Purpose: We report new electrocardiographic criteria (ECG) for localizing premature ventricular complexes (PVCs) originating from the base of the left ventricle (LV).
Methods: QRS deflection (positive negative or negative positive) in lead aVR and aVL respectively, were evaluated in 41 PVC/VT cases.
Results: There were a total of 41 patients, age 64 ± 11 years.
Introduction: Ventricular arrhythmias/premature ventricular complexes (VA/PVCs) that can be ablated from within the coronary venous system (CVS) have not been described in the United States Veterans Health Administration (VHA) population. We retrospectively studied the VA/PVCs ablations that were performed in the VHA population.
Methods: Data from 42 consecutive patients who underwent VA/PVCs ablation at Veterans Affairs Hospital, Indianapolis, IN, with 44 VA/PVCs was included in the study.
Digoxin has been a key therapeutic for heart failure and atrial tachyarrhythmias for over 200 years following Withering's groundbreaking work depicting the therapeutic benefit of the common botanical foxglove in his 1785 monograph. The use of digoxin preceded any randomised evidence or even basic understanding of its mechanism of action. Over the past two decades, there has been mounting evidence further challenging the safety and efficacy of digoxin, while multiple other therapies for both heart failure and atrial tachyarrhythmias have proven to be more effective and safe.
View Article and Find Full Text PDFBackground: The mechanism of sinoatrial node (SAN) dysfunction in atrial fibrillation (AF) is unclear.
Objective: The purpose of this study was to test the hypothesis that defective spontaneous sarcoplasmic reticulum (SR) Ca(2+) release (Ca(2+) clock) is in part responsible for SAN dysfunction in AF.
Methods: Arrhythmic events and SAN function were evaluated in pacing-induced AF dogs (n = 7) and in normal dogs (n = 19) with simultaneous intracellular calcium (Ca(i)) and membrane potential recording.
Background: Recent evidence indicates that membrane voltage and Ca2+ clocks jointly regulate sinoatrial node (SAN) automaticity. Here we test the hypothesis that sinus rate acceleration by beta-adrenergic stimulation involves synergistic interactions between these clock mechanisms.
Methods And Results: We simultaneously mapped intracellular calcium (Ca(i)) and membrane potential in 25 isolated canine right atrium, using previously described criteria of the timing of late diastolic Ca(i) elevation (LDCAE) relative to the action potential upstroke to detect the Ca2+ clock.