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Background: Left atrial appendage closure (LAAC) became an alternative method for stroke prevention in patients with non‐valvular atrial fibrillation (AF) intolerant to long term oral anticoagulation therapy. This study aimed to compare endocardial (Amulet and LAmbere occluders) and epicardial (Lariat) LAAC techniques. Methods: A retrospective, observational case‐control study included 223 consecutive CHA2DS2‐VAS score–matched patients with AF who underwent LAAC in two centers. Results: There were 55 matched cases with the mean CHA2DS2‐VASs score 4.4 ± 1.22 (p = 1). Overall follow‐up was 308.2 patient‐years. The Endocardial group patients were older and more often females with congestive heart failure and peripheral vascular disease. The epicardial group more frequently had a stroke/transient ischemic attack history. There were no differences in hypertension, diabetes mellitus, and indications for procedure between both groups. The mean HAS‐BLED score was significantly higher in the endocardial group than in the epicardial group (4.3 ± 0.9 vs. 3.7 ± 1.3, p =.011). There were no differences in annual rates of thromboembolic events (2.6% vs 0.5%) and annual stroke (0.87% vs. 0%) between the endocardial and epicardial groups. Conclusion: Endocardial and Epicardial LAAC techniques show comparable implantation outcomes and safety profile and stroke prevention in patients with AF. Future randomized studies are needed to corroborate these initial results and assess long term mortality. [ABSTRACT FROM AUTHOR]

Introduction: Resuscitation from ventricular fibrillation (VF), particularly from prolonged VF, frequently is complicated by postfibrillatory myocardial dysfunction (postresuscitation stunning). We tested whether this dysfunction can be caused by reduced myofilament Ca2+ responsiveness after VF-induced myocyte Ca2+ overload. We also tested whether electrical defibrillation shocks contribute to this dysfunction. Methods and Results: Myofilament Ca responsiveness was estimated as ratio of left ventricular developed pressure over myocyte Ca2+ transient amplitudes (assessed as indo-1 fluorescence) in isolated perfused rat hearts before, during, and after VF (1.5 or 10 min) comparing three modes of defibrillation (bipbasic electrical shocks, lidocaine, or spontaneous). We found that, independent of these defibrillation modes, myofilament Ca responsiveness was significantly reduced, particularly after prolonged VF, although hearts were not ischemic or acidotic during and after VF (unchanged coronary flow, myocardial oxygen consumption, and pH of the coronary effluent). This reduction was associated with VF-induced myocyte Ca2+ overload and increasing or decreasing Ca2+ overload during VF (using 1 µM diltiazem or 6 mM extracellular calcium) led to parallel changes of myofilament Ca responsiveness. However, myofilament Ca2+ responsiveness was not associated with the defibrillation shock energy (range 0.1-15.0 J/g wet heart weight). Conclusion: Postfibrillatory myocardial dysfunction can be caused by reduced myofilament Ca2+ responsiveness after VF-induced myocyte Ca2+ overload. Electrical defibrillation shocks (up to 15 J/g wet heart weight). however, do not significantly contribute to this dysfunction. Our findings suggest that early additional therapy targeting intracellular Ca2+ overload may normalize myocyte Ca2+ and partially prevent postresuscitation stunning. [ABSTRACT FROM AUTHOR]