A Case of a Human Ventricular Fibrillation Rotor Localized to Ablation Sites for Scar-mediated Monomorphic Ventricular Tachycardia

Introduction

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most common causes of sudden cardiac death. Currently, knowledge of the reentrant mechanism of monomorphic VT circuits in relation to complex scar anatomy allows for various mapping techniques including electroanatomic and entrainment mapping to accomplish catheter ablation of VT.^{1, 2} Clinically, it may be observed that ablation to eliminate recurrent macro-reentrant VT may also eliminate recurrent VF, as defined for instance by electrograms from implanted cardioverter-defibrillators (ICD).^{3, 4} However, whether this represents elimination of the VT trigger for VF, or directly of the substrate for VF, is unclear since the mechanism of VF in relation to scar is not known. Recent work targeting localized rotors in atrial fibrillation ablation has shown promise,⁵ but its implications for VF are unknown. We report here a case where VT termination and a VF rotor occurred at spatially coincidental sites in a patient with ischemic cardiomyopathy, suggesting that VF rotors may localize to the same anatomic substrate that promotes VT.

Case Report

The patient was a 55 year old male with a history of coronary artery disease, ischemic cardiomyopathy with an ejection fraction of 23%, history of cardiac arrest with subsequent placement of a bi-ventricular ICD 6 years prior, history of premature ventricular contraction ablation procedure 9 months prior, on sotalol (amiodarone was discontinued due to decreasing diffusing lung capacity) who presented with palpitations, dizziness, and shortness of breath. He had single vessel disease of the right coronary artery with multiple prior percutaneous coronary interventions. Device interrogation showed the patient to be in slow VT at 135 bpm for the past 3 days. (Figure 1A and 1B) The VT was refractory to anti-tachycardia pacing (ATP) therapy, and no shock therapies were programmed in this zone. In the emergency department he was sedated, and he underwent successful cardioversion with a programmed ICD shock at 31J. He was admitted, and his sotalol dose was increased. His ICD was also reprogrammed with a VT-1 zone to detect at 130–150 bpm, provide 8 runs of ATP, then one shock at 21J, then a 31J shock up to four times. He was discharged with plans to undergo endocardial VT ablation the following week.

Figure 1.

(A) Baseline ECG demonstrating sinus bradycardia with a left bundle branch block. (B) Admission ECG prior to first endocardial ablation demonstrating ventricular tachycardia with rate of 135 bpm. (C) Admission ECG prior to epicardial ablation demonstrating ventricular tachycardia with rate of 111 bpm.

Under IRB-approved protocol, mapping was obtained from 128 biventricular sites using two 64-pole basket catheters – one advanced transvenously to the right ventricle and another transseptally into the left ventricle. At electrophysiology study (EPS), both rapid pacing (cycle length 230 ms) and shock-on-T induced VF, which was defibrillated after external defibrillator charging. Focal impulse and rotor maps (FIRM) of both instances of VF revealed a rotor at the mid-posterolateral left ventricle (Figure 2). Voltage mapping determined this rotor to be located within an area of dense scar. Endocardial ablation of the targeted monomorphic VT at a region in the mid-lateral wall within this scar, which included the site of the rotor, was acutely successful, rendering the patient non-inducible for VT or VF by burst pacing.

Figure 2.

(top left) Isochronal analysis of the left ventricle (LV) during ventricular fibrillation showing a sustained electrical rotor in the mid-posterolateral LV. (top right) Endocardial image from initial ablation procedure and epicardial image from repeat ablation procedure demonstrating similar termination sites in the mid-lateral LV wall. (bottom left) Fluoroscopic images from the epicardial ablation procedure demonstrating ablation catheter location in mid-lateral LV wall. (bottom right) Epicardial electrogram demonstrating mid-diastolic potential during clinical VT with termination of VT during ablation.

However, approximately 10 months later, VT recurred with different morphology, (Figure 1C) and the patient presented with multiple ICD shocks. On device interrogation, he had had 26 episodes of ventricular tachycardia treated with 26 rounds of ATP and 2 ICD shocks within a 24-hour period. Mexiletine was added to his current regimen of sotalol, but he continued to have symptomatic sustained VT. Due to concern for an epicardial circuit, an initial attempt at epicardial access was made at an outside facility but was unsuccessful due to adhesions. He was subsequently referred for percutaneous epicardial ablation.

During this procedure, percutaneous access was severely restricted by epicardial adhesions, but a limited region in the mid to basal lateral wall was accessible. An isolated late potential was found in this mapped region and single paced beat at this site resulted in a matched pacemap (12/12) of clinical VT (tachycardia cycle length 540ms). Entrainment at this site, that showed diastolic potentials during VT, confirmed an epicardial isthmus site (with basal scar exit morphology). Rapid termination of VT was achieved by ablation at this site in the mid-posterolateral left ventricle. This epicardial site of termination was spatially adjacent to the endocardial scar for the VT termination site and VF rotor core seen on prior ablation. (Figure 2)

In the week following the procedure, the patient had recurrence of VT with rate of 130 bpm that was accelerated to VF zone with 4 bursts of ATP resulting in 2 ICD shocks. This prompted restarting amiodarone therapy. Since then, the patient has had follow-up for over one year with no ICD shocks or ATP therapies.

Discussion

Electroanatomic mapping combined with entrainment mapping, pacemapping, and targeting of late potentials have become powerful tools in the armamentarium of electrophysiologists for ablation of scar-mediated VT.^{1, 2} However, VF is a more difficult entity to characterize and target mechanistically, anatomically, and spatially. Multiple mechanisms have been proposed, and observed, to sustain VF including: stable rotors,⁶ transient rotational patterns of reentry,⁷ focal sources,⁸ and multiple wavelets.⁷ Recent work in canine models has suggested that rotors may be important drivers for VF.⁹ However, the precise mechanistic importance of such theories to the perpetuation of human scar-mediated VF remains unclear.

Currently, it is hypothesized that mechanisms that sustain VF preferentially localize in diseased tissue,^10–12 or sites of source-to-sink mismatch in areas of anatomic heterogeneity such as near papillary muscle or Purkinje-muscle junctions.^{13, 14} The dependence of such sites upon substrate is an important issue, as this may potentially allow targeted intervention of the sustaining mechanisms of VF. In this case, it is intriguing that the location of the VF rotor was found to be in a similar scar location as the termination sites for VT. While such a finding may be coincidental, it is also plausible that the specific characteristics of scar that form functional isthmuses for VT may serve as the substrate for wavebreak and subsequent phase singularities to sustain VF as seen in this patient.¹⁵ This hypothesis is timely, given recent studies showing the success of rotor-targeted ablation for atrial fibrillation at many centers.^{5, 16, 17} Notably for our patient, VF was non-inducible following ablation at the site of the endocardial rotor seen during the initial procedure. Whether ablation of the rotor had any effect in suppressing our patient’s arrhythmias is an important question that will require much future study to determine the role, if any, of targeted rotor ablation in the management of VF.

One potential confounder to this hypothesis, however, is the re-addition of amiodarone to his medical regimen. Although it is likely that the epicardial ablation reduced his VT burden, it is difficult to know the relative contribution of the ablation versus the addition of amiodarone. Nevertheless, this case represents a unique and intriguing illustration of the potential overlap in scar substrate between VT and VF in human cardiomyopathy.

Conclusion

This case report is an interesting example of human VF that was characterized by an electrical rotor, which may lie spatially adjacent to isthmuses for clinical VT. Targeted ablation may have suppressed recurrence of both arrhythmias in this patient. This finding suggests that rotors, a potential sustaining mechanism of VF, may be anchored to the same scar substrate for monomorphic VT; however, future studies are required to define the electrophysiologic properties that promote VF rotors. Further investigation is needed to determine whether these rotors consistently lie in areas of scar that may promote both VT and VF, such as the rotor correlation with VT isthmus site seen in this patient, and whether catheter ablation can reduce all clinically relevant forms of ventricular arrhythmias.