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1.
ESC Heart Fail ; 7(6): 3601-3609, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32940421

RESUMO

AIMS: Cardiomyopathies are a heterogeneous group of disorders that increase the risk for atrial fibrillation (AF). The aim of the study is to assess the prevalence of AF, anticoagulation management, and risk of stroke/transient ischaemic attack (TIA) in patients with cardiomyopathy. METHODS AND RESULTS: Three thousand two hundred eight consecutive adult patients with cardiomyopathy (34.9% female; median age: 55.0 years) were prospectively enrolled as part of the EURObservational Research Programme Cardiomyopathy/Myocarditis Registry. At baseline, 903 (28.2%) patients had AF (29.4% dilated, 27.5% hypertrophic, 51.5% restrictive, and 14.7% arrhythmogenic right ventricular cardiomyopathy, P < 0.001). AF was associated with more advanced New York Heart Association class (P < 0.001), increased prevalence of cardiovascular risk factors and co-morbidities, and a history of stroke/TIA (P < 0.001). Oral anticoagulation was administered in 71.7% of patients with AF (vitamin K antagonist: 51.6%; direct oral anticoagulant: 20.1%). At 1 year follow-up, the incidence of cardiovascular endpoints was as follows: stroke/TIA 1.85% (AF vs. non-AF: 3.17% vs. 1.19%, P < 0.001), death from any cause 3.43% (AF vs. non-AF: 5.39% vs. 2.50%, P < 0.001), and death from heart failure 1.67% (AF vs. non-AF: 2.44% vs. 1.31%, P = 0.033). The independent predictors for stroke/TIA were as follows: AF [odds ratio (OR) 2.812, P = 0.005], history of stroke (OR 7.311, P = 0.010), and anaemia (OR 3.119, P = 0.006). CONCLUSIONS: The study reveals a high prevalence and diverse distribution of AF in patients with cardiomyopathies, inadequate anticoagulation regimen, and high risk of stroke/TIA in this population.

2.
J Cardiol Cases ; 21(3): 106-109, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32153685

RESUMO

This clinical case report describes the simultaneous development of an acute myocardial infarction, stroke, and a massive pulmonary thromboembolism in a 44-year-old patient - a carrier of the thrombophilia gene polymorphisms: MTHFR C677T, А1298C, PAI-1 4G/5G, ITGA2 C807T. Multifocal thrombosis was probably due to the initial congenital deficiency of anticoagulants, accompanied by a decrease in antithrombin III and protein C, against the background of their critical consumption in cascade thrombosis, in combination with the carrier of polymorphisms of moderate and low thrombogenic risk. This case is unique in that there is usually a tendency toward clinical thrombosis when the level of antithrombin III is less than 70%. Such patients develop thrombosis at a younger age, and by the age of 35-40 years usually have a verified diagnosis of extremely high-risk hereditary thrombophilia. In this case, multifocal thrombosis was accompanied by critically low values of anticoagulants: antithrombin III - 3.4%, and protein C - 36.8%. The patient had suffered from epilepsy since childhood and took anticonvulsant drugs that increase the deficit of active folic acid and can lead to hyperhomocysteinemia, which in this case, against the background of an innate decrease in the activity of methyltetrahydrofolate reductase, could have aggravated the situation. .

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