsmo
                SAGE Open Medicine
                SAGE Publications (Sage UK: London, England )
                2050-3121
                17 June 2020
                2020
                : 8
                : 2050312120932703
                Affiliations
                [1 ]Internal Medicine Department, Cardiology Service, Vascular Intervention Unit, Fundación Valle del Lili, Cali, Colombia
                [2 ]Health Science Faculty, Icesi University, Cali, Colombia
                [3 ]Clinical Research Center, Fundación Valle del Lili, Cali, Colombia
                Author notes
                [*]Diana Cristina Carrillo-Gómez, Internal Medicine Department, Cardiology Service, Fundación Valle del Lili, Av Simón Bolivar, Kr 98 #18-49 4th Floor Tower 1, Cali 760032, Colombia. Email: diana.carrillo@ 123456fvl.org.co
                [*]

                These authors takes responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.

                Author information
                https://orcid.org/0000-0002-9085-9083
                Article
                10.1177_2050312120932703
                10.1177/2050312120932703
                7301652
                32595970
                324d39d2-32b5-4522-a452-e4b64bb488f7
                © The Author(s) 2020

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 1 December 2019
                : 13 May 2020
                Funding
                Funded by: Fundación Valle del Lili, FundRef https://doi.org/10.13039/501100003402;
                Categories
                Original Article
                Custom metadata
                January-December 2020
                ts1

                risk factors,cardiovascular diseases,myocardial infarction,acute coronary syndrome,adult

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