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Premature ventricular complexes (PVCs) are increasingly recognized, as the use of ECG wearables becomes more widespread. In particular, PVCs arising from both the right ventricular outflow tract (RVOT) and left ventricular outflow tract (LVOT) comprise the majority of these arrhythmias and form a significant component of an electrophysiology practice. A keen understanding of the correlative anatomy of the outflow tracts, in addition to recognizing key ECG indices illustrating PVC sites of origin, are fundamental in preparing for a successful ablation. Patient selection, incorporating symptomatology, structural disease, and PVC burden can pose a challenge, though tools such as the ABC-VT risk score may help identify those patients with a higher risk of clinical deterioration. Utilizing intracardiac echocardiography to highlight salient anatomic features not visible with fluoroscopy allows for a more precise and safer ablation. Interpretation of intracardiac EGMs, and the careful examination for low amplitude highly fractionated pre-potentials, enhanced by the advent of new developed mapping/ablation catheters, remains crucial. Utilizing these tools will guide the electrophysiologist to an efficient and effective outflow tract PVC ablation., (© 2021 Wiley Periodicals LLC.)

Primary prevention trials have demonstrated that patients with coronary disease, reduced left ventricular function, and nonsustained ventricular tachycardia (NSVT) have improved survival with implantable cardioverter defibrillator (ICD) therapy, presumably secondary to effective termination of life-threatening arrhythmias. However, stored intracardiac electrograms were not always available and specific arrhythmias leading to ICD therapy were not always known. We examined the occurrence of ICD events in 51 consecutive patients who match the described patient profile to determine the frequency of appropriate and inappropriate ICD therapy. ICD detections were noted in 18 (35%) patients during a median follow-up period of 13.1 months. Appropriate therapy for sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) occurred in 11 (22%) patients, with appropriate shocks in 8 (16%) patients and appropriate antitachycardia pacing (ATP) in 4 (8%) patients. The time to first appropriate therapy occurred at a mean of 17 +/- 12 months (median 18 months, range 3-36 months). Inappropriate therapy occurred in 5 (10%) patients with inappropriate shocks in 4 patients and inappropriate ATP in 2 patients. Inappropriate therapy was delivered for supraventricular arrhythmias (SVAs) in 4 patients and for T wave oversensing in 1 patient. The reason for shock therapy was unknown in 1 patient (2%) due to ICD malfunction. The mean arrhythmia rate leading to appropriate therapy for VT/VF was 232 +/- 72 beats/min (range 181-400 beats/min), and the mean rate leading to inappropriate therapy for SVT was 168 +/- 10 beats/min (range 160-180 beats/min). Patients with coronary disease and asymptomatic NSVT commonly receive appropriate defibrillator therapy. These results support the need for ICD implantation for primary prevention, with attention to careful programming of the detection rate to prevent inappropriate therapy.

Background: The circulating wavelet hypothesis suggests that atrial fibrillation could terminate by either progressive fusion or simultaneous block of all wavelets., Methods: Intraatrial recordings from the right atrial free wall were made during procainamide induced (n = 8) or spontaneous (n = 7) termination of electrically induced atrial fibrillation in 14 patients. Atrial rate, mean magnitude squared coherence, and direction of activation during sequential electrograms were measured. Rate and coherence were calculated from the earliest point within 5 minutes prior to termination as well as from the 4-second interval just prior to termination., Results: Termination was directly to sinus rhythm (13 episodes) or to atrial flutter (2 episodes). For the eight procainamide induced terminations, rate decreased between the first measurement and the measurement just prior to termination, from 443 +/- 127 beats/min to 322 +/- 119 beats/min. For the seven spontaneous terminations, rate also decreased from 373 +/- 119 beats/min to 323 +/- 88 beats/min; however, a slight increase in atrial rate prior to termination was observed in three episodes. No specific patterns of atrial cycle lengths were seen during the final few seconds of fibrillation. No increase in coherence was observed. In seven episodes, recordings were made using orthogonal bipoles in the x, y, and z directions, allowing direction of activation of wavefronts to be measured. Three episodes showed multiple instances where direction of activation remained similar over several electrograms as we have previously reported for chronic fibrillation. However, no such instances precipitated termination in any of the seven episodes., Conclusions: Atrial fibrillation usually terminates directly to sinus rhythm and does so abruptly and without forewarning. While we and others have previously reported that the rate of atrial fibrillation decreases with procainamide infusion, a decrease in the rate of atrial fibrillation is not required for the rhythm to terminate and consequently may not be a part of the termination process at all. Coherence does not demonstrate a progressive increase in the organization of atrial fibrillation prior to termination. Lack of stabilization in the direction of activation of wavefronts in the final few seconds also fails to support fusion of wavefronts as the mechanism of termination of atrial fibrillation. Simultaneous block of all wavelets is consistent with, but not proven by, our observations.