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      The Association of Hereditary Prothrombotic Risk Factors with ST-Elevation Myocardial Infarction Translated title: Kalıtsal Protrombotik Risk Faktörlerinin ST Yükselmeli Miyokart Enfarktüsü ile İlişkisi

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          Abstract

          Objective

          The ST- elevation myocardial infarction (STEMI), a serious health care problem, is commonly a thrombotic complication of coronary artery disease. We compare the STEMI patients and control group in terms of the possible causes of inherited thrombophilia including FactorV Cambridge G1091C, FactorV Leiden G1691A, MTHFRC677T, MTHFR A1298C, FactorII G20210A, Factor XIII (V34L), PAI-1, FGB, ITGB3, APOB, FVHR2, ACE gene variants.

          Methods

          Fifty-three patients with STEMI and 47 individuals without diagnosis of acute coronary syndrome were included in the study. Percutaneous coronary intervention was performed for patients with STEMI. Echocardiography was performed and inherited thrombophilia genes were evaluated in all subjects.

          Results

          The MTHFR A1298C, Factor XIII (V34L), ITGB, ACE and homozygous or compound heterozygous gene varations of inherited thrombophilia are significantly related with STEMI (p<0.05). Also significantly higher MTHFR A1298C, FactorV Leiden G1691A, PAI and ACE gene variations in MI patients who were smokers; Factor XIII (V34L), PAI and ACE gene variations in MI patients with HT; PAI and ACE gene variation in MI patients with FH and PAI gene variations in MI patients with HL were detected when compared with the control groups with all of the same risk factors (p<0.05).

          Conclusion

          Hereditary thrombophilia factors may show promise in the prevention and management of STEMI when supported studies with larger case series.

          ÖZ

          Amaç

          Ciddi bir sağlık sorunu olan ST yükselmeli miyokart enfarktüsü (STEMI), genellikle koroner arter hastalığının trombotik bir komplikasyonudur. STEMI hastalarını ve kontrol grubunu, FactorV Cambridge G1091C, FactorV Leiden G1691A, MTHFRC677T, MTHFR A1298C, FactorII G20210A, FaktörXIII (V34L), PAI-1, FGB, ITGB3, APOB, FVHR2 dahil olmak üzere kalıtsal trombofilinin olası nedenleri açısından karşılaştırdık.

          Yöntem

          Çalışmaya STEMI’li 53 hasta ve akut koroner sendrom tanısı olmayan 47 kişi dahil edildi. STEMI’li hastalara perkütan koroner girişim uygulandı. Tüm olgulara ekokardiyografi yapıldı ve tüm olgular kalıtsal trombofili genleri açısından değerlendirildi.

          Bulgular

          Kalıtsal trombofilinin MTHFR A1298C, FaktörXIII (V34L), ITGB, ACE ve homozigot veya bileşik heterozigot gen varyasyonu STEMI ile anlamlı olarak ilişkilidir (p<0.05). Ayrıca sigara içen MI hastalarında MTHFR A1298C, FactorV Leiden G1691A, PAI ve ACE gen varyasyonu, HT’li MI hastalarında Faktör XIII (V34L), PAI ve ACE gen varyasyonu, aile öyküsü olan MI hastalarında PAI ve ACE gen varyasyonu ve HL’li MI hastalarında PAI gen varyasyonu anlamlı derecede kontrol grubundan daha yüksek bulundu.

          Sonuç

          Kalıtsal trombofili faktörleri, daha büyük seri çalışmalarla desteklendiğinde STEMI’nin ön-lenmesi ve tedavisinde umut vaat edebilir.

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          Most cited references29

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          Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging.

          The rapid technological developments of the past decade and the changes in echocardiographic practice brought about by these developments have resulted in the need for updated recommendations to the previously published guidelines for cardiac chamber quantification, which was the goal of the joint writing group assembled by the American Society of Echocardiography and the European Association of Cardiovascular Imaging. This document provides updated normal values for all four cardiac chambers, including three-dimensional echocardiography and myocardial deformation, when possible, on the basis of considerably larger numbers of normal subjects, compiled from multiple databases. In addition, this document attempts to eliminate several minor discrepancies that existed between previously published guidelines.
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            Fourth Universal Definition of Myocardial Infarction (2018)

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              • Article: not found

              Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines.

              The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management in 2001. Since the publication of ATP III, 5 major clinical trials of statin therapy with clinical end points have been published. These trials addressed issues that were not examined in previous clinical trials of cholesterol-lowering therapy. The present document reviews the results of these recent trials and assesses their implications for cholesterol management. Therapeutic lifestyle changes (TLC) remain an essential modality in clinical management. The trials confirm the benefit of cholesterol-lowering therapy in high-risk patients and support the ATP III treatment goal of low-density lipoprotein cholesterol (LDL-C) <100 mg/dL. They support the inclusion of patients with diabetes in the high-risk category and confirm the benefits of LDL-lowering therapy in these patients. They further confirm that older persons benefit from therapeutic lowering of LDL-C. The major recommendations for modifications to footnote the ATP III treatment algorithm are the following. In high-risk persons, the recommended LDL-C goal is <100 mg/dL, but when risk is very high, an LDL-C goal of <70 mg/dL is a therapeutic option, ie, a reasonable clinical strategy, on the basis of available clinical trial evidence. This therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100 mg/dL. Moreover, when a high-risk patient has high triglycerides or low high-density lipoprotein cholesterol (HDL-C), consideration can be given to combining a fibrate or nicotinic acid with an LDL-lowering drug. For moderately high-risk persons (2+ risk factors and 10-year risk 10% to 20%), the recommended LDL-C goal is <130 mg/dL, but an LDL-C goal <100 mg/dL is a therapeutic option on the basis of recent trial evidence. The latter option extends also to moderately high-risk persons with a baseline LDL-C of 100 to 129 mg/dL. When LDL-lowering drug therapy is employed in high-risk or moderately high-risk persons, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels. Moreover, any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglycerides, low HDL-C, or metabolic syndrome) is a candidate for TLC to modify these risk factors regardless of LDL-C level. Finally, for people in lower-risk categories, recent clinical trials do not modify the goals and cutpoints of therapy.
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                Author and article information

                Journal
                Medeni Med J
                Medeni Med J
                medj
                Medeniyet Medical Journal
                Istanbul Medeniyet University (Turkey )
                2149-2042
                2149-4606
                2020
                25 December 2020
                : 35
                : 4
                : 295-303
                Affiliations
                [1]Duzce University, Faculty of Medicine, Department of Cardiology, Duzce, Turkey
                [2]Duzce University, Faculty of Medicine, Department of Medical Genetics, Duzce, Turkey
                Author notes

                Ethics Committee Approval: This study approved by the Duzce University Ethic Committee, 20 January 2020, 2019/290.

                Conflict of interest: The authors declare that they have no conflict of interest.

                Funding: None.

                Informed Consent: Informed consent was taken from the participants of the study.

                Cite as: Damar İH, Eroz R. The association of hereditary prothromboticrisk factors with ST-elevation myocardial infarction. Medeni Med J. 2020;35:295-303.

                Author information
                https://orcid.org/0000-0001-6420-0122
                https://orcid.org/0000-0003-0840-2613
                Article
                10.5222/MMJ.2020.67366
                7945729
                33717621
                1e65ef5b-cfb1-4ccd-9ab9-d9f712c1be0d
                © Copyright Istanbul Medeniyet University Faculty of Medicine.

                This journal is published by Logos Medical Publishing. Licenced by Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

                History
                : 11 October 2020
                : 23 November 2020
                Categories
                Original Study

                coronary artery disease,inherited thrombophilia,stemi,thrombosis,hypercoagulation,koroner arter hastalığı,kalıtsal trombofili,tromboz,hiperkoagülasyon

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