Nils Bögeholz

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The cardiac Na+/Ca2+ exchanger (NCX) generates an inward electrical current during SR-Ca2+ release, thus possibly promoting afterdepolarizations of the action potential (AP). We used transgenic mice 12.5 weeks or younger with cardiomyocyte-directed overexpression of NCX (NCX-Tg) to study the proarrhythmic potential and mechanisms of enhanced NCX activity.(More)
BACKGROUND Ranolazine has been reported to have an antiarrhythmic potential. The aim of this study was to assess the electrophysiologic effects of ranolazine and to compare its effects to vernakalant in an experimental whole-heart model of short-QT syndrome. METHODS Rabbit hearts were isolated and Langendorff-perfused. After obtaining baseline data,(More)
Der myokardiale Kalziumstoffwechsel ist für eine physiologische Herzfunktion von essentieller Bedeutung. Diese Übersichtsarbeit beschreibt die Rolle von Ca2+ Ionen während des kontraktilen Zyklus und der myokardialen Erregung sowie den modulierenden Einfluss β-adrenerger Stimulation. Cardiac calcium (Ca2+) handling subsumes the mechanisms maintaining the(More)
BACKGROUND The Na(+)/Ca(2+) exchanger (NCX) has been implied to cause arrhythmias. To date, information on the role of NCX in arrhythmogenesis derived from models with increased NCX expression, hypertrophy, and heart failure. Furthermore, the exact mechanism by which NCX exerts its potentially proarrhythmic effect, ie, by promoting early afterdepolarization(More)
INTRODUCTION The antihistaminic antazoline (ANT) was reported to be highly effective and safe for rapid conversion of atrial fibrillation (AF). We therefore analyzed underlying mechanisms in an experimental whole-heart model. METHODS AND RESULTS Isolated and retrogradely perfused rabbit hearts underwent a standardized protocol employing atrial burst(More)
AIMS In atrial fibrillation, increased function of the Na+/Ca2+-exchanger (NCX) is one among several electrical remodeling mechanisms. METHODS/RESULTS Using the patch-clamp- and Ca2+ imaging-methods, we investigated atrial myocytes from NCX-homozygous-overexpressor (OE)- and heterozygous-knockout (KO)-mice and their corresponding wildtypes (WTOE; WTKO).(More)
BACKGROUND Slow pathway modification (SPM) is the therapy of choice for AV-nodal reentry tachycardia (AVNRT). When AVNRT is not inducible, empirical ablation can be considered, however, the outcome in patients with two AV nodal echo beats (AVNEBs) is unknown. METHODS Out of a population of 3003 patients who underwent slow pathway modification at our(More)