124 research outputs found

    Fulminant myocarditis parvovirus B19 related in a young woman

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    We present the case of a 18-year-old female with fulminant lymphocytic myocarditis caused by Parvovirus B19 (PVB19), successfully treated using temporary LVAD. In the literature there is no consensus on the surgical strategy. While some surgeons prefer to use a single device supporting only the LV, others prefer to start immediately with a biventricular supporting. At pre-procedural ultrasound evaluation, her anatomical features were not suitable for a percutaneous device such as the Impella. Thus, a temporary paracorporeal continuous flow LVAD was inserted. The heart recovery allowed LVAD removal 9 days after the implant

    292. Extracorporeal membrane oxygenation for refractory cardiogenic shock: a bridge to decision?

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    Cardiogenic shock refractory to conventional therapy has very high mortality and limited therapeutical options. Aim of the study was to evaluate the impact of the use of ECMO as a life-saving measure when optimal conventional treatment has been reached and mechanical circulatory support is the only option for survival. Material and methods: Between January 2009 and May 2011, 32 patients in cardiogenic shock refractory to optimal conventional therapy (inotropes and intra-aortic-balloonpump) were treated with the extracorporeal life support implantation. Veno-arterial extracorporeal membrane oxygenation has been implanted either at bedside under local anesthesia or in operating room. Results: The mean age of the population (24 male and 8 female) was 49 ± 16 years, all patients presented with cardiogenic shock refractory to medical therapy due to various etiology. Veno-arterial extracorporeal membrane oxygenation was implanted at bedside under local anesthesia in 20 awake patients (63%) and in the operating room in the remaining 12 (37%). Average duration of ECMO support was 12.3 ± 10.2 days (range 1–46). Twenty-six patients (81%) were weaned from veno-arterial extracorporeal membrane oxygenation or bridged to either a ventricular assist device or heart transplantation. ECMO was used as bridge to transplantation in 7 patients (22%), bridge to recovery in 10 patients (31%) and bridge to bridge in 9 patients (28%). Six patients (18.7%) died during ECMO support, whereas 30-day overall survival after ECMO removal was 80.7% (21/26 pts). Sixteen patients (50%) were discharged from the hospital, with a 100% survival at sixmonths follow-up. Conclusions: In our experience the use of ECMO as a "bridge to decision" significantly improved the outcome of cardiogenic shock patients, greatly reducing the expected mortality

    No evidence of association between prothrombotic gene polymorphisms and the development of acute myocardial infarction at a young age

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    Background : we investigated the association between 9 polymorphisms of genes encoding hemostasis factors and myocardial infarction in a large sample of young patients chosen because they have less coronary atherosclerosis than older patients, and thus their disease is more likely to be related to a genetic predisposition to a prothrombotic state Methods and Results : this nationwide case-control study involved 1210 patients who had survived a first myocardial infarction at an age of 45 years who underwent coronary arteriography in 125 coronary care units and 1210 healthy subjects matched for age, sex, and geographical origin. None of the 9 polymorphisms of genes encoding proteins involved in coagulation (G-455A -fibrinogen: OR, 1.0; CI, 0.8 to 1.2; G1691A factor V: OR, 1.1; CI, 0.6 to 2.1; G20210A factor II: OR, 1.0; CI, 0.5 to 1.9; and G10976A factor VII: OR, 1.0; CI, 0.8 to 1.3), platelet function (C807T glycoprotein Ia: OR, 1.1; CI, 0.9 to 1.3; and C1565T glycoprotein IIIa: OR, 0.9; CI, 0.8 to 1.2), fibrinolysis (G185T factor XIII: OR, 1.2; CI, 0.9 to 1.6; and 4G/5G plasminogen activator inhibitor type 1: OR, 0.9; CI, 0.7 to 1.2), or homocysteine metabolism (C677T methylenetetrahydrofolate reductase: OR, 0.9; CI, 0.8 to 1.1) were associated with an increased or decreased risk of myocardial infarction Conclusions : this study provides no evidence supporting an association between 9 polymorphisms of genes encoding proteins involved in hemostasis and the occurrence of premature myocardial infarction or protection against it
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