EP 101

An Interesting Case of Arrhythmia-Induced Cardiomyopathy

Rakesh Gopinathannair, MD, MA, FHRS, Director of Cardiac Electrophysiology, Assistant Professor of Medicine, Division of Cardiovascular Medicine, Section of Electrophysiology, University of Louisville, Louisville, Kentucky

Rakesh Gopinathannair, MD, MA, FHRS, Director of Cardiac Electrophysiology, Assistant Professor of Medicine, Division of Cardiovascular Medicine, Section of Electrophysiology, University of Louisville, Louisville, Kentucky

Case Presentation

A 66-year-old white male with a history of coronary artery disease needing bypass surgery (CABG) in 1999 was referred for further management of atrial flutter and cardiomyopathy. The patient had a several-month history of palpitations, fatigue, leg swelling, and progressively worsening dyspnea. He was diagnosed to have atrial flutter with rapid ventricular rates 3 months prior, and had failed cardioversion and amiodarone therapy. Physical exam was consistent with left heart failure. Echocardiogram showed a left ventricular ejection fraction (LVEF) of 35% with increased left ventricular end-diastolic dimension (LVEDD) and global hypokinesis. Twelve-lead ECG showed atrial flutter with a ventricular rate of 90-95 bpm and frequent premature ventricular contractions (PVCs) of RBBB, inferior axis morphology (Figure 1). The flutter wave morphology (biphasic in V1, positive in lead 1 and aVL, negative in inferior leads) was consistent with typical right atrial flutter. His cardiac medications included amiodarone 200 mg daily, metoprolol XL 25 mg daily, diltiazem CD 180 mg daily, and losartan 50 mg daily. His CHA2DS2-VASC score was 5 and he was on apixaban 5 mg twice daily for anticoagulation. 

Persistent atrial flutter refractory to medical therapy and associated decline in LVEF raised suspicion for atrial flutter-induced cardiomyopathy; therefore, catheter ablation was pursued for rhythm control. During electrophysiology (EP) study, the patient was in atrial flutter with a cycle length of 276 msec with proximal to distal coronary sinus activation and a counterclockwise activation on a halo catheter spanning the lateral right atrium (Figure 2). Entrainment mapping from the ablation catheter placed in the cavotricuspid isthmus showed a post-pacing interval equal to the tachycardia cycle length. Ablation using an 8 mm tip, large curl, non-irrigated ablation catheter at 70W and 60° C resulted in termination of flutter and restoration of sinus rhythm. Bidirectional block across the cavotricuspid isthmus was achieved and maintained. Diltiazem and amiodarone were discontinued, and the rest continued. Post procedure, the patient remained in normal sinus rhythm with frequent RBBB morphology PVCs. 

At 4-week follow-up after ablation, the patient mentioned a marked improvement in shortness of breath and exercise tolerance. He denied any palpitations, and a 12-lead ECG showed sinus rhythm and no PVCs. Anticoagulation was continued, given his high CHA2DS2-VASC score. Echocardiogram performed at the 2-month mark following flutter ablation showed reduction in LVEDD. LVEF had increased to 50%. 

However, soon after that, the patient had an emergency room visit for complaints of chest discomfort, palpitations, and dyspnea. ECG showed sinus rhythm with frequent PVCs. A Holter monitor showed normal sinus rhythm with a PVC burden of 28,000 PVCs/day, with intermittent bigeminy and episodes of non-sustained ventricular tachycardia. Two different PVC morphologies were noted on Holter. Given the recurrence of symptoms and potential for decline in left ventricular function from PVCs, management options including antiarrhythmic therapy and PVC ablation were discussed, and the patient chose to undergo PVC ablation.

During the second EP study, bidirectional block was still present across the cavotricuspid isthmus. Two different PVC morphologies were noted and will be denoted as PVC1 and PVC2, respectively (Figure 3). PVC1 was the predominant morphology at baseline, and had a QR pattern in lead V1 and transition to prominent R-wave in V2, a left superior axis and a QRS duration of 125 msec. Interestingly, when the patient underwent the EP study and atrial flutter ablation several weeks prior, PVC2 (RBBB, inferior axis) was the only morphology seen. The relatively narrow QRS and the morphology suggested a septal location for the PVC1. We initially placed a coronary sinus catheter, a His bundle catheter, and a right ventricular catheter. 

Activation mapping was then performed, first in the right ventricle followed by the left ventricle using a 4 mm tip non-irrigated ablation catheter (Safire, St. Jude Medical). Earliest activation in the right ventricle was located at the basal mid to inferior septal tricuspid annulus, slightly inferior to the His bundle potential, and was 52 msec pre-QRS (Figure 4, panel A). Radiofrequency energy delivered at this located at 50W and 55°C resulted in a decrease in frequency of PVC1 but did not eliminate the PVCs. Interestingly, with the decrease in frequency of PVC1, PVC2 frequency increased significantly. PVC2 had a RBBB morphology with no precordial transition and an inferior axis with negative complexes in aVL and aVR (Figure 3). This was suggestive of a basal anterior/anterolateral left ventricular location. Transseptal catheterization was performed using the standard technique with intracardiac echo guidance, a steerable sheath (Agilis, St. Jude Medical) was placed in the left ventricle, and the same 4 mm ablation catheter was used for activation mapping of PVC2. Earliest activation was at the anterolateral basal mitral annulus, where the local electrogram was 24 msec pre-QRS (Figure 6, panels A-C) and showed a 12/12 pace match. Ablation here resulted in elimination of PVC focus within 20 seconds. Following this, attention was focused again on PVC1, which was still present. Mapping identified a site at the inferoseptal left ventricle where the local activation during PVC1 was 63 msec pre-QRS and was fractionated (Figure 4, panel B). This location was directly across the septum from the earliest right ventricular site (Figure 5, panels A-C), and ablation here (50W, 55°C) resulted in elimination of PVC1 in 14 seconds. No further PVCs or ventricular tachycardia were inducible with programmed stimulation and burst pacing in the presence of high-dose isoproterenol. 

The patient was discharged the following day, and had complete resolution of dyspnea and marked improvement in exercise capacity over the next several days. Repeat echocardiogram in 3 months showed normalization of LVEF, and the patient hasn’t had any atrial or ventricular arrhythmias at 6 months following the second ablation. 


This case is a great example of how tachyarrhythmias and frequent ventricular ectopy can result in development of cardiomyopathy and heart failure in a patient, irrespective of underlying structural heart disease, and how successful treatment of culprit arrhythmias resulted in resolution of heart failure and complete recovery of left ventricular function. 

Arrhythmia-induced cardiomyopathy (AIC) is a condition in which a persistent tachycardia or frequent ectopy either directly induces or contributes to development of cardiomyopathy and heart failure in patients with either a structurally normal or abnormal heart.1 The key component of this particular condition is that it can be potentially reversed, when measured by heart failure symptoms and LVEF, with aggressive treatment of the culprit arrhythmia. Reversal of heart failure and cardiomyopathy following arrhythmia suppression confirms diagnosis of AIC. 

A full discussion of the mechanisms, clinical features, diagnosis, and management of AIC is beyond the scope of this article. Atrial fibrillation or flutter with rapid ventricular rate is the common reason for AIC.1,2 This condition, however, is often missed and a high degree of suspicion is needed for early identification. In this case, it is easy to overlook the importance of atrial flutter and/or PVCs as culprits for this patient’s cardiomyopathy and to just assume that he had ischemic cardiomyopathy given the coronary artery disease and prior CABG. Aggressive rhythm control, focused at elimination of both atrial flutter followed by PVCs, in this case resulted in stepwise improvement in heart failure and LVEF, confirmed the diagnosis of AIC, and disproved that underlying ischemic heart disease was the sole reason for the decline in LVEF.

An interesting aspect of this case is the potential contribution of more than one arrhythmia to the cardiomyopathic process. The initial insult was from rapid atrial flutter, and following flutter ablation, the patient’s symptoms and LVEF substantially improved to 50% from 35% previously. The patient, however, did have frequent PVCs at the time of initial EP study, but no clear quantification of PVC burden was available. Another interesting part was that the RBBB, inferior axis morphology PVC was the only type seen during the initial EP study. It is unclear what the PVC burden of the patient was in the immediate 2-month period following atrial flutter ablation. However, given that the patient initially felt better and then had recurrent symptoms of worsening dyspnea and fatigue associated with PVCs 2 months after successful atrial flutter ablation suggests worsening PVC burden, which was confirmed by Holter monitoring. Our patient had a PVC burden of 28%, which according to prior studies,3-5 is high enough to result in PVC-mediated cardiomyopathy. The fact that elimination of PVCs resulted in incremental improvement in LVEF supports how frequent PVCs also contributed to cardiomyopathy in this patient. 

In patients with AIC, suppression of the culprit arrhythmia often results in gradual recovery of LVEF and resolution of heart failure. However, recurrent tachyarrhythmia can result in rapid decline in left ventricular function.6 In this particular case, complete recovery of LVEF following atrial flutter ablation was possibly impeded by high PVC burden.

In this case, both PVC1 and PVC2 were not located to the common outflow tract locations, and perhaps the underlying ischemic heart disease substrate may have had a role to play in the origin of these different morphologies. Local electrogram on the left ventricular side of the septum was highly fractionated and of low amplitude, suggesting scar in the inferoseptal LV. Another key teaching point to recognize with respect to PVCs or ventricular tachycardias that arise from the interventricular septum is that although early local activation was seen on the right side of the septum (52 msec, in this case), lack of complete success with ablation at that site should prompt mapping the left side of the septum. In this case, earliest activation on the left side of the septum was earlier than that on the right side, and thus was the successful site. In terms of approach to the inferoseptum, both retrograde and transseptal approaches can be used. Here the patient had bilateral iliac artery stents, and so a transseptal approach was used.


In this patient with pre-existing ischemic heart disease, two different arrhythmias — persistent atrial flutter and frequent PVCs — contributed to the development of cardiomyopathy and heart failure. Early recognition led to a focused rhythm control strategy, and catheter ablation resulted in successful elimination of atrial flutter and 2 different morphologies of PVCs. Arrhythmia suppression led to resolution of heart failure symptoms and recovery of left ventricular function, and also confirmed the diagnosis of AIC. In any patient presenting with persistent tachyarrhythmia, heart failure, and cardiomyopathy, AIC should be suspected and aggressive attempts at arrhythmia suppression/elimination should be initiated to give the patient the best chance at recovery of myocardial function. 

Disclosures: The author has no conflicts of interest to report regarding the content herein. Outside the submitted work, Dr. Gopinathannair reports personal fees from St. Jude Medical, Abiomed, Inc., and Bristol-Myers Squibb/Pfizer.  


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