173 research outputs found

    Is it worth closing the atrial septal defect in patients with insignificant shunt?

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    Introduction: Closure of the atrial septal defect in patients with insignificant shunt is controversial. Aim: To evaluate the outcomes of transcatheter closure of atrial septal defect (ASD) in symptomatic patients with borderline shunt. Material and methods: One hundred and sixty patients (120 female, 40 male) with a mean age of 30.1 ±16.2 (20–52) years with a small ASD who underwent transcatheter closure were analyzed. All patients had a small ASD with Qp : Qs ratio ≤ 1.5, mean 1.2 ±0.9 (1.1–1.5) in echo examination. Cardiopulmonary exercise tests, clinical study, transthoracic echocardiographic study as well as quality of life (QoL) (measured using the SF36 questionnaire (SF36q)) were repeated in all patients before and after the procedure. Results: The devices were successfully implanted in all patients. After 12 months of ASD closure, all the patients showed a significant improvement of exercise capacity (oxygen consumption – 21.9 ±3.1 vs. 30.4 ±7.7, p > 0.001). The QoL improved in 7 parameters at 12-month follow-up. The mean SF36q scale increased significantly in 141 (88.1%) patients of mean 43.2 ±20.1 (7–69). A significant decrease of the right ventricular area (20.3 ±1.3 cm2 vs. 18.3 ±1.2 cm2, p < 0.001) and the right atrial area (15.2 ±1.9 cm2 vs. 12.0 ±1.6 cm2, p < 0.001) was observed at 12-month follow-up. Conclusions: Closure of ASD in the patients with insignificant shunt resulted in significant durable clinical and hemodynamic improvement after percutaneous treatment

    Resynchronization therapy transvenous approach in dextrocardia and congenitally corrected transposition of great arteries

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    Cardiac resynchronization therapy (CRT) is an acknowledged treatment for advanced heart failure in acquired dilated cardiomyopathy, resistant to pharmacotherapy. Although there are no therapeutic standards regarding heart failure originating from congenital heart defects with systemic right ventricle, a number of CRT implantations by transvenous approach in congenitally corrected transposition of the great arteries (CCTGA) have been reported since 2001, even though none of them expressly referred to a case concomitant with dextrocardia and situs inversus anomaly. We present a 57 year-old patient with dextrocardia and CCTGA, who underwent surgical closure of interatrial and interventricular septal defects at the age of 19, and in whom a VVI pacemaker was subsequently implanted at age 36. A three-lead CRT system was implanted by transvenous approach. Imaging techniques, including multi-slice computed tomography, targeted to pacing system and unusual anatomical relationships were applied. Within a 20-month follow-up, a significant improvement of functional NYHA class, systemic right ventricle ejection fraction and exercise capability were observed. Entirely transvenous CRT system implantation is feasible in patients with dextrocardia and CCTGA, and has substantial potential for long-term benefits. (Cardiol J 2010; 17, 5: 503-508

    Flow cytometric assessment of endothelial and platelet microparticles in patients with atrial fibrillation treated with dabigatran

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    The prothrombotic state in patients with atrial fibrillation (AF) is related to endothelial injury, the activation of platelets and the coagulation cascade. We evaluated the levels of platelet- (CD42b) and endothelial-derived (CD144) microparticles in the plasma patients with non-valvular AF treated with dabigatran at the time of expected minimum and maximum drug plasma concentrations. Following that, we determined the peak dabigatran plasma concentration (cpeak ). CD42b increased after taking dabigatran (median [IQR] 36.7 [29.4-53.3] vs. 45.6 [32.3-59.5] cells/mL; p ¼ 0.025). The concentration of dabigatran correlated negatively with the post-dabigatran change in CD42b (DCD42b, r ¼ -0.47, p ¼ 0.021). In the multivariate model, the independent predictors of DCD42b were: cpeak (HR -0.55; with a 95% confidence interval, CI [-0.93, -0.16]; p ¼ 0.007), coronary artery disease (CAD) (HR -0.41; 95% CI [-0.79, -0.02]; p ¼ 0.037) and peripheral artery disease (PAD) (HR 0.42; 95% CI [0.07, 0.74]; p ¼ 0.019). CD144 did not increase after dabigatran administration. These data suggest that low concentrations of dabigatran may be associated with platelet activation. PAD and CAD have distinct effects on CD42b levels during dabigatran treatment
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