Case Study
A 59 year old man with a medical history of end stage renal failure on dialysis presented with nausea, vomiting and diarrhea. While in the hospital, he was noted to have incessant bigeminal premature ventricular contractions (PVCs) (figure 1). Serum potassium was 5.9 mEq/L and was corrected without effect on arrhythmic burden. Echocardiogram showed mild concentric left ventricular hypertrophy, mildly reduced left ventricular ejection fraction (LVEF), and grade III diastolic dysfunction.
Past medical history is remarkable for IDDM, end stage renal disease on dialysis for 4 years, HTN, PVD, and non-obstructive coronary disease on recent ischemic workup. A year ago, cardiac MRI performed for non-sustained VT showed LVEF of 40% (patient had bigeminal PVCs during the study) and no late gadolinium enhancement. He had previously undergone electrophysiology study for frequent PVCs and non-sustained VT, and was non inducible for sustained arrhythmia.
Because of palpitations, LV dysfunction, and inadequate response to beta blocker therapy, he was taken to the EP laboratory. The PVC was present in a bigeminal pattern with a coupling interval of 460 ms. PVC morphology was LBBB with precordial QRS transition in v4 and a left superior axis. QRS duration of the PVCs was 140 msec. Intracardiac echocardiography was used to create a 3-D shell of the right ventricle and septal and anterior papillary muscle. The trabeculations from the mid/apical septum to the anterior papillary muscle were traced as the moderator band (MB), as a clear structure traversing the chamber was not visualized. Activation mapping of the PVCs showed earliest activation at the trabeculation close to the septum and was 25 ms presystolic (figure 2). A clear Purkinje potential could not be recorded. Ablation at the site resulted in PVCs suppression. The ablation also resulted in right bundle branch block. During an observation period of an hour, no further PVCs were seen. Programmed ventricular stimulation with triple extra-stimulation at 600 and 400 ms drive cycle lengths failed to induce ventricular arrhythmias. The patient returned to the coronary care unit.
Six hours after the ablation, PVCs of the same morphology returned with a shorter coupling interval of 240 ms and runs of non-sustained ventricular tachycardia. Intravenous lidocaine was begun for suppression. Ventricular fibrillation was triggered by the same PVC (Figure 3 A and B). This required resuscitation with external cardiac compressions, repeated external defibrillation, amiodarone bolus and use of a temporary transvenous pacemaker for overdrive pacing suppression. No alterations in serum electrolytes were recorded. The patient was taken back to the EP lab after discontinuation of intravenous antiarrhythmic drugs. Pacing was stopped. No PVCs were evident. Based on prior mapping data, the septal aspect of the MB was targeted for ablation using a 23 mm Arctic Front IV cryoballoon (Medtronic, MN). A multipolar Achieve catheter (Medtronic, MN) was advanced beyond the moderator band to the apex of the RV and the cryoballoon was positioned at the septal end of the MB under intracardiac echocardiographic guidance (figure 4). Two lesions were applied for 180 and 140 sec with lowest temperature recordings of -55 and -45 degrees Celsius, respectively. The cryoballoon was repositioned more laterally toward the anterior papillary muscle and two further lesions created. Post ablation, a period of observation of 2 hours and stimulation with epinephrine and programmed ventricular stimulation were performed. No arrhythmias were observed. A voltage map of the RV using a mapping/ablation catheter showed small area of low voltage at the distal septum. All other areas appeared to have a voltage >1.5 mV.
The patient had no further ventricular arrhythmia during subsequent hospitalization and observation on telemetry for 48 hours off of all anti-arrhythmic drug therapy. Given the documentation of ventricular fibrillation, the patient was implanted with a cardioverter defibrillator prior to hospital discharge for prevention of sudden death.
At one month follow up, no further arrhythmias were seen on ICD interrogation and 24-hour Holter monitoring showed no further clinical PVCs.