Evaluation of the pulmonary artery potential using a 20-polar circumferential catheter and three-dimensional integrated intracardiac echocardiography

Abstract

Prolongation of the pulmonary artery potentials (PAPs) in response to short coupling intervals was related to polymorphic QRS configurations during the ventricular tachycardia originating above the pulmonary valve (PA-VT). This prospective study was aimed to investigate the mechanisms of polymorphic changes during the PA-VT. We performed the mapping above the pulmonary valve using a 20-polar circumferential catheter and three-dimensional integrated intracardiac echocardiography in 9 consecutive patients with outflow tract arrhythmias undergoing catheter ablation (UMIN ID: UMIN000021682). The location of successful ablation was right ventricular outflow tract (RVOT) in 6 patients, above the pulmonary valve in 1 patient, left coronary cusp in 1 patient, and unknown in 1 patient. The PAP was detected in six (67%) patients with bipolar voltage of 0.56 ± 0.27 mV. Pacing from bipolar electrodes of the circumferential catheter located above the pulmonary valve captured the PA myocardium only in 1 patient who had the PA-VT (100% in PA-VT vs 0% in non-PA-VT, P = 0.0046), and slight changes of the QRS morphology was observed in accordance with the conduction delay from the stimulus to activation of the RVOT myocardium. The selective PAP capture with conduction delays evoked by bipolar stimulations through a 20-polar circumferential catheter may be a characteristic property of patients with the PA-VT. Conduction delays within the PA and PA-RVOT junction appears to contribute polymorphic QRS changes during the PA-VT.

Catheter ablation in a pediatric patient with idiopathic ventricular tachycardia and arrhythmia‐induced cardiomyopathy

“…However, with ventricular arrhythmias (VAs) originating from the RVOT, there have been reports of a few occurrences of cardiac events such as syncope or sudden cardiac death in pediatric patients 1,2 . Although cardiac complications are very rare in pediatric patients with VT arising from RVOT, the rapid excitation and conduction delays of ventricular arrhythmia originating above pulmonary valve appear to contribute polymorphic VT, suggesting its malignant electrophysiological characteristics 3,4 . We believed that this patient developed heart failure and arrhythmia‐induced cardiomyopathy because of the persistence of VT, which was at a relatively low heart rate with no accompanying palpitations, rather than frequent PVCs.…”