Voltage mapping and pulmonary vein isolation in master athletes with atrial fibrillation.

BACKGROUND: Master athletes encompass a wide range of exercise enthusiasts. At the extreme, there is an increased risk of atrial fibrillation (AF). Therapies aimed at rate or rhythm control are often limited given unfavorable side effects. Although studies suggest an increase in left atrial (LA) fibrosis in this population, minimal electrophysiologic data exist regarding the LA voltage mapping and the efficacy of AF ablation with pulmonary vein isolation (PVI). METHODS: In a retrospective single-center study, we reviewed AF ablations (pulmonary vein isolation and assessment/ablation of non-pulmonary vein triggers) performed in extreme master athletes with AF. We define "extreme" as those who have repeatedly competed in long distance endurance events for a > 10-year period. Bipolar voltage mappings obtained through PENTARAY Catheter (Biosense Webster) were reviewed using CARTO. LA scarring was defined as an area of less than 0.1 mV. All patients were monitored as outpatients for AF recurrence. RESULTS: Between January 2018 and February 2022, 16 patients (11 marathon runners, four long distance cyclers, and one marathon swimmer) underwent AF ablations. All patients in the cohort were male with an average CHA2DS2-VASc score of 1.2 ± 0.8 and left atrial volume of 34.4 cc/m2  ± 9.9. A total of eight patients (50%) had persistent AF. One patient (6.3%) had LA scar on bipolar voltage mapping, whom also had a non-pulmonary vein trigger of AF. Bidirectional blocks of the four pulmonary veins were achieved by radiofrequency (RF) ablation in all patients. Freedom from documented recurrence of AF up to 24 months was 93.8%. One patient (6.3%) had recurrence of AF at 14 months and underwent successful cardioversion. CONCLUSION: In our series of extreme master athletes with AF, the incidence of LA scarring on bipolar voltage mapping was low and the recurrence of AF following PVI by RF ablation was minimal.

Loop Recorder Implantation on a Telemetry Ward.

The implantable loop recorder (ILR) is a valuable tool used in the evaluation of syncope, arrhythmia, and cryptogenic stroke. In the inpatient setting, ILRs are routinely implanted in the electrophysiology (EP) lab despite the low complication rate. The purpose of this study was to evaluate the safety, feasibility, and cost of implanting ILRs at the patient's bedside by both electrophysiologists and advanced practice providers (APPs). This was a single center, retrospective study of consecutive ILR implantations performed from February 2018 to May 2019. We examined 3 groups: implantations in the EP lab by electrophysiologists (EP Lab/MD), implantations at the bedside by electrophysiologists (Floor/MD), and implantations at the bedside by APPs (Floor/APP). Over 15 months, 152 patients underwent ILR implantation: 48 in the EP Lab/MD group, 57 in the Floor/MD group, and 47 in the Floor/APP group. The procedure duration was longer in the Floor/APP group (14.2 ± 5.9 minutes) compared with the EP Lab/MD and Floor/MD groups (6.8 ± 4.3 minutes, 9.1 ± 4.9 minutes, p <0.001). The overall complication rate was low (2.6%) with no differences between the groups (p = 0.83). The calculated costs per implant for the EP Lab/MD group, Floor/MD group, and Floor/APP group were $482.05, $162.82, and $73.08, respectively.

Electrophysiologic study: its predictive value for ventricular arrhythmias.

Studies have shown the predictive value of inducible ventricular tachycardia and clinical arrhythmia in patients who have structural heart disease. We examined the possible predictive value of electrophysiologic study before the placement of an implantable cardioverter-defibrillator. Our retrospective study group comprised 315 patients who had ventricular tachycardia that was inducible during electrophysiologic study and who had undergone at least 1 month of follow-up (247 men; mean age, 66.9 +/- 13.5 yr; mean follow-up, 24.9 +/- 14.8 mo). Recorded characteristics included induced ventricular tachycardia cycle length, atrio-His and His-ventricular electrograms, PR and QT intervals, QRS duration, and drug therapy. Of the 315 patients, 97 experienced ventricular arrhythmia during the follow-up period, as registered by 184 of more than 400 interrogations. There were 187 episodes of ventricular arrhythmia (tachycardia, 178; fibrillation, 9) during 652.5 person-years of follow-up. Subjects with a cycle length > or =240 msec were more likely to have an earlier 1st arrhythmia than those with a cycle length <240 msec (P=0.032). A quarter of the subjects with a cycle length > or =240 msec had their 1st arrhythmia by 19.14 months, compared with 23.8 months for a quarter of the subjects with a cycle length <240 msec (P <0.032). Among the electrophysiologic characteristics examined, inducible ventricular tachycardia with a cycle length > or =240 msec is predictive of appropriate implantable cardioverter-defibrillator therapy at an earlier time. This may have prognostic implications that warrant implantable cardioverter-defibrillator programming to enable appropriate antitachycardia pacing in this group of patients.

Dual atrioventricular-nodal physiology, elicited by pacing and leading to a reversible cardiomyopathy.

Atrioventricular nodal re-entry tachycardia is the most common form of regular paroxysmal tachycardia in the adult population. This tachycardia is a re-entrant rhythm that uses the anatomic location of the atrioventricular node and its surrounding perinodal atrial tissue. The simplest concept regarding the atrioventricular nodal physiology that allows re-entry is founded upon the postulated existence of 2 atrioventricular nodal pathways with different conduction velocities and refractory periods. Herein, we present the case of a 64-year-old man who had a history of paroxysmal atrial fibrillation; he had a permanent pacemaker for sick-sinus syndrome. He developed a tachycardia-induced cardiomyopathy with a perpetual dual response to the pacemaker stimulus. The tachycardia displayed characteristic dual atrioventricular-nodal physiology that was suppressed by amiodarone therapy, leading to a reversal of the cardiomyopathy. We discuss the mechanisms that surround such phenomena.