Fascicular and Nonfascicular Left Ventricular Tachycardias in the Young: An International Multicenter Study : Left Ventricular Tachycardia in Pediatrics

The purpose of this study was to determine the relation of diastolic and presystolic potentials recorded during verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) to reentry circuit. Successful ablation of verapamil-sensitive ILVT at the zone of slow conduction from which the diastolic potential is recorded has been reported. However, the relationship between the diastolic potential and the reentrant circuit remains a matter of debate. Radiofrequency (RF) ablation was performed in 20 patients with verapamil-sensitive ILVT. After identifying the ventricular tachycardia (VT) exit site, we searched for the mid-diastolic potential (P1) during VT. Entrainment followed by RF current application was performed. If the mid-diastolic potential could not be detected, RF current was applied at the VT exit site showing the earliest ventricular activation with a single fused presystolic Purkinje potential (P2). In 15 of 20 patients, both P1 and P2 were recorded during VT from midseptal region. Entrainment pacing captured P1 orthodromically and reset the VT. The interval from stimulus to P1 was prolonged as the pacing rate was increased. Radiofrequency ablation was successfully performed at this site in all 15 patients. After successful ablation, P1 appeared after the QRS complex during sinus rhythm with the identical sequence to that during VT. In the remaining five patients, the diastolic potential could not be detected, and a single fused P2 was recorded only at the VT exit site. Successful ablation was performed at this site in all five patients. This study demonstrates that P1 and P2 are critical potentials in a circuit of verapamil-sensitive ILVT and suggests the presence of a macroreentry circuit involving the normal Purkinje system and the abnormal Purkinje tissue with decremental property and verapamil-sensitivity.

Several distinct forms of focal ventricular tachycardia (VT) from the left ventricle (LV) have been described. We report a new syndrome of VT arising from the base of the posterior papillary muscle in the LV. Among 290 consecutive patients who underwent ablation for VT or symptomatic premature ventricular complexes (PVCs) based on a focal mechanism, 7 patients were found to have an ablation site at the base of the posterior papillary muscle in the LV. All patients had normal LV systolic function and a normal baseline electrocardiogram. The electrocardiogram during VT or PVCs demonstrated a right bundle-branch block and superior-axis QRS morphology in all patients. VT was not inducible by programmed atrial or ventricular stimulation. In 2 patients with sustained VT, overdrive pacing neither terminated VT nor demonstrated any criterion for transient entrainment. Activation mapping localized the earliest site of activation to the base of the posterior papillary muscle in all patients. When Purkinje potentials were recorded at the site of successful ablation, these potentials preceded local ventricular muscle potentials during sinus rhythm. During VT or PVCs, however, the ventricular muscle potential always preceded the Purkinje potentials. After recurrence of VT or PVCs with standard radiofrequency ablation, irrigated ablation was successful in eliminating the arrhythmia in all patients. Over a mean follow-up period of 9 months, all patients have been free of PVCs and VT. We present a distinct syndrome of VT arising from the base of the posterior papillary muscle in the LV by a nonreentrant mechanism. Ablation can be challenging, and irrigated ablation may be necessary for long-term success.

A 28-year-old man is described with no demonstrable organic heart disease and recurrent paroxysmal attacks of sustained ventricular tachycardia. Lignocaine and ajmaline failed to terminate the first attack but a bolus infection of verapamil succeeded. This drug was subsequently successful on six more occasions. During electrophysiological study of the eighth attack, slow intravenous administration of verapamil significantly reduced the rate of the tachycardia and prevented its subsequent reinitiation by pacing. Two mechanisms are postulated to explain both the arrhythmia and the beneficial effects of verapamil in this case.