ELECTROPHYSIOLOGY
Monomorphic ventricular tachycardia related to Wolff–Parkinson–White surgery
Department of Cardiology, The Royal Melbourne Hospital, Grattan Street, Parkville, Melbourne 3052, Australia
Manuscript submitted 12 August 2006. Accepted after revision 12 November 2006.
* Corresponding author. Tel: +613 93428879; fax: +613 93472808 E-mail address: richard.hillock{at}mh.org.au
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Abstract |
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Monomorphic ventricular tachycardia (MVT) is well described in patients who have had a ventricular scar due to repair of congenital heart disease. A 54-year-old woman presented with MVT 20 years after WPW surgery for a left-sided accessory pathway. The circuit was mapped to an area at the base of the left ventricle consistent with the incision described in the operation report. Entrainment confirmed the re-entrant circuit. Successful radiofrequency ablation was performed in a zone of slowed conduction consistent with the circuit isthmus. Any iatrogenic ventricular scar may form the substrate for MVT and be treated with standard electrophysiology techniques.
Key Words: Electrophysiology-clinical, Ablation, Wolff–Parkinson–White syndrome, Ventricular tachycardia
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Introduction |
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Monomorphic ventricular tachycardia (MVT) is a significant cause of morbidity and mortality in patients with ventricular incisions particularly in those who have had curative or palliative repair of congenital heart disease.1
Tetralogy of Fallot (TOF) repair, where a right ventriculotomy is used to relieve infundibular stenosis, is associated with an annual incidence of ventricular tachycardia in 0.3–3% of patients2 and long-term prevalence of ventricular tachycardia of 5%.3
Scar-mediated MVT is classically related to a zone of slow conduction around the ventricular incision establishing the substrate for re-entry and may also have some autonomic component.1,4 The development of MVT may be delayed by many years, which may point to progressive remodelling over time as an important factor in formation of substrate. We report a case of ventricular tachycardia related to previous cardiac surgical correction for Wolf–Parkinson–White (WPW) and its successful treatment by radiofrequency ablation.
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Case report |
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A 54-year-old woman with mild Ebstein's anomaly and previous WPW surgery developed recurrent palpitations 20 years after curative surgery. She was having multiple episodes per week. Non-sustained MVT was documented on exercise treadmill; transthoracic echo demonstrated moderate left ventricular systolic impairment without hypertrophy. Coronary angiography was normal.
Her medical history included syncope and palpitations since she was 6 with surgical interruption of the bypass tract at the age of 34. At surgery orthodromic re-entry tachycardia was mapped to a postero-septal bi-directional accessory tract. A standard right atriotomy was performed 2 mm from the hinge point of tricuspid leaflets and extended down through atrialized myocardium to the true ventricle. This was extended to the right free wall, then medially across the septum to the left free wall several centimetres beyond the postero-septal region. The delta wave was abolished after cardioplegia was reversed.
At electrophysiology study for her MVT 20 years later there was antegrade conduction with dual AV nodal physiology and absent VA conduction with no evidence of an AV bypass tract. Standard programmed ventricular stimulation induced right bundle branch block-like basal MVT (Figure 1) which was mapped, via a retro-aortic approach, to a left ventricular basal/postero-septal site (Figure 2). Low amplitude fractionated signals were found consistent with a surgical scar at this site over an area involving the septum and postero-basal area below the aortic valve. A re-entrant mechanism was proven by reproducibility of induction with programmed extra-stimuli, concealed entrainment at pacing sites around the scar (Figure 3 lower panel), and reliable termination with ventricular overdrive pacing. A zone suggestive of slowed conduction was demonstrated by low voltage fractionated signals around the unexcitable ventricular scar (Figure 3 upper panel). With the ablating catheter in this area, VT could no longer be initiated. Focal radiofrequency ablation (Irrigated ablation catheter, 30 W, 45°C) during sinus rhythm at this site rendered the VT non-inducible. There has been no recurrence of VT in the following 22 months.
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Discussion |
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This is the first case report of VT due to a ventricular scar from a surgical WPW cure successfully treated by radiofrequency ablation. The first case of iatrogenic WPW scar VT was described by Kimman et al., in which a young man presented 9 years after WPW surgery with a right ventricular basal aneurysm and ventricular tachycardia related to an incision for a postero-septal pathway.5
In that case, a repeat surgical procedure was performed with successful elimination of the ventricular tachycardia. In our case, the ventricular endocardial scar, used to interrupt the accessory AV connection, formed the substrate and one anatomical boundary for ventricular tachycardia. There was no indication of aneurysm at the time of mapping or in the pre-procedural echocardiogram. The incision formed one boundary of the circuit and the mitral annulus the other. Surgical division of the deep vascular perforators in the incision may have left patchy infarction in the area (small vessels and bands are typically divided within the ventricular incision, and the AV nodal artery and fibrous body are dissected out within the septal space.6 The successful ablation site correlated closely with the description of the leftward extension of the incision appearing in the operation report. This incision may be more extensive than other reported procedures because of the presence of Ebstein's anomaly, however, endocardial incisions were common in the early 1980s7 before an epicardial approach was developed that did not require cardiopulmonary bypass.8
Histology from right ventricular scar in TOF patients with VT demonstrates that these areas typically show degeneration, adiposis, fibrosis, inflammatory cell infiltration, and scattered myocyte islets9 and have also been shown in TOF patients who died suddenly.10 Abnormal cellular architecture, aneurysmal dilatation and ultrastructural change, correlates with electrophysiological areas of delay.9 Triggers for re-entry also become more prevalent in particular the frequency of ventricular premature beats over time.11 While these findings have not been described in patients who have undergone radiofrequency ablation for arrhythmia there is evidence that RF energy lesions may also be proarrhythmic many years after the ablation was performed.12
Transvenous catheter techniques allow mapping of the circuit and subsequent ablation.13,14 Entrainment, pace-mapping, and diastolic potentials in sinus rhythm are useful and successful techniques for identification and ablation of re-entrant circuits.15,16
Incisional scar mediated VT has previously been described in the repaired congenital heart disease population. This case demonstrates that any iatrogenic scar in the ventricle may form the substrate for re-entrant VT. It demonstrates that VT can occur late after WPW surgery.
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[1] Folino AF, Russo G, Bauce B, Mazzotti E, Daliento L. Autonomic profile and arrhythmic risk stratification after surgical repair of tetralogy of Fallot. Am Heart J 2004; 148: 985–9.[CrossRef][Web of Science][Medline]
[2] Harken AH, Horowitz LN, Josephson ME. Surgical correction of recurrent sustained ventricular tachycardia following complete repair of tetralogy of Fallot. J Thorac Cardiovasc Surg 1980; 80: 779–81.[Abstract]
[3] Gatzoulis MA, Till JA, Somerville J, et al. Mechanoelectrical interaction in tetralogy of Fallot: QRS prolongation relates to right ventricular size and predicts malignant ventricular arrhythmias and sudden death. Circulation 1995; 92: 231–7.
[4] Daliento L, Folino AF, Menti L, Zanco P, Baratella MC, Dalla Volta S. Adrenergic nervous activity in patients after surgical correction of tetralogy of Fallot. J Am Coll Cardiol 2001; 38: 2043–7.
[5] Kimman GP, van Hemel NM, Defauw JJAM. Proarrhythmia of surgery for Wolff–Parkinson–White syndrome. Cardiologie 1998; 5: 31–3.
[6] Kirklin JW and Barratt-Boyes BG. Tachycardias. In Kirklin JW and Barrattt-Boyes BG (Eds.). Cardiac Surgery 1986; New York John Wiley & Sons pp. p1359–83.
[7] Iwa T, Kawasuji M, Misaki T, Iwase T, Magara T. Localization and interruption of accessory conduction pathway in the Wolff–Parkinson–White syndrome. J Thorac Cardiovasc Surg 1980; 80: 271–9.[Abstract]
[8] Guiraudon GM, Klein GJ, Gulamhusein S, Jones DL, Yee R, Perkins DG, et al. Surgical repair of Wolff–Parkinson–White syndrome: a new closed-heart technique. Ann Thorac Surg 1984; 37: 67–71.[Abstract]
[9] Misaki T, Tsubota M, Watanabe GY, Watanabe Y, Matumoto Y, Ishida K, et al. Surgical treatment of ventricular tachycardia after surgical repair of tetralogy of Fallot. Relation between intraoperative mapping and histological findings. Circulation 1994; 90: 264–71.
[10] Deanfield JE, Ho SY, Anderson RH, McKenna WJ, Allwork SP, Hallidie-Smith KA. Late sudden death after repair of tetralogy of Fallot: a clinicopathologic study. Circulation 1983; 67: 626–31.
[11] Simpson RJ Jr, Cascio WE, Schreiner PJ, Crow RS, Rantaharju PM, Heiss G. Prevalence of premature ventricular contractions in a population of African American and white men and women: the atherosclerosis risk in communities (ARIC) study. Am Heart J 2002; 143: 535–40.[CrossRef][Web of Science][Medline]
[12] Kimman GP, Bogaard MD, van Hemel NM, van Dessel PF, Jessurun ER, Boersma LV, et al. Ten year follow-up after radiofrequency catheter ablation for atrioventricular nodal reentrant tachycardia in the early days forever cured, or a source for new arrhythmias? Pacing Clin Electrophysiol 2005; 28: 1302–9.[CrossRef][Medline]
[13] Cai CJ, Morton JB, Azegami K, et al. Linear segmental ablation of the scar border in sinus rhythm for post infarction ventricular tachycardia. Pacing Clin Electrophysiol 2003; 26: 12.[Medline]
[14] Stevenson WG and Delacretaz E. Strategies for catheter ablation of scar-related ventricular tachycardia. Curr Cardiol Rep 2000; 2: 537–44.[Medline]
[15] Soejima K, Stevenson WG, Maisel WH, Delacretaz E, Brunckhorst CB, Ellison KE, et al. The N+1 difference: a new measure for entrainment mapping. J Am Coll Cardiol 2001; 37: 1386–94.
[16] Stevenson WG, Sager PT, Friedman PL. Entrainment techniques for mapping atrial and ventricular tachycardias. J Cardiovasc Electrophysiol 1995; 6: 201–16.[Web of Science][Medline]
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