ISSN 0326-646X





Sumario Vol. 42 - Nº 1 Enero - Marzo 2013

Epicardial radiofrequency ablation of arrhythmic storm.

Andrés Martellotto, José L. Velarde, Ricardo Martellotto.

Unidad de Arritmias y Electrofisiología, Servicio de Cardiología Hospital Italiano de Córdoba. Sarmiento 1595, Barrio Gral. Paz.
Córdoba (5400), Argentina.
Correo electrónico

Recibido 30-OCT-12 – ACEPTADO después de revisión el 19-Diciembre de 2012.

The authors declare not having a conflict of interest.

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Chagas disease is an endemic disease, very common in Latin America. Its chronic cardiac compromise is frequently characterized by an entire myocardial involvement, leading to myocardial dysfunction and sustained ventricular arrhythmias. We present a 65-year-old lady, with Chagas cardiomyopathy and a ventricular tachycardia storm after an ICD implantation, for secondary prevention of sudden cardiac death. She was ablated from the epicardial space after a failed endocardial ablation attempt. We discuss the ablation protocol used, limitations and the result of the case.

Key words: Chagas cardiomyopathy. Ventricular tachycardia storm. Epicardial ablation
Rev Fed Arg Cardiol. 2013; 42(1): -




Chagas disease is an endemic parasitosis very prevalent in South America, mainly in Argentina, Brazil, Bolivia, and Venezuela with a prevalence estimated in 16-18 million people [1]. The etiologic agent is the Trypanosoma cruzi, a parasite, and its vector, the Triatoma infestans or vinchuca (kissing bug). Currently it is estimated that there are approximately 2.5 million people infected in Argentina, from whom 600,000 present clinical symptoms [2].

This parasitosis is rarely symptomatic in the acute phase, so much so that up to 90% of the patients go undetected. The cardiovascular involvement occurs over time, affecting up to 25-30% of infected patients [3-4].

The cardiac involvement, when acute, includes myocarditis with variable severity, manifesting as heart failure in its most severe appearance, and by the presence of electrocardiographic alterations, with the most common being: repolarization alterations (T wave alterations), 1st degree AVB, low-voltage QRS and premature ventricular contractions. In general, this type of severe manifestations are uncommon, and mild or concealed myocarditis predominate [5].

Chronic cardiac involvement generally manifests as dilated cardiomyopathy, accompanied up to 50%, by dyskinetic areas (generally postero-basal and apical in the LV) and ventricular arrhythmias. Myocardial damage in this stage is widespread and diffuse, as expression of a panmyocarditis (affecting the three myocardial layers, besides the excitoconductor system), with frequent electrocardiographic correlation, with CRBBB and LAFB maybe being the most emblematic ones.


We present a 64-year-old female patient, chagasic, who was referred to our institution for evaluation and treatment, because she suffered a first episode of ventricular arrhythmia in a scenario of a surgical intervention (cholecystectomy). The patient arrived lucid, hemodynamically stable, in sinus rhythm. When questioned, she mentioned asthenia and dyspnea of a one year evolution, accompanied occasionally by dizziness, never passing out. Her baseline ECG presented sinus rhythm with preserved AV and IV conduction and frequent PVC. Figure 1A. An echocardiogram was conducted, that showed dilated LV (LVEDD 5.85 cm, LVESD 4.51 cm) with mild dysfunction, with LVEF estimated in 45% and presence of two aneurysms, one at posterobasal level and another apical in the LV. Her medication included: carvedilol 12.5 mg every 12 h, losartan 50 mg every 24 h, and ASA 100 mg every 24 h. The physical examination did not show signs of decompensated heart failure (HF). The presence of CAD was ruled out through catheterization that showed coronary arteries without lesions and confirmed the presence of aneurysms. Thus, the diagnosis of chagasic cardiomyopathy was confirmed.

Figure 1. A: Baseline ECG of the patient. B: Induction of sustained monomorphic ventricular arrhythmia (SMVT). C: 12-lead ECG of the SMVT.


Faced with the absence of documentation on the arrhythmia, it was decided to perform an electrophysiology study (EPS), showing induction of sustained monomorphic ventricular arrhythmia (SMVT) with morphology of CRBBB with superior axis (QS in II, III and aVF) and positive R from V1-5, V6 starting with small q, Figure 1B-C. Such SMVT was terminated by ventricular overdrive (secondary termination). An ICD Medtronic MAXIMO DR was implanted. Successful defibrillation test with 15 J concluded the implant. Five days after the discharge, she consulted in the clinic of devices due to arrhythmic storm, with presence of multiple ineffective shocks, Figure 2A-B. Because of her good hemodynamic tolerance the device was turned off, and IV bolus of amiodarone was administered (150 mg slow) was administered, the patient was admitted and amiodarone in a load IV dose was prescribed (5 mg/Kg in 250 cc to be delivered over 2 hours); after 30 min she reversed to sinus rhythm. Interestingly, the morphology of the SMVT was similar to that induced during EPS.

Figure 2. A1: Mapped site and successful application, RAO. A2: Mapped site and successful application, LAO. B: Successful application of RF and removal of SMVT at 15 sec. C: Local electrogram (EGM) with fractionated signal of low amplitude and pre-systolic during SMVT.

A first endocardial ablation attempt was carried out, during which the protocol of ablation was similar to the one we will explain later. First and after seven days without SMVT, the patient was discharged, with amiodarone 200 mg every 24 h being added to her usual treatment. On the 9th post-ablation day, she was readmitted with asthenia, dizziness, and signs of decompensated HF; when the device was interrogated, SMVT below the range of detection was documented. Next, and once she was compensated, a new ablation was made with endo and epicardial access.

In our center, we don’t have electroanatomic mapping systems, so the protocol used for this type of arrhythmias was the following:

  1. Careful analysis of the ECG of tachycardia to delimit the ventricular area of interest (“gross tuning”). Figure 3A.
  2. Endocardial and epicardial access (prior failed endocardial ablation). Figure 3D.
  3. Mapping of the substrate (during SR) looking for fractionated electrograms (EGMs) of low amplitude and late, from the endo and the epicardium in areas of interest (“fine tuning”). Figure 3C.
  4. Pace mapping in areas previously identified during substrate mapping and comparison to documented SMVT (to identify areas of circuit exit). Figure 3B.
  5. SMVT induction.
  6. Activation mapping, identifying modification of the sequence of activation, where fractionated and late EGMs become early and precede QRS.
  7. Resetting and entrainment; comparing the morphology of the captured beat (concealed entrainment), measuring time of QRS spike vs. EGM local to QRS and evaluating post-pacing interval minus tachycardia cycle (PPI-TCL).

Figure 3 .A: Clinical VT morphology. B: Mapping of stimulation from the epicardium. C: Local electrograms in activation mapping site. D: Punctures for endo (RV apex quadripolar, coronary sinus and ablating in LV) and epicardial access.


With the use of this protocol, from the endo and epicardium, it was possible to identify an epicardial EGM (Figure 4C) of low amplitude, fractionated, 39 ms previous to QRS with an almost perfect pacing mapping, showing concealed entrainment with 34 ms of PPI-TCL and 15 ms of difference between the QRS spike vs. QRS EGM. This site was considered optimal and so, the target of the ablation, Figure 4A. Two radiofrequency (RF) pulses with a solid catheter, deflectable IBI, 4-mm tip, with 50 Watts of power limited by 60°C resulted in the abolition of the tachycardia after 15 sec of the second application.  

Once again the protocol of ventricular pacing was repeated, reaching the ventricular effective refractory period without induction and arrhythmia. More aggressive pacing (with basic cycle of 400 ms and up to 3 extrastimuli) resulted in induction of four different kinds of faster and not tolerated VT, which required overdrive pacing to end them. These were considered non-clinical arrhythmias and were not the target of ablation.

After 24 months post-ablation, the patient suffered two appropriate shocks; the first at 17 months and the second at 23 months, both times related to the decrease and suspension of amiodarone.


The purpose of this case is to show that in spite of being very helpful for the ablation of this type of arrhythmias, the lack of electroanatomic mapping systems in this particular type of arrhythmias (hemodynamically tolerated) should not be a limitation.

The careful analysis of the ECG of SMVT allows with a certain degree of certainty, to “regionalize” the site of origin (exit) of the tachycardia – gross tuning -. In this case, the morphology similar to CRBBB identifies the origin in the LV; the superior axis (negativity in II, III and aVF) warns us that the depolarization vector is getting away from the inferior side; the presence of prominent R from V1 through V4 places it at basal level, and q waves in V5-6 tells us that the vector is getting away from the lateral wall. To conclude we could say that the site of circuit exit originates in the LV, in its infero-lateral and basal region, close to the mitral annulus, where coincidentally there is an aneurysm. Moreover, the morphology of the QRS during tachycardia presents “Wolffian” characteristics, resembling the delta wave of the Wolff-Parkinson-White syndrome, which may express an epicardial origin [6].

Once access is obtained to the epicardial space, through the techniques described above [7] and during sinus rhythm, the search (in the area of interest) of fractionated and late potentials (areas of slow conduction), constitute a part of what we call “fine tuning”. Subsequently the use of the electrophysiological maneuvers described previously, in the ablation protocol, constitute the fundamental basis of the procedure. The hemodynamic tolerance during the arrhythmia, clearly related to her ventricular function with mild depression, offers us the invaluable chance of adjusting even more the fine tuning and identifying with greater accuracy the area of circuit exit and thus increasing our chances of success at the time of making the ablation.

This is the result of this particular case, part of the special group of patients (chagasic cardiomyopathy with hemodynamically stable SMVT). However, it constitutes a considerable part of our daily clinical practice.

We did not use contrast at the level of the coronary arteries to identify their location before applying RF. In this regard, our choice was based on our previous clinical and in vitro experience[8-9]. This showed that even during the emission of RF, in direct contact by the catheter with an epicardial coronary vessel, endothelial disruption, narrowing (stenosis) or the formation of thrombi in the lumen of the vessel do not occur. Even so, we are aware of the presence of reports of complications [9].

Only one morphology of arrhythmia was the target of our ablation, leaving the others without ablation. In this regard, the international experience advises to seek and remove all arrhythmias, but because they were hemodynamically not tolerated, it was not possible to fulfill the protocol of ablation. On the other hand, none of these arrhythmias was documented, and the arrhythmia removed was consistently reproduced during the EPS and documented spontaneously.


The lack of electroanatomic systems should not be a limitation to ablate patients with chagasic heart disease and well tolerated SMVT.

The use of a clear and graded algorithm allowed us to reduce significantly the area of interest, decreasing the time in VT and identifying the area of the circuit exit, optimizing the result of the ablation.

The use of protocols with combined access (endo and epicardial) in patients where the previously described electrocardiographic characteristics are identified, as first approach, would probably increase the percentage of success, decreasing the number of procedures to be made. This conclusion is still a speculation.



  1. Alderete PN, Di Pietro L, Calatroni M. Actualización sobre diagnóstico y control de la enfermedad de Chagas a profesionales de área endémica. Resultados relevantes. Congreso Argentino de Protozoología y Reunión sobre Enfermedad de Chagas. Córdoba-Argentina. 1984.
  2. Jörg M, Storino R. La enfermedad de Chagas en el siglo XXI: Consenso para una asignatura pendiente. Consenso de Enfermedad de Chagas SAC. Rev Arg Cardiol 2002; 70 Suplemento 1.
  3. Marin-Neto JS, Rassi A Jr, Morillo CA, et al. Rationale and design of a randomized placebo-controlled trial assessing the effects of etiologic treatment in Chagas cardiomyopathy: The Benznidazol Evaluation for Interrupting Trypanosomiasis (BENEFIT). Am Heart J 2008; 156: 37-43.
  4. Evequoz MC, Chuit R. Enfoque Globalizado del Impacto Médico Social de la Enfermedad de Chagas grupos II y III. 1° Simposio Virtual Enfermedad de Chagas. Federación Argentina de Cardiología. Disponible en
  5. Jörg M, Storino R. Tópico I: Enfermedad de Chagas con parasitemia evidente. Consenso de Enfermedad de Chagas SAC. Rev Arg Cardiol 2002, Vol. 70, Sup 1.
  6. Berruezo A, Mont L, Nava S. Electrocardiographic Recognition of the Epicardial Origin of Ventricular Tachycardias. Circulation 2004; 109: 1842-1847.
  7. Sosa E, Scanavacca M, Dcahgas’Avila A: A new technique to perform epicardial mapping in the electrophysiology laboratory. J Cardiovasc Electrophysiol 1996; 7: 531-536.
  8. Brugada J, Berruezo A, Cuesta A, et al. Non Surgical Transthoracic Epicardial Radio Frequency Ablation. An Alternative in Incesant Ventricular Tachycardia. J Am Coll Cardiol 2003; 41 (11): 2036-2043.
  9. D'avila A, Gutierrez P, Scanavacca M, et al. Effects of radiofrequency pulses delivered in the vicinity of the coronary arteries: Implications for nonsurgical transthoracic epicardial catheter ablation to treat ventricular tachycardia. PACE 2002; 25 (10): 1488-1495.  



Publication: March 2013

Editorial Electrónica
de FAC

8vo. Congreso Virtual de Cardiología

1º Setiembre al
30 Noviembre, 2013

XXXI Congreso Nacional de Cardiología

30-31 Mayo,
1º Junio, 2013
Organiza: Región Patagónica

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