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Resolution of ventricular tachycardia following cavotricuspid isthmus ablation for atrial flutter: Potential implications of cross-chamber induction on catheter ablation strategies

  • Norman C. Wang
    Correspondence
    Address reprint requests and correspondence: Dr Norman C. Wang, UPMC Presbyterian, 200 Lothrop St, South Tower, 3rd Floor, Room E352.9, Pittsburgh, PA 15213.
    Affiliations
    Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
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Open AccessPublished:December 19, 2022DOI:https://doi.org/10.1016/j.hrcr.2022.12.014

      Keywords

      Introduction

      For decades, atrial fibrillation (AF) and/or atrial flutter (AFL) have been described to have positive associations with sudden death and/or ventricular arrhythmias.
      • Rattanawong P.
      • Upala S.
      • Riangwiwat T.
      • et al.
      Atrial fibrillation is associated with sudden cardiac death: a systematic review and meta-analysis.
      The pathophysiologic basis may be related to electrophysiologic changes that heighten the probability for ventricular tachycardia (VT) and ventricular fibrillation (VF).
      • Chen L.Y.
      • Benditt D.G.
      • Alonso A.
      Atrial fibrillation and its association with sudden cardiac death.
      They may also be reflective of advanced heart disease, noncardiac comorbid illnesses, or proarrhythmic adverse consequences of antiarrhythmic drugs. Translating these data and theories into treatment strategies has been elusive.
      Case reports have described “cross-chamber induction” of ventricular arrhythmias from atrial stimulation or arrhythmias. In 1979, Zipes and colleagues
      • Zipes D.P.
      • Foster P.R.
      • Troup P.J.
      • Pederson D.H.
      Atrial induction of ventricular tachycardia: reentry versus triggered automaticity.
      demonstrated that atrial pacing could induce VT owing to reentry and triggered automaticity. In 2010, Venkataraman and Strickberger
      • Venkataraman G.
      • Strickberger S.A.
      Atrial fibrillation degenerates into ventricular fibrillation.
      described a patient without ventricular pre-excitation who received a successful implantable cardioverter-defibrillator (ICD) shock for VF that developed after an R-on-T event during AF. In 2020, Koya and colleagues
      • Koya T.
      • Temma T.
      • Watanabe M.
      • Kamada R.
      • Nagai T.
      • Anzai T.
      Radiofrequency catheter ablation of a sporadically occurring ventricular arrhythmia originating from the right ventricular outflow tract: a novel arrhythmia induction strategy involving atrial fibrillation provocation.
      reported an increase in premature ventricular complex and nonsustained VT frequency after induction of AF, which facilitated catheter ablation of idiopathic VT from the right ventricular outflow tract (OT). Herein, I describe the first report where successful catheter ablation of the cavotricuspid isthmus for typical AFL also resulted in resolution of VT.

      Case report

      In June 2022, an 87-year-old man with a reported history of paroxysmal AF, sinus node dysfunction, and a dual-chamber pacemaker (Boston Scientific, Marlborough, MA) presented to an outside medical center with syncope. He collapsed while playing golf after experiencing loss of consciousness without prodromal symptoms. Physical examination was notable for head trauma and rapid heart rate, but was otherwise unremarkable. Blood tests were significant for serum calcium of 8.2 mg/dL, serum phosphorus of 1.9 mg/dL, and brain natriuretic peptide of 112 pg/mL. He was taking rivaroxaban as an outpatient and computed tomography revealed a subarachnoid hemorrhage. This was managed with observation and rivaroxaban was resumed after improvement.
      Pacemaker interrogation demonstrated onset of a persistent atrial tachy response (ATR) episode beginning at 10:48 PM the prior evening. On the morning of presentation, there was a 23-second VT episode with a rate of 205 beats/min at 8:03 AM. An additional 9 nonsustained VT episodes between 12 and 17 seconds in duration with rates between 153 and 181 beats/min were recorded from 9:57 AM to 10:22 AM.
      Hospital records stated that he had multiple episodes of monomorphic VT and continuous AF with periods of rapid ventricular rate. Symptoms of lightheadedness correlated with VT, rather than AF. As an outpatient, dronedarone and sotalol had been ineffective for treating AF. Amiodarone was discontinued for ocular side effects. He was not on a class III antiarrhythmic drug on presentation.
      Oral verapamil was attempted but was held owing to hypotension. Intravenous (IV) lidocaine effectively suppressed VT. Cardiac catheterization estimated a left ventricular ejection fraction of 55%–60% by ventriculography, a 60% stenosis of a small left atrial branch, and mild disease elsewhere. For logistical reasons, catheter ablation of the atrioventricular junction and for suspected idiopathic VT was arranged at a later date with a tertiary care center. He was transitioned to sotalol 120 mg twice daily and mexiletine 150 mg 3 times daily, then discharged with a wearable cardioverter-defibrillator (WCD) (ZOLL LifeVest, Pittsburgh, PA). An outpatient echocardiogram demonstrated mild concentric left ventricular hypertrophy, but was otherwise normal.
      Eighteen days after discharge, he experienced episodes of lightheadedness that were associated with alarms from his WCD. He returned to the outside medical center, where recurrent VT was diagnosed. IV lidocaine was started and he was transferred for expedited catheter ablation.
      At the tertiary care center, episodes of nonsustained VT were noted on WCD recordings and 12-lead electrocardiogram (ECG) rhythm strips (Figure 1). These were associated with initiation coupling intervals, between anterograde conducted ventricular depolarizations and ectopic ventricular depolarizations, of approximately 440–500 ms. Despite IV lidocaine, frequent nonsustained VT episodes continued.
      Figure thumbnail gr1
      Figure 1Samples of nonsustained ventricular tachycardia. A: Wearable cardioverter-defibrillator recording from the side-to-side (SS) channel. B: Twelve-lead electrocardiogram rhythm strip.
      The VT morphology was left bundle branch block and inferior axis with an R-to-S wave precordial transition in lead V3. The V2 transition ratio was approximately 0.78. The sinus rhythm precordial transition was in lead V4. These characteristics favored a left ventricular OT origin.
      • Lerman B.B.
      Mechanism, diagnosis, and treatment of outflow tract tachycardia.
      The electrocardiogram suggested AFL, rather than AF, with variable atrioventricular conduction ratios and ventricular rates generally between 100 and 110 beats/min. Comprehensive review of electrograms from his pacemaker memory log demonstrated only AFL.
      In the electrophysiology laboratory, there was near-total suppression of VT after anesthesia administration, which included dexmedetomidine, fentanyl, and propofol. A right atrial activation map using the CARTO 3 electroanatomic mapping system (Biosense Webster, Irvine, CA) suggested typical clockwise AFL with a cycle length of 253 ms. Radiofrequency ablation of the cavotricuspid isthmus was successfully performed with a 3.5 mm irrigated-tip THERMOCOOL SMARTTOUCH catheter (Biosense Webster) using a power of 40 W and a temperature limit of 43°C (Figure 2). Bidirectional block was achieved and the postablation transisthmus conduction time was 166 ms. Isoproterenol was started and increased in a stepwise fashion to 6 mcg/min. Programmed stimulation from the right ventricular apex was performed using drive trains of 8 stimuli with 2 cycle lengths, 600 ms and 400 ms, followed by single and double extrastimuli. Sustained arrhythmias were not induced. No ablation lesions were delivered outside of the cavotricuspid isthmus. The final procedure time was 126 minutes. After ablation, he was in sinus rhythm (Figure 3A).
      Figure thumbnail gr2
      Figure 2Catheter ablation of the cavotricuspid isthmus. A: Atrial flutter terminated during ablation and transitioned to an atrial- and ventricular-paced rhythm. Recording speed 50 mm/second. B: Right atrial activation map in the left anterior oblique (LAO) projection accounted for 100% of the 253 ms cycle length. C: LAO caudal projection highlighting the cavotricuspid isthmus with points for His bundle recordings (yellow), ablation lesions (red), and the ablation lesion at site of termination (green).
      Figure thumbnail gr3
      Figure 3A: The immediate postablation 12-lead electrocardiogram demonstrated sinus rhythm at 83 beats/min with a corrected QT interval of 432 ms. B: One-month postablation pacemaker data demonstrated a continuous period of recorded AT/AF (atrial tachycardia or atrial fibrillation) that started 1 day prior to his initial presentation with syncope and ended on the day of catheter ablation.
      He remained hospitalized for an additional 6 days for noncardiac reasons, during which time he had no further VT episodes or even premature ventricular complexes. He was discharged with the WCD and metoprolol tartrate 25 mg twice daily, but no other antiarrhythmic drugs.
      At his 1-month clinic follow-up appointment, 34 days after ablation, pacemaker interrogation demonstrated a continuous period of atrial arrhythmias from 1 day prior to his initial hospitalization with head trauma until the day of his catheter ablation procedure (Figure 3B). In the postablation period, there were only 2 atrial tachy response episodes. There was a 9-second and a 4-second episode, both consistent with atrial tachycardia, on postablation days 1 and 14, respectively. His WCD, which estimated 97% wear time, did not detect any ventricular arrhythmias with a VT rate threshold set at 150 beats/min. He was instructed to discontinue the WCD and cleared to resume normal activity.
      During a telephone follow-up 3 months after ablation, he stated he felt back to his normal condition. He was back to golfing 2–3 times per week.

      Discussion

      To the best of my knowledge, this is the first description of VT resolution after catheter ablation for typical AFL. The VT was likely idiopathic, originating from the left ventricular OT, and caused by triggered activity. This was supported by absence of structural heart disease and the QRS morphology,
      • Lerman B.B.
      Mechanism, diagnosis, and treatment of outflow tract tachycardia.
      but other mechanisms were not definitively excluded. This case provides a real-world example to support the hypothesis that treating atrial arrhythmias may decrease the risk for ventricular arrhythmias and sudden death. Further, it raises considerations for catheter ablation strategies for coexisting atrial and ventricular arrhythmias when cross-chamber induction is suspected.
      The pathophysiologic relationship between AFL and idiopathic VT was unclear, although autonomic nervous system involvement was probable. Sympathetic activation and/or parasympathetic withdrawal has been described minutes before the onset of AFL.
      • Wen Z.C.
      • Chen S.A.
      • Tai C.T.
      • Huang J.L.
      • Chang M.S.
      Role of autonomic tone in facilitating spontaneous onset of typical atrial flutter.
      Patients with idiopathic right ventricular OT tachycardia are sensitive to catecholamines owing to reductions in both presynaptic catecholamine reuptake and postsynaptic β-adrenoreceptor density.
      • Schäfers M.
      • Lerch H.
      • Wichter T.
      • et al.
      Cardiac sympathetic innervation in patients with idiopathic right ventricular outflow tract tachycardia.
      Elevation of intracellular calcium may be a critical component, given its role in OT VT.
      • Lerman B.B.
      Mechanism, diagnosis, and treatment of outflow tract tachycardia.
      AFL may produce similar molecular and cellular changes on the ventricle as AF, but data are sparse and mostly derived from animal models.
      • Wijesurendra R.S.
      • Casadei B.
      Atrial fibrillation: effects beyond the atrium?.
      For stepwise ablation, where both atrial and ventricular arrhythmias are to be targeted during catheter ablation, it may be advantageous to first target the arrhythmia associated with higher success rates, lower complication rates, and lower procedural times. Noninducibility of 1 arrhythmia may also dictate which arrhythmia to prioritize. Finally, successful ablation of the first arrhythmia may obviate pursuing ablation for the second arrhythmia.
      In the case report patient, VT was associated with more malignant symptoms compared to AFL. However, it may have been desirable to target AFL first, even if VT was active during the electrophysiology study. Cessation of VT following cavotricuspid isthmus ablation would avoid femoral arterial access and anticoagulation that is generally required for left-sided mapping and ablation, presuming a left ventricular OT origin.
      For adjunctive ablation, where 1 arrhythmia is the primary target, ablation of a secondary arrhythmia may improve outcomes if cross-chamber induction is present. Given the number and consistency of prior publications, populations with AF and at risk for VT/VF may have the most relevance.
      • Rattanawong P.
      • Upala S.
      • Riangwiwat T.
      • et al.
      Atrial fibrillation is associated with sudden cardiac death: a systematic review and meta-analysis.
      ICD recipients make an attractive potential study population, given continuous arrhythmia monitoring. A caveat would be the potential for heart failure status to act as a confounding variable. The case report patient did not have heart failure and, as such, the causal relationship between AFL and VT was more likely to be purely arrhythmogenic in nature.
      Early ICD randomized trials reported variable rates of AF.
      • Botto G.L.
      • Luzi M.
      • Ruffa F.
      • Russo G.
      • Ferrari G.
      Atrial tachyarrhythmias in primary and secondary prevention ICD recipients: clinical and prognostic data.
      AF was a stronger predictor of mortality in secondary prevention trials. More recently, a meta-analysis evaluating 25 studies and more than 63,000 patients with ICDs for primary and secondary prevention found positive associations between AF and the separate outcomes of all-cause mortality and appropriate ICD shocks.
      • Mustafa U.
      • Dherange P.
      • Reddy R.
      • et al.
      Atrial fibrillation is associated with higher overall mortality in patients with implantable cardioverter-defibrillator: a systematic review and meta-analysis.
      Although point estimate effects sizes of the odds ratios were small, there was consistency among the individual studies.
      Reduction of AF burden may in turn reduce cross-chamber induction of VT/VF and subsequent death. Degeneration of AF into VF is assumed to be rare, but robust data are sparse.
      • Venkataraman G.
      • Strickberger S.A.
      Atrial fibrillation degenerates into ventricular fibrillation.
      For example, 29% of adjudicated sudden deaths in ICD recipients in 1 study occurred owing to electromechanical dissociation after appropriate ICD shocks for VT/VF, or cardiac annihilation, yet whether AF was involved in VT/VF initiation was not analyzed.
      • Mitchell L.B.
      • Pineda E.A.
      • Titus J.L.
      • Bartosch P.M.
      • Benditt D.G.
      Sudden death in patients with implantable cardioverter defibrillators: the importance of post-shock electromechanical dissociation.
      The Catheter Ablation versus Standard Conventional Therapy in Patients with Left Ventricular Dysfunction and Atrial Fibrillation (CASTLE-AF) trial reported a statistically significant reduction for death from any cause in the pulmonary vein isolation arm compared to the medical therapy arm.
      • Marrouche N.F.
      • Brachmann J.
      • Andresen D.
      • et al.
      Catheter ablation for atrial fibrillation with heart failure.
      All subjects had ICDs and 89% were for primary prevention. The relationship between AF burden reduction and VT/VF was unclear, as mode of death and appropriate ICD therapy events were not published.
      Probably the most intriguing population to explore the potential of adjunctive ablation for AF/AFL are patients with ICDs and previously documented VT/VF. In the Ventricular Tachycardia Ablation versus Escalated Antiarrhythmic Drug Therapy in Ischemic Heart Disease (VANISH) trial,
      • Sapp J.L.
      • Wells G.A.
      • Parkash R.
      • et al.
      Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs.
      38.2% of enrolled subjects had AF/AFL. Follow-up event rates remained high in the catheter ablation group, with deaths at 27.3%, VT storm after 30 days at 33.1%, and appropriate ICD shocks after 30 days at 37.9%. Therefore, the opportunity for improving outcomes may be substantial.
      Mechanisms other than reentry may be present for sustained monomorphic VT in ischemic cardiomyopathy.
      • Pogwizd S.M.
      • Hoyt R.H.
      • Saffitz J.E.
      • Corr P.B.
      • Cox J.L.
      • Cain M.E.
      Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart.
      Even for reentrant VT, initiating PVCs may be due to automaticity or triggered activity. Noninducibility or multiple VT morphologies may also be theoretical situations where adjunctive ablation of AF/AFL leads to reduction in VT/VF burden.
      It is difficult to assess when cross-chamber induction may be present. In the case report patient, the temporal relationship between persistent AFL and VT was recognized only retrospectively. Future studies should define variables that suggest cross-chamber induction. Even if the population that can benefit from adjunctive AF/AFL ablation is ultimately modest, the potential benefit for individual patients may be vast.
      There were several limitations. Programmed atrial stimulation was not performed. Long-term follow-up was not available and subsequent development of AF could result in VT recurrence. The possibility of an infiltrative disorder, such as arrhythmogenic right ventricular cardiomyopathy, was not definitively excluded.

      Conclusion

      This case report serves as proof of concept that successful catheter ablation of the cavotricuspid isthmus for typical AFL may also resolve idiopathic VT. Considering cross-chamber induction may have important implications for stepwise and adjunctive catheter ablation strategies for patients with coexisting atrial and ventricular arrhythmias.
      Key Teaching Points
      • Successful catheter ablation of the cavotricuspid isthmus for typical atrial flutter may also resolve idiopathic ventricular tachycardia arising from the left ventricular outflow tract.
      • Cross-chamber induction may explain some of the positive associations between atrial arrhythmias and sudden death owing to ventricular arrhythmias that have been reported in observational studies.
      • A temporal relationship between coexisting atrial and ventricular arrhythmias may suggest the presence of cross-chamber induction.
      • Cross-chamber induction may have important implications for stepwise and adjunctive catheter ablation strategies in patients with coexisting atrial and ventricular arrhythmias.

      Acknowledgments

      The author thanks Josiah Parkinson, CAS, of Biosense Webster for creation of the electroanatomic maps.

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