Europace Advance Access originally published online on March 8, 2007
Europace 2007 9(4):212-215; doi:10.1093/europace/eum016
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ABLATION
Epicardial catheter ablation of ventricular tachycardia using surgical subxyphoid approach
Federation of Cardiology, University Hospital Rangueil, 31059 Toulouse Cedex 09, France
Manuscript submitted 17 September 2006. Accepted after revision 31 December 2006.
* Corresponding author: Tel: +33 5 61 32 20 94; fax: +33 5 61 32 22 46. E-mail address: mauryjphil{at}hotmail.com
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Abstract |
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We report the case of a patient presenting with a previous inferior myocardial infarction complicated by incessant monomorphic ventricular tachycardia resistant to antiarrhythmic drugs. Because endocardial catheter ablation failed and because of focal endocardial activation arising from the left ventricular inferior wall, an epicardial location of the reentry circuit was suspected. Catheter mapping of the pericardial space through a surgical subxyphoid approach performed in the electrophysiological laboratory confirmed the epicardial location of the arrhythmogenic substrate and allowed us successfully to ablate and cure the patient. Surgical subxyphoid approach can be performed in the electrophysiological laboratory when epicardial ablation is needed in case of inadvisable, difficult, or failed non-surgical percutaneous access.
Key Words: Epicardial ventricular tachycardia, Epicardial catheter ablation, Surgical subxyphoid approach
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Case report |
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A 74-year-old man was admitted due to incessant well-tolerated monomorphic sustained ventricular tachycardia (VT) with left bundle branch block pattern and left axis (Figure 1). He presented with a previous inferior Q wave-myocardial infarction and left ventricular ejection fraction of 45%. Coronary arteriography revealed a chronically occluded right coronary vessel without significant abnormality of the left coronary artery, aneurysm, or wide severe left ventricular akinetic or dyskinetic area. Inefficiency of antiarrhythmic drugs (beta blockers, amiodarone, and flecainide) led us to perform general anaesthesia in order transiently to overcome the electrical storm.
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A first radio frequency (RF) ablation procedure was attempted using a non-fluoroscopic navigation system (CARTO, Biosense Webster, Inc. Diamond Bar, CA, USA). No significant scar was present on the left ventricle voltage map. A focal pattern of activation was documented on activation map, arising at the septal side of the inferior wall, with endocardial activation representing 40% of the VT cycle length. No satisfactory electrophysiological criteria could be found, even at the site of earliest activation, where pre-systolic smooth fragmented activities were present, suggesting far-field potentials. Lack of local capture did not allow entrainment mapping. Ventricular tachycardia persisted despite several long RF applications at this site, using an irrigated catheter with 50 W power output.
Despite the absence of ECG pattern evoking an epicardial origin, we decided to perform a second ablation procedure using epicardial mapping through surgical pericardial access. Three catheters were introduced through the right femoral vein and placed at the right ventricular apex in the coronary sinus and at the left ventricular apex through patent foramen ovale. The pericardial space was exposed using a surgical subxyphoid approach. A standard 8F sheath mounted over a guidewire was then simply introduced into the pericardium through a small incision (Figure 2). The sheath was maintained with a holding suture that could be released to allow removal of the irrigation fluid during the ablation procedure. An externally irrigated RF catheter (F curve, Thermocool Celsius, Cordis Webster, Inc. Diamond Bar, CA, USA) was then introduced through the sheath and carefully pushed into the pericardial space. The catheter was constantly irrigated with saline (1 mL/min flow rate). Manipulation of the catheter was never hampered by adhesion or fibrosis. The catheter could easily be placed and stabilized under the inferior ventricular wall after complete looping around the entire heart (Figure 2). Anatomic location of the ablation catheter was assessed using intracardiac catheters as landmarks. At an epicardial location facing the presumed site of endocardial activation breakthrough, low voltage electrograms and late ventricular potentials were present during sinus rhythm. Ventricular tachycardia could be easily induced, and sharp and ample pre-systolic potentials preceding far-field QRS complexes were consistently recorded in this area during VT. Efficient local capture using 10 mA and 2 ms pulse duration allowed entrainment mapping. Several RF test applications were performed at some sites in this area with acceptable entrainment criteria, interrupted after 15–20 s due to inability to stop the VT. Finally, at an optimal site displaying concealed entrainment, sinus rhythm resumed after 7 s of RF delivery using 40 W and 20 mL/min irrigation (Figure 3). Radio frequency was then applied for 3 min at this site.
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Ventricular tachycardia could not be induced thereafter, even with isoprenaline and the procedure was stopped. The whole procedure duration was 180 min, of which 30 min for surgical access and closure and 90 min for the ablation procedure itself (with the catheter in the pericardial space). Fluoroscopy time was 26 min.
Surgical approach was closed after insertion of an intrapericardial chest tube, which was removed on the next day. Anaesthesia could be interrupted without arrhythmia recurrence, which was maintained over a follow-up of 6 months. Repeated echocardiograms did not reveal pericardial effusion. The patient did not complain of chest pain or present symptoms suggestive of pericarditis. No ventricular arrhythmia could be induced during electrophysiological testing performed 1 month later.
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Discussion |
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Monomorphic sustained VT occurring late after myocardial infarction is known to be related to reentry circuits located in or at the border of the scar zone. Most of these circuits are subendocardially located, so that they are amenable to intracardiac catheter ablation, which, however, failed in 25–55% of cases.1
Intraoperative mapping had already suggested that epicardial circuits were common in VT related to prior infarction of the left ventricular inferior wall.2 Ventricular tachycardias originate from the epicardium in 15% of patients with previous myocardial infarction, particularly in case of inferior wall infarction.1
Following their encouraging results in non-surgical catheter epicardial ablation of VT in patients with Chagas' disease, Sosa et al. first reported their experience in 14 patients with an old, inferior myocardial infarction.2 Most of them presented with mildly impaired systolic function, inferior akinesia and occluded right coronary artery. By transthoracic puncture, RF catheters could have been placed in the pericardial space. Though not concealed, entrainment could be demonstrated due to the high pacing threshold, epicardial RF applications were able to interrupt 39% of all mappable VTs.2
Brugada et al. using the same technique were able successfully to cure incessant VTs in 8 of 10 patients, of whom eight had previous myocardial infarction (inferior in five).1 Such a non-surgical transthoracic epicardial approach was later performed by Ouyang et al. for successful ablation of VT in three of four patients presenting with isolated aneurysms of the left ventricular inferior-lateral wall without coronary abnormalities,3 by Schweikert et al. in 17 of 18 epicardial VTs occurring in various clinical settings after failure of endocardial ablation,4 then by Soejima et al. in six of seven patients with epicardial VTs related to non-ischaemic dilated cardiomyopathy.5 Percutaneous pericardial access has then become a not exceptional—if not a routine procedure—in some centres for RF ablation of epicardial VT.6
Soejima et al. first recently reported their initial experience in two patients with coronary artery disease and four patients with dilated cardiomyopathy with epicardial VT, in whom catheter ablation was successfully performed after subxyphoid surgical approach realized under general anaesthesia in the electrophysiology laboratory,7 in a procedure quite similar to the one here presented. Complications inherent in transthoracic puncture2 and necessity of anaesthesia or deep sedation2 prompted us to perform such a surgical approach without anticipating morbidity. Convenience in manipulating the RF catheter in the pericardial space would favour similar combined approaches in case of subepicardially located substrates, particularly in patients with previous heart surgery or difficult pericardial access using transthoracic puncture, or when electro-anatomic mapping, not available in operating room, is mandatory.7
The main risk in epicardial RF ablation would be that of damaging epicardial vessels, especially when the catheter is located close to a coronary artery or tributaries of the coronary sinus. This risk was minimized in our case due to the occluded right coronary artery, but coronary angiography is usually recommended before any RF application in order to avoid ablation when the catheter tip is <10–12 mm from a major coronary vessel.2,3
The 12-lead ECG of our patient did not match with the published criteria leading to recognition of epicardial origin of VT.8 For Sosa and colleagues, no remarkable ECG pattern was able to distinguish between epicardial and endocardial VTs occurring after inferior myocardial infarction.2 In our opinion, epicardial VT should be suspected in patients with previous inferior myocardial infarction in case of inability to perform endocardial RF ablation, regardless of ECG patterns, even in the case of left bundle branch block pattern.1,2 Subepicardially located circuits are probably more frequent in cases of non-transmural infarction,1 so that epicardial VT should particularly be suspected when occurring in patients with preserved left ventricular systolic function.
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References |
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[1] Brugada J, Berruezo A, Cuesta A, Osca J, Chueca E, Fosch X, et al. Non surgical transthoracic epicardial radiofrequency ablation. J Am Coll Cardiol 2003; 41: 2036–43.
[2] Sosa E, Scanavacca M, d'Avila A, Oliveira F, Ramires JAF. Nonsurgical transthoracic epicardial catheter ablation to treat recurrent ventricular tachycardia occurring late after myocardial infarction. J Am Coll Cardiol 2000; 35: 1442–9.
[3] Ouyang F, Antz M, Deger FT, Bänsch D, Schaumann A, Ernst S, et al. An underrecognized subepicardial reentrant ventricular tachycardia attributable to left ventricular aneurysm in patients with normal coronary arteriograms. Circulation 2003; 107: 2702–9.
[4] Schweikert RA, Saliba WI, Tomassoni G, Marrouche N, Cole CR, Dresing TJ, et al. Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablation. Circulation 2003; 108: 1329–35.
[5] Soejima K, Stevenson WG, Sapp JL, Selwyn AP, Couper G, Epstein LM. Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy. J Am Coll Cardiol 2004; 43: 1834–42.
[6] De Ponti R, Tritto M, Marazzi R, Salerno-Uriarte JA. How to approach epicardial ventricular tachycardia: electroanatomical mapping and ablation by transpericardial nonsurgical approach. Europace 2003; 5: 55–6.
[7] Soejima K, Couper G, Couper JM, Sapp JL, Epstein LM, Stevenson WG. Subxyphoid surgical approach for epicardial catheter-based mapping and ablation in patients with prior cardiac surgery or difficult pericardial access. Circulation 2004; 110: 1197–1201.
[8] Berruezo A, Mont L, Nava S, Chueca E, Bartholomay E, Brugada J. Electrocardiogram recognition of the epicardial origin of ventricular tachycardias. Circulation 2004; 109: 1842–7.
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