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Introduction: Biventricular pacing (BiVp) improves outcomes in systolic heart failure patients with electrical dyssynchrony. BiVp is delivered from epicardial left ventricular (LV) and endocardial right ventricular (RV) electrodes. Acute electrical activation changes with different LV‐RV stimulation offsets can help guide individually optimized BiVp programming. We sought to study the BiVp ventricular activation with different LV‐RV offsets and compare with 12‐lead ECG. Methods: In five patients with BiVp (63 ± 17‐year‐old, 80% male, LV ejection fraction 27 ± 6%), we evaluated acute ventricular epicardial activation, varying LV‐RV offsets in 20 ms increments from −40 to 80 ms, using electrocardiographic imaging (ECGI) to obtain absolute ventricular electrical uncoupling (VEUabs, absolute difference in average LV and average RV activation time) and total activation time (TAT). For each patient, we calculated the correlation between ECGI and corresponding ECG (3D‐QRS‐area and QRS duration) with different LV‐RV offsets. Results: The LV‐RV offset to attain minimum VEUabs in individual patients ranged 20–60 ms. In all patients, a larger LV‐RV offset was required to achieve minimum VEUabs (36 ± 17 ms) or 3D‐QRS‐area (40 ± 14 ms) than that for minimum TAT (−4 ± 9 ms) or QRS duration (−8 ± 11 ms). In individual patients, 3D‐QRS‐area correlated with VEUabs (r 0.65 ± 0.24) and QRS duration correlated with TAT (r 0.95 ± 0.02). Minimum VEUabs and minimum 3D‐QRS‐area were obtained by LV‐RV offset within 20 ms of each other in all five patients. Conclusions: LV‐RV electrical uncoupling, as assessed by ECGI, can be minimized by optimizing LV‐RV stimulation offset. 3D‐QRS‐area is a surrogate to identify LV‐RV offset that minimizes LV‐RV uncoupling. [ABSTRACT FROM AUTHOR]

Background: Smoking is a major risk factor for cardiovascular disease. The impact of smoking on the right and left atrial substrates is unknown. Methods: This study included 88 patients (age 50 ± 13 years, M/F = 71/17) who underwent four pulmonary veins isolation (PVI) for paroxysmal atrial fibrillation (AF). The mean voltage and total activation time of the individual atria were obtained by using a NavX mapping system, and were compared between the patients with and without a previous smoking history. The dose effect was evaluated by the smoking intensity-duration, defined as the number of packs per day plus how many years they had been smoking. Results: The right atrial (RA) mean voltage was lower in the patients with a previous history of smoking than in those without a history of smoking (1.92 ± 0.49 vs 2.17 ± 0.56 mV, P < 0.05). The left atrial (LA) mean voltage was similar between the two groups (1.73 ± 0.67 vs 1.82 ± 0.48 mV, P = 0.488). Further, the total activation time of the RA was longer in the patients with a previous history of smoking than in those without a history of smoking, but not so for the LA. Furthermore, the voltage reduction in the RA was related to the smoking intensity-duration (Pearson's correlation, r = 0.650, P < 0.001). Conclusions: In patients with atrial fibrillation, the RA mean voltage and total activation time were significantly correlated to smoking and had a dose-dependent effect. [ABSTRACT FROM AUTHOR]

Spontaneous Arrhythmias in Acute Ischemia. Introduction: Ventricular tachycardia (VT) and ventricular fibrillation (VF) induced by thrombotic coronary occlusion were mapped in three dimensions In ten dogs. Methods and Results: Thrombotic occlusion was induced using a wire to deliver current to the proximal left circumflex artery (LCX). In nine dogs, nonsustained VT (NSVT) arose from numerous focal sites. Sustained VT was initiated in six dogs (VT group) by a focus near or in the ischemic region. VT was maintained by a focus in the ischemic border In three dogs and by macroreentry that involved both the Ischemic and nonischemic regions in the other three dogs. In five dogs, VT degenerated into VF due to intramural reentry in different locations. Mean total activation time (AT), the time for activation to traverse the ventricles, for a sinus beat when LCX current was first applied was 40 ± 4 msec. In the four dogs in which VT occurred 3 to 7 minutes after total occlusion, sinus AT increased to 98 to 146 msec just before VT. Sinus AT in the four dogs without VT was always <98 msec. Mean AT of the first ten cycles of VT was significantly longer in those VTs that degenerated Into VE (169 ± 29 msec) than in those that did not (81 ± 12 msec). Conclusion: Thrombotic LCX occlusion Induced NSVT In 90%, VT In 60%, and VF in 50% of dogs. Focal mechanisms caused most NSVTs and VT Initiation. VT was maintained by a focus near or in the ischemic region or by macroreentry involving both the ischemic and nonischemic regions. AT identified animals in which VT occurred soon after LCX occlusion and in which VT progressed to VF. [ABSTRACT FROM AUTHOR]