Ann Thorac Surg 2009;87:631-633. doi:10.1016/j.athoracsur.2008.06.065
© 2009 The Society of Thoracic Surgeons
Case Reports
Recurrent Ventricular Arrhythmia After Coronary Artery Bypass Grafting Treated With Radiofrequency Catheter Ablation
Fernando A. Atik, MDa,*,
Maria Fernanda M. Garcia, MDb,
Jose Mario Baggio, Jr, MDb,c,
Cristiano N. Faber, MDa,
Ricardo B. Corso, MDa,
Luiz Fernando Caneo, MDa,
Alvaro V. Sarabanda, MDb,c
a Department of Cardiovascular Surgery, Heart Institute of Federal District, Zerbini Foundation, Brasilia, Brazil
b Department of Cardiology, Heart Institute of Federal District, Zerbini Foundation, Brasilia, Brazil
c Department of Clinical Arrhythmia and Pacemaker Unit, Heart Institute of Federal District, Zerbini Foundation, Brasilia, Brazil
Accepted for publication June 19, 2008.
* Address correspondence to Dr Atik, Heart Institute of Federal District, Zerbini Foundation, Estrada Parque Contorno do Bosque s/n, 1 Andar, Sala 13, Brasília-DF, 70658-700, Brazil (Email: fernando.atik{at}incordf.zerbini.org.br).
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Abstract
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A 63-year-old diabetic woman was emergently submitted to coronary artery bypass grafting in the setting of acute myocardial infarction. Recurrent, drug-refractory episodes of ventricular arrhythmia occurred for 2 weeks postoperatively, despite no documentation of ongoing myocardial ischemia and optimum medical treatment. Ventricular arrhythmia was initiated by premature ventricular contractions originating from the Purkinje system within the infarct border zone. Radiofrequency catheter ablation was performed at sites where Purkinje potentials were recorded, leading to arrhythmia cessation. A week later, an implantable cardioverter defibrillator was inserted and she was discharged home a few days later. At 15-month follow-up, there were no further episodes of arrhythmia and ventricular function had improved.
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Introduction
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Recurrent, drug-refractory, new onset ventricular tachycardia (VT) and ventricular fibrillation (VF) after coronary artery bypass grafting (CABG) is uncommon, but may be associated with increased morbidity and mortality. The most likely mechanism is residual myocardial ischemia that usually relates to suboptimal anastomosis or incomplete revascularization. However, other factors may be implicated [1], including inadequate myocardial protection, myocardial reperfusion, metabolic imbalance, and anti-arrhythmic drug pro-arrhythmia.
We herein report a patient who had drug-refractory, recurrent VT/VF early after CABG, and we discuss the possible mechanisms and the successful use of radiofrequency catheter ablation.
A 63-year-old diabetic woman was admitted in the emergency room with a 3-hour history of sudden onset chest discomfort irradiated to the left arm and the back. On physical examination, she was found hemodynamically unstable, with early signs of pulmonary edema. Admission electrocardiogram revealed sinus rhythm, 80 beats per minute, and 1-mm ST segment elevation deviation on the posterolateral wall leads. Her cardiac enzymes were 2.5 times greater than expected. She was treated according to standardized protocols and immediately submitted to cardiac catheterization, which revealed an occluded left main trunk and patent right coronary artery that supplied the distal left anterior descending coronary artery through collateral arteries. She remained hemodynamically unstable throughout the procedure, requiring intravenous inotropes and an intra-aortic balloon pump.
Emergent CABG with cardiopulmonary bypass was then performed approximately 3 hours after hospital admission. The operation consisted of an in situ left internal thoracic artery to the left anterior descending coronary artery and reversed saphenous vein grafts to diagonal and obtuse marginal branches. Although her initial postoperative recovery was unremarkable, she had recurrent episodes of fast VT degenerating into VF starting on postoperative day 5. She was initially managed with intravenous amiodarone (600 mg bolus, 1.8 g/day), lidocaine (150 mg bolus, 4 mg/min) and β-blocker therapy (metoprolol, 10 mg IV bolus; enteral, 100 mg/day), but all these anti-arrhythmic drugs were ineffective to suppress the VT, which recurred every other day. Coronary angiogram assured wide patency of all conduits, and echocardiography revealed severe left ventricular dysfunction with wall motion abnormalities at the mid-inferior septum and apex.
A 24-hour Holter electrocardiogram recording identified that VT episodes were reproducibly initiated by premature ventricular contractions with right bundle-branch block morphology and superior axis configuration, and QRS duration between 80 to 120 ms, which were coupled to the preceding ventricular beat by 400 to 480 ms (Fig 1).
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Fig 1. Holter electrocardiographic recordings on postoperative day 7. Premature ventricular contractions ( ) initiating (A) monomorphic nonsustained ventricular tachycardia (VT), (B) fast monomorphic sustained VT, and (C) degeneration into ventricular fibrillation (VF) that required external defibrillation.
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On postoperative day 9, the patient had a central line related bacteremia, and shortly thereafter, despite absence of QT interval prolongation, she exhibited incessant VT–VF episodes, which required external defibrillation for approximately 90 times during a 3-hour period. Therefore, an intra-aortic balloon pump was reinserted, broad-spectrum antibiotics were initiated, and the central line was removed. The patient was then kept sedated with midazolam and fentanyl, and was mechanically ventilated. Even though deep sedation was successful to suppress VT–VF, antiarrhythmic drugs were ineffective to control it on discontinuing the sedation, and VT–VF recurred for the following days. Considering that arrhythmia remission was unlikely, she was taken to the electrophysiology laboratory to attempt catheter ablation.
The electrophysiologic study was performed under general anesthesia. Multi-polar catheters were positioned from the femoral veins into the right ventricular apex and at the His bundle. The left ventricle (LV) was mapped using a 7-French 4-mm tip quadripolar electrode catheter (Biosense Webster, Diamond Bar, CA) through a retrograde aortic approach, which was also used for radiofrequency ablation. During the electrophysiologic study, no spontaneous premature ventricular contractions were observed, probably due to deep sedation. Nonsustained VT and sustained monomorphic fast VT (cycle length, 250 ms) degenerating into VF were induced by programmed ventricular stimulation (Fig 2). During VT induction, pre-systolic, high-frequency Purkinje potentials were recorded continuously from the LV inferobasal septum to the inferior midseptal segment (Fig 2). Purkinje potentials preceded ventricular activation with a regular interval for the first few tachycardia beats. Then, during VT degeneration into VF, Purkinje potentials were recorded in random intervals. Bundle branch re-entry VT was excluded based on absence of His depolarization preceding the QRS complex during VT, at a site where a His depolarization was recorded during sinus rhythm (Fig 2). Pace mapping during sinus rhythm at the LV inferoseptal region showed a matching QRS morphology with the induced VT. A total of 16 radiofrequency energy (60°C and maximum power 50 W) applications were delivered to the LV inferoseptal region, at sites where Purkinje potentials were recorded. No conduction abnormalities were noted after the procedure.
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Fig 2. Twelve-lead electrocardiogram at electrophysiologic study of (A) a sustained ventricular tachycardia (VT) induced by programmed ventricular stimulation. (B) Intracardiac electrocardiograms during induction of monomorphic fast sustained VT. Purkinje potentials (*) precedes the very first narrow VT beat () and the subsequent beats.
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After the ablation session, there was marked improvement on arrhythmia frequency, being able to wean off intravenous medications and optimize beta blockade use. A week later, an implantable cardioverter defibrillator was inserted because of impaired ventricular function. She was discharged home a few days later. At 15-month follow-up, the implantable cardioverter defibrillator showed no further arrhythmia episodes; she was found to be in functional class I and LV function had improved.
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Comment
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The present case illustrated the occurrence of drug-refractory, incessant VT–VF early after CABG, despite no documentation of graft occlusion or ongoing myocardial ischemia. The patient had known risk factors for postoperative ventricular arrhythmia, such as left ventricular dysfunction, female gender, and acute myocardial infarction [1]. Likewise, the present case, grafting a non-collateralized, totally occluded vessel, supplying an infarct zone has been associated with postoperative VT due to restoration of electrophysiologic function to cells embedded within the borders of myocardial scar and creation of re-entrant circuits [2].
In the present patient, the most likely mechanism underlying VT–VF storm seemed to be related to Purkinje triggered activity and re-entry along the infarct border zone. Indeed, LV mapping during VT induction by programmed stimulation showed pre-systolic, high-frequency Purkinje potentials, continuously recorded from the inferobasal septum to the inferior midseptal segment. It is noteworthy that immediately after VT induction, Purkinje potentials preceded ventricular activation at regular intervals, but during VT degeneration into VF, these local potentials occurred in random intervals. Finally, radiofrequency energy delivered within the scar border zone, at sites where Purkinje potentials were recorded, were effective to suppress ventricular arrhythmia for a relatively long follow-up period. Bloodstream infection may have played an additional role in arrhythmia perpetuation, probably due to increased serum catecholamines.
Both experimental and clinical data have shown that the Purkinje system may be responsible for electrical storm in patients after myocardial infarction [3, 4]. It is widely known that endocardial Purkinje fibers are more resistant to ischemia than myocardial cells due to cavity blood derived nourishment [5]. Such surviving Purkinje fibers demonstrate abnormal electrophysiologic properties, including decreased resting membrane potential and reduced maximum depolarization velocity [3], which may lead to development of re-entrant arrhythmia.
Postoperative ventricular arrhythmia is usually manageable with medical therapy. Implantable cardioverter defibrillator therapy may be useful and dramatically improves prognosis of patients with ventricular dysfunction after CABG [6]; however, implantable cardioverter defibrillator is not indicated for patients with electrical storms. Anti-arrhythmic drugs and heart failure management are indicated and are usually enough to suppress electrical storms. However, Purkinje triggered activity and re-entry along the infarct border zone may be responsible for medical refractory cases, and these arrhythmias can be easily cured by catheter ablation [4]. In this patient, no episode of ventricular arrhythmia has recurred after the ablation procedure, indicating the relatively benign course once they have survived the electrical storm.
In conclusion, incessant VT–VF early after CABG may be triggered by premature ventricular contractions originating from the Purkinje system within the infarct border zone. Radiofrequency catheter ablation may be used as an adjunctive therapy in these patients, after excluding the possibility of ongoing myocardial ischemia.
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References
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- Ascione R, Reeves B, Santo K, Khan N, Angelini GD. Predictors of new malignant ventricular arrhythmias after coronary surgery J Am Coll Cardiol 2004;43:1630-1638.[Abstract/Free Full Text]
- Steinberg JS, Gaur A, Sciacca R, Tan E. New-onset sustained ventricular tachycardia after cardiac surgery Circulation 1999;99:903-908.[Abstract/Free Full Text]
- Friedman PL, Stewart JR, Fenoglio Jr JJ, Wit AL. Survival of subendocardial Purkinje fibers after extensive myocardial infarction in dogs Circ Res 1973;33:597-611.[Abstract/Free Full Text]
- Bansch D, Oyang F, Antz M, et al. Successful catheter ablation of electrical storm after myocardial infarction Circulation 2003;108:3011-3016.[Abstract/Free Full Text]
- Arnar DO, Bullinga JR, Martins JB. Role of the Purkinje system in spontaneous ventricular tachycardia during acute ischemia in a canine model Circulation 1997;96:2421-2429.[Abstract/Free Full Text]
- Bolad I, MacLellan C, Karanam S, et al. Effectiveness of early implantation of cardioverter defibrillator for postoperative ventricular tachyarrhythmia Am J Cardiol 2004;94:376-378.[Medline]
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Abstract
Introduction
