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Europace 2003 5(4):375-380; doi:10.1016/S1099-5129(03)00091-6
© 2003 by European Society of Cardiology
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CASE REPORT

Ablation of postinfarction ventricular tachycardia guided by isolated diastolic potentials

B. Strohmer1 and C. Hwang2

1Department of Cardiology, Landeskliniken Salzburg Salzburg, Austria; 2Utah Valley Regional Medical Center Provo, UT, USA

Manuscript submitted 14 January 2003. Accepted after revision 22 June 2003.

Correspondence: Bernhard Strohmer, MD, Department of Cardiology, Landeskliniken Salzburg, Muellner Hauptstrasse 48, A-5020 Salzburg, Austria. Tel.: +43-662-4482-3401; Fax: +43-662-4482-3486. E-mail: b.strohmer{at}lks.at


    Abstract
 Top
 Abstract
 Introduction
 Case report
 Discussion
 Conclusion
 Acknowledgements
 References
 
Frequent recurrences of ventricular tachycardia (VT) despite implantable cardioverter-defibrillator (ICD) and antiarrhythmic drug therapy are a typical indication for catheter ablation. We performed endocardial mapping of an haemodynamically tolerated VT in a 67-year-old male patient. Isolated diastolic potentials (IDPs) of similar morphology were recorded during atrial paced rhythm at baseline and during monomorphic VT. The isolated potentials were required for initiation and maintenance of ventricular arrhythmia. These diastolic electrograms were considered to be part of the reentry circuit, as they remained constantly associated with VT during oscillations of cycle length and resetting. Validation of the ablation target was not performed by exact entrainment pacing in order to test the predictive value of the observed diagnostic phenomena. Radiofrequency (RF) energy applications were successful at the site where IDPs were recorded during atrial paced rhythm and VT. Ablation decreased the need for ICD therapies effectively in a patient with scar-related, slow VT.

Key Words: Radiofrequency catheter ablation, ventricular tachycardia, isolated diastolic potentials


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 Conclusion
 Acknowledgements
 References
 
Patients with an implantable cardioverter-defibrillator (ICD) frequently require concomitant antiarrhythmic drug therapy. Despite that, some patients have to be treated by adjunctive catheter ablation to decrease the frequency of defibrillator therapies[1]Go. Ventricular tachycardia (VT) after previous myocardial infarction is presumed to result from intraventricular reentry[2,Go3]Go. Slow conduction through surviving fibres of the infarct zone may produce fractionated electrograms, late or isolated diastolic potentials (IDP) during sinus rhythm (SR). Previous studies demonstrated that delayed electrograms during SR were nonspecific and frequently recorded from adjacent bystander sites, even though they were sites of slow conduction[4]Go. Hence, combinations of several strict mapping criteria based on entrainment technique have been proven useful for choosing target sites during radiofrequency (RF) catheter ablation of infarct-related VT[5]Go. However, IDP with identical morphology during SR and VT may be a marker for a narrow isthmus of the reentry circuit[6]Go. The following report will highlight the potential value of IDPs for locating a desirable ablation region, if these potentials are required for initiation and maintenance of haemodynamically tolerated VT.


    Case report
 Top
 Abstract
 Introduction
 Case report
 Discussion
 Conclusion
 Acknowledgements
 References
 
We report a 67-year-old male patient with a history of monomorphic VT after remote inferior myocardial infarction. Angiography showed diffuse coronary artery disease, with patent infarct related right coronary artery and inferobasal akinesia. The left ventricular ejection fraction determined by echocardiography was 0.30. A dual chamber ICD (Guidant Ventak Prizm 2 DR, model 1861) was implanted due to symptomatic sustained VT despite sotalol medication. Frequent recurrences of haemodynamically tolerated VT were detected properly by the device and terminated by antitachycardia pacing (ATP). However, premature atrial or ventricular complexes (PVC) reinitiated repetitive episodes of VT. For 30 days before the ablation procedure the patient received more than hundred ATP therapies and one 30 J-shock due to acceleration of VT. The surface ECG of the clinical VT showed an RBBB configuration with a ‘late reverse’ R-wave progression pattern, left superior axis deviation, and a cycle length (CL) of 450 ms.

During the ablation procedure the ICD was programmed to ‘therapy off’. The pacemaker was set to the DDD mode with a lower rate limit of 80 bpm and AV-delay of 220 ms allowing intrinsic atrioventricular nodal conduction. The electrophysiological study was performed in the fasting state after obtaining informed consent. Access to the left ventricle was achieved retrogradely across the aortic valve after exclusion of a mobile thrombus by echocardiography. Left ventricular mapping and ablation were performed with an 8F quadripolar, steerable catheter (5-mm tip electrode, 2-5-2 mm spacing, EP Technologies). The catheter position was assessed by biplane fluoroscopy. Bipolar intracardiac electrograms were filtered at 30–500 Hz. All data were digitally recorded using the CardioLabTM System (GE, Prucka, Houston, Texas). RF current (500 kHz) was applied under temperature control of 60°C at 50 W power. Systemic anticoagulation was achieved with heparin, sedation with propofol and fentanyl.

Clinical VT started either spontaneously after atrial (Fig. 1A) or ventricular ectopy, or was easily induced by programmed ventricular stimulation. More than one VT morphology was inducible, but only the clinical prevalent VT was targeted. Detailed endocardial mapping of the inferobasal septum revealed abnormal electrograms with distinct IDPs. The diastolic electrograms were recorded during atrial paced rhythm with ventricular pseudofusion due to the long AV delay. The interval from QRS onset to the inscription of the IDP at the distal ablation catheter bipole measured 234 ms. The initiation of monomorhic VT by premature atrial beats (Fig. 1B) was preceded by the appearance of IDPs during baseline rhythm. However, at this catheter location the potentials showed different characteristics during ongoing VT. After refined mapping we recorded identical IDPs during atrial paced rhythm and VT, which started after a late ventricular extrasystole at a CL of 430 ms (Fig. 2). Again, onset of VT was preceded by appearance of an IDP, which occurred at a constant relationship (160 ms) to the subsequent QRS complexes during VT despite minor oscillations of CL. A spontaneous PVC during VT advanced the isolated potential before resetting the subsequent QRS complex, resulting in a less than compensatory pause (Fig. 3A). The IDP showed again a fixed position to the subsequent QRS of 164 ms. The loss of the IDP after a PVC from that site was associated with termination of tachycardia (Fig. 3B). Based on these phenomena we assumed that the diastolic potentials were recorded from an early site of the reentry pathway and entrainment criteria were not further defined. RF energy applications delivered to this specific site with IDPs terminated VT within 5 s (Fig. 4). Enlargement of the initial lesion was performed and the IDPs were no longer present after a total number of five energy applications, each lasting for 2 min. Following ablation, the clinical VT was noninducible by programmed ventricular stimulation from two sites at baseline and on orciprenaline infusion. No procedure-related complications occurred. The patient remained free of VT recurrences and required no tiered defibrillator therapies since then. Unexpectedly, the patient died a month later due to pneumonia and acute respiratory distress syndrome.



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Figure 1 (A) Ventricular tachycardia (VT) induced by a premature atrial beat (*), as recorded by the ICD onset electrogram (atrial, ventricular and shock leads from top to bottom, 25 mm/s). (B) Similar onset mechanism recorded during endocardial mapping. The morphology of the isolated diastolic potentials (arrows) during atrial paced rhythm differs from the multicomponent morphology during VT (small arrows) at this point of mapping. ABL d and ABL p, distal and proximal poles of the ablation catheter, respectively; RVA, right ventricular apex; CS, coronary sinus; STIM, stimulation.

 



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Figure 2 IDPs (arrows) were recorded during atrial paced rhythm and during VT. At baseline, the isolated potentials were present 234 ms after QRS onset. A late ventricular extrasystole (*) initiated VT (CL 430 ms) with subtle spontaneous oscillations after onset. Despite these minor variations of CL, IDPs of similar morphology preceded the subsequent QRS by a fixed relationship of 160 ms. This was considered as a criterion indicating that the diastolic electrogram was required for initiation and maintenance of VT. Abbreviations same as in Fig. 1B.

 



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Figure 3 (A) A single premature ventricular beat (*) advanced the mid-diastolic potential (arrow) and resulted in resetting of the monomorphic VT. Again, the IDP showed a fixed position to the subsequent QRS of 164 ms. (B) Loss of the IDP (open arrow) after a spontaneous PVC (*) was associated with the termination of VT. Both observations provided evidence that the isolated potentials were part of the reentry circuit. Abbreviations same as in Fig. 1B.

 



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Figure 4 During ongoing radiofrequency catheter ablation at this specific site VT terminated within 5 s by blocking between this diastolic site (arrow) and the systolic (QRS) electrogram. The IDPs decreased in amplitude until they vanished completely after delivery of energy application. Abbreviations same as in Fig. 1B.

 

    Discussion
 Top
 Abstract
 Introduction
 Case report
 Discussion
 Conclusion
 Acknowledgements
 References
 
During SR, slow conduction through an old infarct region may depolarize tissue after the end of the QRS complex. Such delayed local depolarization of surviving fibres is considered to be the cause of late or isolated potentials[3]Go. IDPs, defined as discrete signals inscribed after the end of the QRS complex, and separated by an isoelectric segment, indicate that they originate in areas of slow conduction bounded by anatomic arcs of block[6Go–8]Go. In a study by Harada et al. ‘late potentials’ were present in 33% of sites where the electrogram was recorded during SR and, without moving the mapping catheter, VT was initiated and RF current was applied[9]Go. These potentials were observed at 54% of sites where ablation terminated VT but only at 21% of sites where it did not. Bogun et al. showed that in two-thirds of cases (10 of 15 VTs) IDPs during SR could be recorded at sites from which IDPs were recorded during VT[10]Go. Eighty-seven percent of the VTs were successfully ablated at sites where IDPs could not be dissociated from monomorphic VT. The higher success rate in this study compared with the previous one may be related to consistent application of strict pacing criteria, such as concealed entrainment and pacing during SR. A recently published study demonstrated that the characteristics of bipolar electrograms recorded during SR and VT are similar at catheter locations that are within the reentry circuit[11]Go. During SR isolated potentials, but not late potentials, were associated with successful ablation.

SR mapping may be helpful in identifying a region of interest for successful ablation in postinfarction VT[12]Go. IDPs often arise from a narrow portion of the reentry circuit, but can also be a nonspecific finding when occurring in abnormal bystander regions. In our case, we considered the IDPs meaningful, as they remained critically related to the clinical VT during initiation, termination, and resetting by a spontaneous PVC[13]Go. Exact entrainment mapping is usually mandatory for validation of a promising target site[5,Go14]Go. However, in this special instance we obviated specific pacing techniques in order to test the predictive value of sharp diastolic potentials with similar shape during SR and VT. Our case demonstrated, that IDPs may probably serve as reliable guide for effective ablation, if the above-mentioned combination of diagnostic criteria are met. Morphological characteristics of IDP during SR and VT seem to be of additional value in predicting a critical reentry site[11]Go. Early termination of VT during RF application was a good indication that a crucial portion of the reentry circuit was heated[14]Go.


    Conclusion
 Top
 Abstract
 Introduction
 Case report
 Discussion
 Conclusion
 Acknowledgements
 References
 
IDPs arising from a zone of slow conduction are known to be activated in a similar way during atrial paced rhythm and monomorphic VT. Isolated potentials with nearly identical morphology during SR and VT were consistently recorded during initiation and maintenance of haemodynamically tolerated ventricular arrhythmia. The IDPs remained critically associated with the VT and pointed to a narrow isthmus of the reentry circuit. RF energy applications were successful at the site where IDPs were recorded during SR and VT. Although it is not recommended to rely on isolated potentials as a sole mapping criterion, our case demonstrated that a target for effective ablation may be defined by isolated potentials when typical diagnostic phenomena are present. Ablation decreased the need for ICD therapies effectively and was an important adjunctive measure in a patient with drug-refractory, slow VT.


    Acknowledgements
 Top
 Abstract
 Introduction
 Case report
 Discussion
 Conclusion
 Acknowledgements
 References
 
We wish to thank Peng-Sheng Chen, MD, for reviewing the manuscript.


    Footnotes
 
Central Utah Medical Clinic, 1055 North 500 West, Provo, UT 84604, USA. Tel.: +1-801-373-4366; Fax: +1-801-429-8191. E-mail: chunhwangmd{at}aol.com Back


    References
 Top
 Abstract
 Introduction
 Case report
 Discussion
 Conclusion
 Acknowledgements
 References
 
[1] Strickberger SA, Man KC, Daoud EG, et al. A prospective evaluation of catheter ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and an implantable cardioverter-defibrillator. Circulation 1997; 96: 1525–1531.[Abstract/Free Full Text]

[2] Stevenson WG, Khan H, Sager P, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation 1993; 88: 1647–1670.[Abstract/Free Full Text]

[3] Morady F, Harvey M, Kalbfleisch SJ, el-Atassi R, Calkins H, Langberg JJ. Radiofrequency catheter ablation of ventricular tachycardia in patients with coronary artery disease. Circulation 1993; 87: 363–372.[Abstract/Free Full Text]

[4] Cassidy DM, Vasallo JA, Buxton AE, Doherty JU, Marchlinski FE, Josephson ME. The value of catheter mapping during sinus rhythm to localize site of origin of ventricular tachycardia. Circulation 1984; 69: 1103–1110.[Abstract/Free Full Text]

[5] El-Shalakany A, Hadjis T, Papageorgiou P, Monahan K, Epstein L, Josephson ME. Entrainment/mapping criteria for the prediction of termination of ventricular tachycardia by single radiofrequency lesion in patients with coronary artery disease. Circulation 1999; 99: 2283–2289.[Abstract/Free Full Text]

[6] Kocovic DZ, Harada T, Friedman PL, Stevenson WG. Characteristics of electrograms recorded at reentry circuit sites and bystanders during ventricular tachycardia after myocardial infarction. J Am Coll Cardiol 1999; 34: 381–388.[Abstract/Free Full Text]

[7] Saito J, Downar E, Doig JC, et al. Characteristics of local electrograms with diastolic potentials: identification of different components of return pathways in ventricular tachycardia. J Interv Card Electrophysiol 1998; 2: 235–245.[Medline]

[8] Cabo C, Schmitt H, Masters G, Coromilas J, Wit AL, Scheinman MM. Location of diastolic potentials in reentrant circuits causing sustained ventricular tachycardia in the infarcted canine heart: relationship to predicted critical ablation sites. Circulation 1998; 98: 2598–2607.[Abstract/Free Full Text]

[9] Harada T, Stevenson WG, Kocovic DZ, Friedman PL. Catheter ablation of ventricular tachycardia after myocardial infarction: relation of endocardial sinus rhythm late potentials to the reentry circuit. J Am Coll Cardiol 1997; 4: 1015–1023.

[10] Bogun F, Bahu M, Knight BP, et al. Response to pacing at sites of isolated diastolic potentials during ventricular tachycardia in patients with previous myocardial infarction. J Am Coll Cardiol 1997; 30: 505–513.[Abstract]

[11] Bogun F, Bender B, Li YG, et al. Analysis during sinus rhythm of critical sites in reentry circuits of postinfarction ventricular tachycardia. J Interv Card Electrophysiol 2002; 7: 95–103.[Medline]

[12] Fitzgerald DM, Friday KJ, Wah JA, Lazzara R, Jackman WM. Electrogram patterns predicting successful catheter ablation of ventricular tachycardia. Circulation 1988; 77: 806–814.[Abstract/Free Full Text]

[13] Fitzgerald DM, Friday KJ, Wah JA, Bowman AJ, Lazzara R, Jackman WM. Myocardial regions of slow conduction participating in the reentry circuit of multiple ventricular tachycardias: report on ten patients. J Cardiovasc Electrophysiol 1991; 2: 193–206.

[14] Stevenson WG, Friedman PL, Sager PT, et al. Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol 1997; 29: 1180–1189.[Abstract]


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