Europace Advance Access originally published online on February 23, 2007
Europace 2007 9(4):208-211; doi:10.1093/europace/eum014
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
ABLATION
Elimination of cavotricuspid isthmus conduction by a single ablation lesion: observations from a maximum voltage-guided ablation technique
Arrhythmia Service, University of Western Ontario, London Health Sciences Centre, 339 Windermere Road, London, Ontario N6A 5A5, Canada
Manuscript submitted 27 September 2006. Accepted after revision 5 January 2007.
* Corresponding author. Tel: +1519 663 3746; fax: +1 519 663 3782. E-mail address: allan.skanes{at}lhsc.on.ca
 |
Abstract |
|---|
 Top Abstract IntroductionMethodResultsDiscussionAcknowledgementsReferences |
|---|
Aims The architecture of the cavotricuspid isthmus has been shown to be highly variable made of a large number of interspersed bundles in the majority. Targeting high-amplitude signals has resulted in short-ablation times, likely due to the selective ablation of such bundles. We report a series of cases where a single site ablation resulted in bidirectional block, supporting the hypothesis that conduction can occur over a discrete portion of the isthmus.
Methods and results Sixty consecutive patients underwent ablation for isthmus-dependent atrial flutter using voltage-guided approach between September 2005 and June 2006. We found in five patients (8.3%) (four male, mean age 58.1 ± 11.4 years), in whom bidirectional block was achieved by ablation at a single site. The isthmus was mapped at the 6 o'clock LAO position, and bipolar amplitude was measured during pull-back to find the site of largest atrial voltage. The atrial and ventricular electrogram (EGM) measured 2.00 ± 1.6 and 0.2 ± 0.1 mV, respectively, at the successful site, resulting in the mean atrium/ventricle ratio of 9.1 ± 4.1. The total radiofrequency time was 83.8 ± 25.3 s, and the procedure time was 68.6 ± 10.4 min, including 30 min waiting time after the procedure. Flutter has not recurred over 5.7 ± 4.0 months follow-up.
Conclusion Targeting the largest atrial EGM in the isthmus can produce bidirectional block with a single site ablation. This supports the hypothesis that trans-isthmus conduction can occur over a discrete part of the isthmus, likely due to the underlying bundle architecture.
Key Words: Atrial flutter, Ablation, Atrial electrogram, Voltage guided, Cavotricuspid isthmus
|
Introduction |
|---|
|
TopAbstractIntroductionMethodResultsDiscussionAcknowledgementsReferences |
|---|
Radiofrequency (RF) ablation of the cavotricuspid isthmus (CTI) has become first line therapy for typical atrial flutter. Although various techniques have been described, the underlying treatment strategy is the creation of a complete line of conduction block from the tricuspid annulus to the Eustachian ridge.1
–6 It is known that the underlying architecture of the CTI is not uniform. In fact, in the majority of pathological specimens, the isthmus was composed of distinct anatomically defined bundles with intervening connective tissue. On the basis of this observation, we developed a ‘bundle hypothesis’ of CTI conduction. Specifically, we hypothesized that CTI conduction is dependent on the unique anatomic architecture of the bundles within the isthmus. Support for this hypothesis comes from the following observations. Intracardiac echo studies have correlated isthmus tissue thickness (bundles) with atrial electrogram (EGM) amplitude. Targeted ablation of high-amplitude atrial EGMs has resulted in short ablation times and bidirectional block in as few as two applications. Such targeted ablation also resulted in sudden, discrete steps in CTI conduction compatible with, loss of a discrete component (bundle) of CTI conduction.
We further hypothesized that the ability to produce bidirectional CTI conduction block with the application of RF at a single site, even in a small number of patients, would provide additional support for a ‘bundle hypothesis’ of CTI conduction.
|
Method |
|---|
|
TopAbstractIntroductionMethodResultsDiscussionAcknowledgementsReferences |
|---|
Ablation procedures between September 2005 and June 2006, using a maximum voltage-guided technique were reviewed. A database maintained for all ablation procedures performed at our centre was searched (Filemaker Pro 8.0v1), and 60 patients undergoing first CTI ablation for typical atrial flutter were reviewed.
Demographics and procedure-related parameters were assessed. Cases where a single ablation site resulted in a bidirectional block were extracted and formed the current study group.
Ablation procedure
The procedure was performed in the fasting state, with conscious sedation and atrial pacing from the proximal coronary sinus in four patients and during atrial flutter in five patients. Patients with prior ablation failure were excluded. A 20-pole catheter with 2–10–2 spacing (Duodeca; Daig Corporation, Minnetonka, MN, USA) was advanced to the right atrium and positioned anterior to the crista terminalis around the tricuspid annulus. A quadripolar catheter was positioned at the right ventricular apex (C.R. Bard Inc., Lowell, MA, USA), and a decapolar catheter in the coronary sinus with 2–8–2 spacing (C.R. Bard Inc.). Mapping of the CTI was performed during coronary sinus pacing at a cycle length of 600 ms. A deflectable ablation catheter was advanced to the inferior tricuspid annulus and into the ventricle.
Ablations were performed using an 8-mm tip catheter (CelciusTMDS, Biosense-Webster Inc., Diamond Bar, CA, USA). Ablation duration was left to the operator. Pacing was performed with an EP-3 clinical stimulator (EP Medical Inc., Budd Lake, NJ, USA) and intracardiac signals were band-pass filtered 30–500 Hz, with amplification 2500–10 000 times using the Prucka Cardiolab® 7000 system (G.E. Medical systems; Milwaukee, WI, USA).
Bidirectional block was the procedural endpoint. This was assessed by splitting of the local atrial EGM,10 reversal of polarity in the low right atrial bipolar EGM, delay in timing from pacing artifact to low right atrium independent of pacing cycle length and by differential pacing.11 Bidirectional block was confirmed at 30 min after the final application in all patients.
Maximum voltage-guided technique
The detailed technique has been described elsewhere.9 On a line in the 6 o'clock region in left anterior oblique view 30°, the isthmus was mapped and peak-to-peak bipolar atrial EGM amplitude was measured continuously during a careful pull back. Radiofrequency energy was applied first at the site of maximum atrial voltage, using an 8-mm tip electrode spacing of 1–6–2, with maximum power set to 70 W and maximum temperature 65°C (CelciusTMDS).
|
Results |
|---|
|
TopAbstractIntroductionMethodResultsDiscussionAcknowledgementsReferences |
|---|
Between September 2005 and June 2006, 60 consecutive patients underwent cavotricuspid ablation using the voltage-guided approach. In five patients (8.3%) [four male and one female, mean age (±SD) was 58.12 ± 11.37 (range 45–76 years)], bidirectional block was achieved with single site ablation within 120 s. Ablation was performed during proximal coronary sinus pacing in four patients and atrial flutter in one case. Clinical data are presented in Table 1.
|
All patients had normal left ventricular function. Mean left atrial size was 39.2 ± 6.3 mm, right atrial size was mildly enlarged in two patients. Four patients were taking antiarrhythmic drugs and/or AV node blocking agent. Three patients had history of atrial fibrillation and one patient had hypertension (Table 1).
Procedural parameters
The mean (±SD) atrial EGM size was 1.99 ± 1.57 mV (range between 0.75–4.4 mV, Table 2). The ventricular EMG size was 0.20 ± 0.087 mV (range between 0.1–0.3 mV). The atrium/ventricle (A/V) ratio at the targeted site was 9.14 ± 4.13 mV (range between 4.65–14.63 mV). The total RF time was 83.8 ± 25.34 s (range 59–120 s). The procedure time was 68.6 ± 10.42 min (range 51–90 min), including a 30-min waiting period after the last RF application. The mean fluoroscopy exposure was 12.76 ± 6.57 min (range 6.1–22 min). Flutter did not recur during 5.7 ± 4.0 months follow up.
|
An example (patient 4) is shown in Figure 1. The A/V ratio at the targeted site is >4. Significant conduction delay was observed during RF ablation, following 19 of the first RF application. Pacing manoeuvres subsequently revealed bidirectional isthmus block.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodResultsDiscussionAcknowledgementsReferences |
|---|
This study demonstrates that CTI conduction can be eliminated by the application of RF energy at a single site by targeting the largest amplitude atrial EGM. Although the numbers are small, this study provides further corroborative evidence that CTI conduction is not uniform in all patients and is likely to be related to the underlying anatomic bundle architecture.
Evidence for a ‘bundle hypothesis’
There is mounting evidence that the CTI does not act like a uniform sheet of muscular tissue in the majority of patients. Pathological studies have demonstrated discrete bundles of atrial muscle interspersed with connective tissue in most specimens. In some cases, large defects between muscular bundles were seen. Our previous work, targeting large amplitude signals on the isthmus has shown that ablation does not require a contiguous line of ablation across the entire isthmus. Using a voltage-guided technique, abrupt changes in CTI conduction were demonstrated during several ablation lesions, presumably due to the elimination of discrete muscle bundles. Hence, CTI conduction block occurred in a stepwise manner, as these functionally distinct routes of conduction were eliminated. The current work provides further evidence for the notion that muscle bundles play a significant role in isthmus conduction, by demonstrating complete elimination of CTI conduction in some patients, with RF application at a single isthmus site. A recent study from Maruyama et al. applied a multipolar catheter across the isthmus (perpendicular to the tricuspid valve) and targeted ‘earliest breakthrough’ EGMs.17 This group also found that ablation across the entire anatomic isthmus was not required to produce bidirectional block. The observations from pathological studies as well as ablation studies, including the current work, strongly suggest that the underlying anatomic bundle architecture of the CTI determines its conduction properties.
Site of ablation
Because the method of ablation targets the largest atrial EGM amplitude first, it is not unexpected that the A:V EGM ratio was relatively large. Nonetheless, the site of ablation was generally far from the tricuspid annulus, where the ventricular EGM would be larger than the atrial due to the relative increased mass of tissue on the ventricular side. The A:V ratio at the ablation site was >4.5 in all cases, suggesting a site relatively far from the AV ring. While we did not prospectively document the ablation sites with fluoroscopy, it is fair to suggest that based on this ratio, such sites were posterior, towards the Eustachian ridge. In cases where the A:V ratio was very large (>8.0), it is interesting to speculate that the Eustachian ridge itself might be the predominant bundle of conduction across the CTI.
Limitations
This analysis was retrospective. Nonetheless, bias was limited in that all the demographic and procedural data were entered in a standing database following each procedure. Only the A:V EGM ratio was retrospectively collected with the use of digital callipers to measure the EGM immediately prior to ablation. The study cohort was relatively small, <10% of the pool of ablation patients using this method.
Compared with that perceived to be associated with a single lesion, the fluoroscopy times were increased by a rigorous method that required several maps of the isthmus to determine the largest EGM. Also, we routinely used a coronary sinus catheter placed via the left subclavian as well as a multipolar catheter placed along the lateral right atrium. Outside the confines of this study, fluoroscopy times could be reduced even further.
Also, no anatomic data from the isthmuses were collected. It is possible that the isthmuses were quite short in these patients. The best estimates for isthmus length from post-mortem studies show a mean length of 37 ± 8 mm (range 21–49 mm).18 Even in this context, the observation of CTI block with ablation of a single site remains striking and highly supportive of the hypothesis that the entire isthmus needs not to be ablated to produce conduction block.
Conclusion
In a select group of patients, CTI conduction can be eliminated with ablation at a single site. This observation is highly supportive of the ‘muscle bundle’ hypothesis of isthmus conduction, with the clinical implication that the entire isthmus need not be ablated to produce conduction block.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionMethodResultsDiscussionAcknowledgementsReferences |
|---|
The authors wish to thank Drs Paul Gould and Uwais Mohamed for assistance on the ablation procedures and collection of data.
|
References |
|---|
|
TopAbstractIntroductionMethodResultsDiscussionAcknowledgementsReferences |
|---|
[1] Klein GJ, Guiraudon GM, Sharma AD, Milstein S. Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol 1986; 57: 587–91.[CrossRef][Web of Science][Medline]
[2] Feld GK, Fleck RP, Chen PS, et al. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation 1992; 86: 1233–40.
[3] Cosio FG, Lopez-Gil M, Goicolea A, Arribas F, Barroso JL. Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993; 71: 705–9.[CrossRef][Web of Science][Medline]
[4] Cosio FG, Lopez GM, Arribas F, Goicolea A. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Circulation 1993; 88: 804–5.
[5] Wellens H.J. Contemporary management of atrial flutter. Circulation 2002; 106: 649–52.
[6] Natale A, Newby KH, Pisano E, et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Card 2000; 35: 1898–1904.
[7] Waki K, Saito T, Becker AE. Right atrial flutter isthmus revisited: normal anatomy favors nonuniform anisotropic conduction. J Cardiovasc Electrophysiol 2000; 11: 90–4.[Web of Science][Medline]
[8] Cabrera JA, Sanchez-Quintana D, Farre J, Rubio JM, Ho SY. The inferior right atrial isthmus: further architectural insights for current and coming ablation technologies. J Cardiovasc Electrophysiol 2005; 16: 402–8.[Web of Science][Medline]
[9] Redfearn DP, Skanes AC, Gula LJ, Krahn AD, Yee R, Klein GJ. Cavotricuspid isthmus conduction is dependent underlying anatomic bundle architecture: observation using a maximum voltage-guided ablation technique. J Cardiovasc Electrophysiol 2006; 17: 832–8.[CrossRef][Web of Science][Medline]
[10] Shah DC, Takahashi A, Jaïs P, et al. Local electrogram-based criteria of cavotricuspid isthmus block. J Cardiovasc Electrophysiol 1999; 10: 662–9.[Web of Science][Medline]
[11] Poty H, Saoudi N, Nair M, et al. Radiofrequency catheter ablation of atrial flutter. Further insights into the various types of isthmus block: application to ablation during sinus rhythm. Circulation 1996; 94: 3204–13.
[12] Ozaydin M, Tada H, Chugh A, et al. Atrial electrogram amplitude and efficacy of cavotricuspid isthmus ablation for atrial flutter. Pacing Clin Electrophysiol 2003; 26: 1859–63.[CrossRef][Medline]
[13] Marrouche NF, Schweikert R, Saliba W, Pavia SV, Martin DO, Dresing T, et al. Use of different catheter ablation technologies for treatment of typical atrial flutter: acute results and long-term follow-up. Pacing Clin Electrophysiol 2003; 26: 743–6.[CrossRef][Medline]
[14] Kirkorian G, Moncada E, Chevalier P, Caru G, Claudel JP, Bellon C, et al. Radiofrequency ablation of atrial flutter. Efficacy of an anatomically guided approach. Circulation 1994; 90: 2804–14.
[15] Takahashi A, Shah DC, Jaïs P, Haïssaguerre M. How to ablate typical atrial flutter. Europace 1999; 1: 151–5.
[16] Thornton AS and Jordaens LJ. Atrial flutter: watch and control? Europace. 2005; 7: 413–4.
[17] Marayuma M, Koayashi Y, Miyauchi Y, et al. Mapping-guided ablation of the cavotricuspid isthmus: A novel simplified approach to radiofrequency catheter ablation of isthmus-dependent atrial flutter. Heart Rhythm 2006; 3: 665–73.[CrossRef][Web of Science][Medline]
[18] Cabrera JA, Sanchez-Quintana D, Ho SY, Medina A, Wanguemert F, Gross E, Grillo J, Hernandez E, Anderson RH. Angiographic anatomy of the inferior right atrial isthmus in patients with and without history of common atrial flutter. Circulation 1999; 99: 3017–23.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J.-A. Cabrera, S. Y. Ho, and D. Sanchez-Quintana How anatomy can guide ablation in isthmic atrial flutter Europace, January 1, 2009; 11(1): 4 - 6. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||