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.