Catheter ablation of electrical storm triggered by monomorphic ventricular ectopic beats after myocardial infarction/Miyyokart enfarktusu sonrasi gelisen monomorfik ventrikuler erken atimlarin tetikledigi elektriksel firtinanin kateter ablasyonu.
Electrical storm is a life threating situation that involves recurrent episodes of ventricular arrhythmias. It is defined as 3 or more sustained episodes of ventricular tachycardia (VT), ventricular fibrillation (VF) or appropriate implantable cardioverter-defibrillator shocks during 24 hours (1). We report a patient who had drug-refractory, repetitive polymorphic VTs after myocardial infarction (MI) which could only be managed by radiofrequency ablation (RF) ablation of triggering ventricular premature beats (VPCs).
A 62-year-old female patient admitted to hospital with inferior MI after 12 hours of symptom onset. Patient immediately underwent successful primary percutaneous intervention. Echocardiogram revealed left ventricular ejection fraction of 40% with segmental wall motion abnormality.
Four days after the revascularization, she suddenly developed recurrent and sustained polymorphic VTs triggered by monomorphic VPCs (Fig. 1). There was no electrolyte imbalance and no recurrent ischemic event. Coronary angiography was also repeated but no significant lesion was observed. She was not taking any QT prolonging medication and QT interval was normal. Combination therapy of amiodarone and metoprolol was ineffective to suppress arrhythmias. Patient was deeply sedated and mechanically ventilated. Overdrive pacing and intra-aortic balloon pump counter pulsation were also tried to stop electrical storm. Despite all these interventions several electrical cardioversions were required (21 times in last 24 hours). Therefore, patient was transferred to electrophysiology laboratory to attempt catheter ablation of the VPCs triggering the polymorphic VTs.
Left ventricle (LV) was accessed retrogradely across the aortic valve (7.5 F Navistar D curve irrigated tip catheter, Biosense Webster). Electro anatomical mapping system (Carto 3, Biosense Webster, Diamond Bar, Ca, USA) was used to create LV map. Initially rapid activation map of presumed location of VPCs was created. VT episodes were so frequent that some of them were being reinitiated by the same VPCs shortly after DC shocks (Fig. 2). Although it was not detailed, activation mapping revealed the possible origin of VPCs at inferior septum near apex (Fig. 3). At these sites, low amplitude and high frequency Purkinje like potentials preceding VPCs were observed (Fig. 4). But they were not constant and hard to target for ablation. Pace mapping was also applied to localize the origin of VPCs. Areas with earliest activation and similar paced QRS morphology were identified as a target for RF ablation. After 5 RF applications VPCs disappeared and electrical storm stopped. Programmed ventricular stimulation with three extra stimuli failed to induce any tachyarrhythmia and the patient was brought to intensive care unit. Antiarrhythmic drug therapy continued. Patient had septicemia during follow up and had 2 VF episodes during febrile spells, which were not triggered by a VPC. On the 10th day of administration she had an ischemic stroke. Unfortunately, we lost her due to septic shock on the 22nd day of administration.
Persistent electrical storm after acute myocardial infarction (MI) is very dramatic condition and sometimes can only be managed by radiofrequency (RF) ablation. The Heart Rhythm Society and the European Heart Rhythm Association support early ablation of recurrent VT (2).
Ablation technique is depending on the mechanism of arrhythmia. Most monomorphic VTs in the presence of ischemic heart disease are due to electrical wave front reentry around a scar tissue. These mechanisms allow identifying critical isthmuses and ablation (3, 4). In contrast, the mechanisms responsible for polymorphic VT are poorly understood. Ventricular premature contractions (VPCs) originating from Purkinje system has been shown to be associated with polymorphic VTs and electrical storms after MI (5-7).
Emerging evidence in patients with polymorphic VT has identified that the Purkinje arborization is a dominant source of triggers initiating arrhythmias (8). Purkinje fibers are more resistant to ischemia than myocardial cells and endocardial fibers may be nourished from cavity blood (9). These surviving Purkinje fibers in infarct region demonstrate enhanced automaticity and triggered activity which may cause polymorphic VT when coupled with prolonged action potential duration (10). In current studies, most of the VPCs originating from Purkinje network were located in the border-zone of MI (5-7).These studies has shown that ablation of these triggers was able to eliminate arrhythmias. Similar results were also demonstrated for patients early after MI (6).
However, it is not always easy to find and abolish Purkinje potentials during electrical storm. For instance, we were not able to localize Purkinje potentials constantly because of repetitive hemodynamically unstable VTs. During the procedure we observed Purkinje like potentials where the earliest endocardial activation regions of VPCs were. After successful RF applications we didn't observe these signals. Our report is result of a single case and more studies are needed to elucidate the mechanisms of polymorphic VT after MI. Unfortunately, followup period was too short due to concomitant diseases and this is an obvious limitation of our report.
Catheter ablation plays increasingly important role in management of electrical storm after MI. RF ablation is indicated in recurrent polymorphic VT or VF when specific triggers can be targeted (2). In these cases accelerated ablation approach may help reaching to a safe harbor.
The study was supported by grants from the National Development Agency of Hungary (Semmelweis Egyetem Magiszter Program, TAMOP-4.2.2/B-10/1-2010-0013) and the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences. RRD
Emin Evren Ozcan, Gabor Szeplaki, Istvan Osztheimer, Tamas Tahin, Laszlo Geller
Department of Cardiology, Heart Center, Semmelweis University, Budapest--Hungary
(1.) Zipes DPP Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006; 48: 247-346. [CrossRef]
(2.) Aliot EM, Stevenson WG, Almendral-Garrote JM, Bogun F Calkins CH, Delacretaz E, et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Heart Rhythm 2009; 6: 886-933. [CrossRef]
(3.) Stevenson WG, Khan H, Sager P Saxon LA, Middlekauff HR, Natterson PD, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation 1993; 88: 1647-70. [CrossRef]
(4.) Soejima K, Suzuki M, Maisel WH, Brunckhorst CB, Delacretaz E, Blier L, et al. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping. Circulation 2001; 104: 664-9. [CrossRef]
(5.) Szumowski L, Sanders P Walczak F Hocini M, JaTs P Kepski R, et al. Mapping and ablation of polymorphic ventricular tachycardia after myocardial infarction. J Am Coll Cardiol 2004; 44: 1700-6. [CrossRef]
(6.) BAnsch D, Oyang F Antz M, Arentz T, Weber R, Val-Mejias JE, et al. Successful catheter ablation of electrical storm after myocardial infarction. Circulation 2003; 108: 3011-6. [CrossRef]
(7.) Peichl P CihAk R, KozeluhovA M, Wichterle D, Vancura V, Kautzner J. Catheter ablation of arrhythmic storm triggered by monomorphic ectopic beats in patients with coronary artery disease. J Interv Card Electrophysiol 2010; 27: 51-9. [CrossRef]
(8.) HaTssaguerre M, Shah DC, JaTs P Shoda M, Kautzner J, Arentz T, et al. Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation. Lancet 2002; 359: 677-8. [CrossRef]
(9.) 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: 2421-9. [CrossRef]
(10.) Berenfeld O, Jalife J. Purkinje-muscle reentry as a mechanism of polymorphic ventricular arrhythmias in a 3-dimensional model of the ventricles. Circ Res 1998; 82: 1063-77. [CrossRef]
Address for Correspondence/Yazisma Adresi: Dr. Emin Evren Ozcan, Department of Cardiology, Heart Center, Semmelweis University, Gaal Jozsef Street 9, 1122 Budapest-Hungary
Phone: +36 14586810
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|Title Annotation:||Case Reports/Olgu Sunumlari|
|Author:||Ozcan, Emin Evren; Szeplaki, Gabor; Osztheimer, Istvan; Tahin, Tamas; Geller, Laszlo|
|Publication:||The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)|
|Date:||Sep 1, 2013|
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