Circulation. Arrhythmia and electrophysiology
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Circ Arrhythm Electrophysiol · Dec 2011
Randomized Controlled Trial Comparative StudyRadiofrequency catheter ablation and antiarrhythmic drug therapy: a prospective, randomized, 4-year follow-up trial: the APAF study.
Information on comparative outcome between radiofrequency catheter ablation (RFA) and antiarrhythmic drugs (AADs) >1 year after randomization is important for clinical decision-making. ⋯ URL: http://www.clinicaltrials.gov. Unique identifier: NCT00340314.
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Circ Arrhythm Electrophysiol · Dec 2011
Randomized Controlled TrialUse of an implantable monitor to detect arrhythmia recurrences and select patients for early repeat catheter ablation for atrial fibrillation: a pilot study.
Catheter ablation of atrial fibrillation (AF) has proved effective in curing highly symptomatic patients with paroxysmal AF. The aim of this prospective, randomized study was to identify the optimal treatment of patients with AF recurrences after the first ablation. ⋯ URL: http://www.clinicaltrials.gov. Unique identifier: NCT01164319.
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Circ Arrhythm Electrophysiol · Dec 2011
Genotype- and mutation site-specific QT adaptation during exercise, recovery, and postural changes in children with long-QT syndrome.
Exercise stress testing has shown diagnostic utility in adult patients with long-QT syndrome (LQTS); however, the QT interval adaptation in response to exercise in pediatric patients with LQTS has received little attention. ⋯ Genotype-specific changes in repolarization response to exercise and recovery exist in the pediatric population and are of diagnostic utility in LQTS. An extended recovery phase is preferable to assess the repolarization response after exercise in the pediatric population.
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Circ Arrhythm Electrophysiol · Dec 2011
Calcium-calmodulin kinase II mediates digitalis-induced arrhythmias.
Digitalis-induced Na(+) accumulation results in an increase in Ca(2+)(i) via the Na(+)/Ca(2+) exchanger, leading to enhanced sarcoplasmic reticulum (SR) Ca(2+) load, responsible for the positive inotropic and toxic arrhythmogenic effects of glycosides. A digitalis-induced increase in Ca(2+)(i) could also activate calcium-calmodulin kinase II (CaMKII), which has been shown to have proarrhythmic effects. Here, we investigate whether CaMKII underlies digitalis-induced arrhythmias and the subcellular mechanisms involved. ⋯ These results show for the first time that CaMKII mediates ouabain-induced arrhythmic/toxic effects. We suggest that CaMKII-dependent phosphorylation of the RyR, resulting in Ca(2+) leak from the SR, is the underlying mechanism involved.