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1.
Europace ; 21(2): 192-193, 2019 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-30052888

RESUMO

In 2014, a joint consensus document dealing with the management of antithrombotic therapy in atrial fibrillation (AF) patients presenting with acute coronary syndrome (ACS) and/or undergoing percutaneous coronary or valve interventions was published, which represented an effort of the European Society of Cardiology Working Group on Thrombosis, European Heart Rhythm Association (EHRA), European Association of Percutaneous Cardiovascular Interventions (EAPCI), and European Association of Acute Cardiac Care (ACCA) endorsed by the Heart Rhythm Society (HRS) and Asia-Pacific Heart Rhythm Society (APHRS). Since publication of this document, additional data from observational cohorts, randomized controlled trials, and percutaneous interventions as well as new guidelines have been published. Moreover, new drugs and devices/interventions are also available, with an increasing evidence base. The approach to managing AF has also evolved towards a more integrated or holistic approach. In recognizing these advances since the last consensus document, EHRA, WG Thrombosis, EAPCI, and ACCA, with additional contributions from HRS, APHRS, Latin America Heart Rhythm Society (LAHRS), and Cardiac Arrhythmia Society of Southern Africa (CASSA), proposed a focused update, to include the new data, with the remit of comprehensively reviewing the available evidence and publishing a focused update consensus document on the management of antithrombotic therapy in AF patients presenting with ACS and/or undergoing percutaneous coronary or valve interventions, and providing up-to-date consensus recommendations for use in clinical practice.


Assuntos
Síndrome Coronariana Aguda/terapia , Anticoagulantes/uso terapêutico , Fibrilação Atrial/tratamento farmacológico , Cateterismo Cardíaco , Fibrinolíticos/uso terapêutico , Doenças das Valvas Cardíacas/terapia , Intervenção Coronária Percutânea , Inibidores da Agregação Plaquetária/uso terapêutico , Acidente Vascular Cerebral/prevenção & controle , Síndrome Coronariana Aguda/diagnóstico , Síndrome Coronariana Aguda/epidemiologia , Anticoagulantes/efeitos adversos , Fibrilação Atrial/diagnóstico , Fibrilação Atrial/epidemiologia , Cateterismo Cardíaco/efeitos adversos , Consenso , Fibrinolíticos/efeitos adversos , Doenças das Valvas Cardíacas/diagnóstico , Doenças das Valvas Cardíacas/epidemiologia , Hemorragia/induzido quimicamente , Humanos , Intervenção Coronária Percutânea/efeitos adversos , Inibidores da Agregação Plaquetária/efeitos adversos , Medição de Risco , Fatores de Risco , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/epidemiologia , Resultado do Tratamento
2.
Thromb Haemost ; 106(3): 511-20, 2011 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21800001

RESUMO

The FXIII-A Leu34 genetic variant increases and accelerates fibrin stabilisation; however, its association with premature coronary artery disease (CAD) and thrombotic events remains controversial. FXIII Val34Leu genotype was determined in 242 young individuals (<45 years old) who survived a myocardial infarction (MI) and 242 healthy controls matched for age and gender. We evaluated its effect on long-term clinical outcome defined as a composite of cardiovascular death, recurrent MI and urgent revascularisation. In addition, fibrin clot stiffness (elastic modulus or EM) and response to rt-PA-mediated fibrinolysis (fibrinolysis rate) were measured ex vivo using the Hemodyne analyser and confocal microscopy as surrogate endpoint. FXIII-A Leu34 genetic variant was not associated with premature CAD (adj. odds ratio 0.83 [0.49-1.4]) nor did it influence clinical outcome in patients, during a median follow-up of 6.3 (± 2.4) years. Patients produced stiffer fibrin clots (median [IQR] EM = 20.3 [14.9-28.1] vs. 12.8 [9.6-17.1] kdynes/cm²; p<0.0001) and displayed reduced response to fibrinolysis with lower fibrinolysis rate (6.7 [3.4-11.0] vs. 9.0 [5.0-16.7] sec-¹ x 10(-4); p<0.0001) than healthy controls. Carriage of factor XIII-A Leu34 led to a stepwise decrease in fibrinolysis rate with a significant gene-dose-effect in patients (7.7 [4.1-12.2] vs. 4.8 [3.0-8.5] vs. 4.3 [2.4-8.1] sec-¹ x 10(-4), for wild-type, heterozygous and homozygous, p for trend = 0.003) and a non-significant trend in controls (p = 0.01). In conclusion, FXIII-A Leu34 is a polymorphism which provides a strong resistance to fibrinolysis with a gene-dose effect, but does not relate to premature CAD or to recurrent coronary events in this study.


Assuntos
Fatores Etários , Doença da Artéria Coronariana/genética , Fator XIII/genética , Adulto , Estudos de Casos e Controles , Doença da Artéria Coronariana/epidemiologia , Doença da Artéria Coronariana/mortalidade , Doença da Artéria Coronariana/fisiopatologia , Trombose Coronária , Análise Mutacional de DNA , Feminino , Seguimentos , Estudos de Associação Genética , Predisposição Genética para Doença , Genótipo , Hemodinâmica , Humanos , Leucina/genética , Masculino , Infarto do Miocárdio , Polimorfismo Genético , Recidiva , Análise de Sobrevida
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