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Radiofrequency catheter ablation of atrial flutter after orthotopic heart transplantation: insights into the redefined critical isthmus
CLINICAL HEART TRANSPLANTATION
Radiofrequency Catheter Ablation of Atrial Flutter After Orthotopic Heart Transplantation: Insights into the Redefined Critical Isthmus Sergio L. Pinski, MD, Audrius J. Bredikis, MD, Elaine Winkel, MD, Richard G. Trohman, MD We report a case of successful radiofrequency catheter ablation of recurrent atrial flutter in a heart transplant recipient and discuss technical aspects of the procedure. A counterclockwise flutter circuit was defined during endocardial mapping of the donor atrium. Termination of atrial flutter was achieved by creating lines of radiofrequency lesions from the tricuspid ring to the suture line between donor and recipient atria. Creation of bidirectional conduction block in the tricuspid ring-suture line isthmus resulted in abolition of atrial flutter. J Heart Lung Transplant 1999;18:292–296.
A
trial arrhythmias, (including atrial fibrillation and atrial flutter), are frequent after orthotopic heart transplantation (OHT).1,2 Recent advances in mapping of cardiac activation and radiofrequency catheter ablation have defined a critical low right atrial isthmus through which typical (counterclockwise or clockwise) atrial flutter routinely traverses. The right atrial anatomy is redefined after OHT. We report a case of successful radiofrequency catheter ablation of recurrent atrial flutter in a heart transplant recipient and discuss technical aspects of the procedure.
CASE REPORT A 47-year-old male with severe heart failure and chronic atrial fibrillation secondary to idiopathic dilated cardiomyopathy underwent OHT with a biatrial anastomosis in November of 1996. His postFrom the Section of Cardiology, Rush-Presbyterian-St. Luke’s Medical Center and Rush Medical College, Chicago, Illinois. Submitted May 19, 1998; accepted August 18, 1998. Reprint requests: Sergio L. Pinski, MD, Rush-Presbyterian-St. Luke’s Medical Center, 1091 Jelke, 1750 West Harrison St, Chicago, IL 60612. Copyright © 1999 by the International Society for Heart and Lung Transplantation. 1053-2498/99/$–see front matter PII S1053-2498(98)00047-3
292
transplantation course was uneventful except for the development of hypertension. On November of 1997, at time of routine surveillance endomyocardial biopsy, he was found to be in atrial flutter with 2:1 atrioventricular block. The surface ECG demonstrated negative flutter waves in inferior leads and positive flutter waves in V1. The arrhythmia was terminated with overdrive atrial pacing. Filling pressures and cardiac output were normal. Coronary angiography and intracoronary ultrasound demonstrated myocardial bridging with mild left anterior descending spasm, moderate intimal thickening with normal endothelial responses to adenosine and nitroglycerin. The endomyocardial biopsy showed mild (ISHLT grade 1A) rejection. An echocardiogram showed normal left ventricular systolic function. He was readmitted a month later with recurrent atrial flutter. The flutter was terminated acutely with intravenous ibutilide. The patient gave informed consent for an ablation procedure.
Electrophysiological Study and Radiofrequency Ablation Technique In the post-absorptive, antiarrhythmic drug-free status, 5 multielectrode catheters were inserted from the right and left femoral veins under fluoroscopic guidance. Conscious sedation was maintained with
The Journal of Heart and Lung Transplantation Volume 18, Number 4
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FIGURE 1 Radiograph of catheter positions in the 45° left anterior oblique projection. The distal (#1) electrode of the tricuspid ring catheter is at the low lateral right atrium in a 7 o’clock position. ABL: ablation; CS: coronary sinus; Rec RA: recipient right atrium. The His bundle catheter is not shown in this picture.
midazolam and fentanyl. Three 6F catheters were positioned into the coronary sinus, in the posterior right atrium to record electrical activity from the recipient atrium, and across the tricuspid valve to record the His bundle electrogram. A 7F steerable (with 2-10-2 mm spacing), duodecapolar catheter (Daig Inc., Minnetonka, Minnesota) was deployed around the tricuspid ring, with the distal pole (#1) at the level of the low lateral right atrium, and the proximal pole (#20) in an 11 o’clock position when viewed in the left anterior oblique projection (Figure 1). Ablation was performed with a 7F quadripolar steerable thermistor catheter with a 4 mm distal tip (Blazer II, EP Technologies, Sunnyvale, California), introduced via a long, preformed intravascular sheath (Daig). Baseline recordings disclosed the recipient atrium to be in a rapid, irregular rhythm compatible with localized atrial fibrillation. The donor atrium was in sinus rhythm with normal conduction intervals (Figure 2). There was atrio-atrial dissociation. Rapid pacing of the donor atrium resulted in the induction of atrial flutter at a cycle length of 238 ms with counterclockwise activation around the tricuspid ring (Figure 3). Pacing during atrial flutter at a cycle
FIGURE 2 Baseline recordings. The recipient right
atrium (Rec RA) is in a rapid irregular rhythm, while the donor atrium is in sinus rhythm with normal intervals. HBE: His bundle electrogram; TR: bipolar electrograms recorded from the tricuspid ring, from the low lateral region (1–2) to the anteroseptal region (19 – 20). CS: bipolar coronary sinus electrograms from distal (1–2) towards its ostium (7– 8).
length of 210 ms from a 6 o’clock position on the tricuspid ring resulted in entrainment with concealed fusion and a postpacing interval equal to the
FIGURE 3 Induced atrial flutter with 2:1 block in the recipient atrium. Note the counterclockwise activation around the tricuspid ring.
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Pinski et al.
flutter cycle length, confirming the participation of the area in the flutter circuit. An anatomical approach was used for ablation of the atrial flutter circuit. The target were the isthmuses between the suture line and the tricuspid ring and coronary sinus ostium. Due to the enlarged right atrium, it was difficult to position the ablation catheter across the tricuspid ring with a standard preformed flutter sheath (SAFL, Daig). The maneuver was more easily accomplished after exchanging this sheath for a SAPD sheath. Starting at the ventricular side of the tricuspid ring at 6 o’clock position, temperature-controlled (65° C) lesions were applied sequentially for 2 minutes each while withdrawing the catheter and sheath towards the inferior vena cava. As the catheter approached the interatrial suture line, atrial fibrillation and atrial flutter were recorded simultaneously (from the recipient and donor atrium, respectively). The operator could also perceive a reproducible ridge when dragging the catheter across the suture line. Radiofrequency lesions were applied on both sides of the suture line to ensure a complete line of block. The line was purposely not continued to the inferior vena cava-right atrium junction, because we hypothesized that the interposed recipient atrium would not participate in the flutter circuit. Atrial flutter was terminated upon completion of an initial line of lesions. However, during pacing from coronary sinus, activation of the lateral right atrium resulted from two wavefronts colliding approximately at the level of electrodes 7– 8 on the tricuspid ring catheter, and indicating residual conduction through our targeted isthmus. It was felt that due to the difficulty in stabilizing the catheter to produce a continuous line of lesions, a gap may have formed. A second, more septallylocated line of radiofrequency lesions was traced from the tricuspid ring to the coronary sinus ostium and continuing to the interatrial suture line. Lesions were applied during pacing from the coronary sinus to monitor the activation sequence of the right atrium. Upon completion of this line, there was a sudden change in activation sequence indicative of conduction block through the isthmus (Figure 4). Pacing from sites medial and lateral to the isthmus confirmed that the block was bidirectional (Figure 5). Atrial flutter was no longer inducible. The patient recovered uneventfully and, after a follow-up of 6 months, remains free of recurrent atrial flutter.
The Journal of Heart and Lung Transplantation April 1999
FIGURE 4 Creation of isthmus block during
radiofrequency energy application during pacing from the coronary sinus ostium at 120 beats per minute. The second beat is the last that conducts through the isthmus. Note the collision in the lateral aspect of the tricuspid ring (TR 7– 8) of clockwise and a counterclockwise waves of activation. The conduction time to the low lateral right atrium (TR 1–2) is 84 ms. Afterwards, conduction occurs only in a counterclockwise fashion, with a conduction time to TR 1–2 of 188 ms.
DISCUSSION Atrial flutter after OHT is frequent and difficult to treat pharmacologically. Restoration and maintenance of sinus rhythm results in a more physiologic rate, prevents atrial electrical remodeling,3 decreases the risk of thromboembolism,4 and restores atrial transport function.5 The standard OHT biatrial anastomosis technique results in alterations in atrial structure and function that may favor the development of reentrant atrial arrhythmias. Brandt et al reported a 40% incidence of atrial flutter or atrial fibrillation during follow-up of heart transplant recipients with right atrial anastomosis. This incidence may be reduced to ,10% by the use of a bicaval anastomosis.6 However, the bicaval anastomosis is technically more demanding, exposes the transplanted heart to a longer ischemic time, and has not been widely adopted. The role of rejection in triggering episodes of atrial flutter in transplant patients is controversial.7 Clinical episodes may occur in patients with no (or minimal) evidence of acute rejection or sinus node dysfunction.
The Journal of Heart and Lung Transplantation Volume 18, Number 4
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FIGURE 6 Proposed low right atrial flutter isthmus in
the native (panel A) and transplanted (panel B) hearts. Idealized depiction of the right atrial endocardium is viewed anterior to posterior, through a reflected anterior wall. In the native heart the isthmus is bounded anteriorly by the tricuspid annulus (TA), and posteriorly by the inferior vena cava (IVC), eustachian ridge (ER), and coronary sinus os. In the transplanted heart, the isthmus is bounded anteriorly by the TA, and posteriorly by the suture line. Note the counterclockwise rotation of the impulse in both circuits (arrows). Other anatomical landmarks include the crista terminalis (CT), the fosa ovalis (FO), the right atrial appendage (RAA) and the superior vena cava (SVC).
FIGURE 5 Demonstration of bidirectional isthmus
block. Panel A shows activation around the tricuspid ring during pacing from the coronary sinus os (medial to the area of block). Activation proceeds with a counterclockwise pattern. The low lateral atrium is activated late. Panel B shows activation around the tricuspid ring during pacing from the low lateral right atrium (lateral to the area of block). Activation proceeds with a clockwise pattern. The proximal coronary sinus is activated late.
Typical atrial flutter is a macrorentrant arrhythmia. In the native heart, the circuit is incompletely elucidated, but the tricuspid ring constitutes the anterior barrier.8 A zone of functional block in the posterior right atrium (most likely constituted by the crista terminalis and its continuation the Eustachian ridge9) creates the posterior barrier. The upper turnaround occurs most frequently anteriorly, be-
tween the superior vena cava and the tricuspid ring.10 For the purposes of catheter ablation there is universal activation through a low right atrial isthmus defined by the orifice of the inferior vena cava, the eustachian ridge, the coronary sinus ostium, and the tricuspid annulus. Catheter ablation approaches aimed at creating a line of bidirectional block through this isthmus are curative.11 Recurrences only occur when permanent bidirectional block is not achieved. The flutter circuit in the transplanted heart is not well characterized. The suture line that connects the recipient and donor right atria could in theory create a sufficiently large anatomic obstacle around which macroreentrant excitation could be established, even in the absence of an area of slow conduction. The surgical incision could also be part of the posterior barrier of the circuit. Using entrainment mapping, Arenal et al found evidence suggesting macroreentry around the tricuspid ring in 5 transplant patients with atrial flutter.12 Activation mapping and the results of ablation in our patient suggest that the suture line constitutes the posterior barrier to the circuit (Figure 6). Li et al reported on an OHT patient who underwent successful atrial flutter ablation in the same region, but their approach was largely based on the recording of double
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Pinski et al.
The Journal of Heart and Lung Transplantation April 1999
decreased morbidity, avoidance of hospital readmissions and improved quality of life. REFERENCES
FIGURE 7 Radiograph of catheter positions in the 30° right anterior oblique projection. Note the distance from the inferior vena cava to the most ventricular aspect the isthmus where the ablation (ABL) catheter lays.
potentials and they did not attempt to define the boundaries of an ablated isthmus.13 Several technical aspects of the ablation procedure deserve comment. Due to the enlarged chamber resulting from the anastomosis of recipient and donor right atria, the distance between the inferior vena cava and the tricuspid ring was wider than usual. This could be better appreciated in the right anterior oblique projection (Figure 7), and required the use of a long reach ablation catheter and a preformed sheath not usually used for this indication. It was especially difficult to maintain a stable catheter position to deliver the most ventricular lesions in each line. We found it particularly helpful to identify these sites in sinus rhythm and to apply the lesions during pacing from the coronary sinus.14 It may therefore be optimal to perform the ablation after termination of atrial flutter. The line of lesions should be extended to the donor-recipient atrial suture line, that can be easily identified by recording dissociated electrical activity (from donor and recipient atria) and by tactile perception of a “jump” in the ablation catheter while crossing it. Radiofrequency catheter ablation is rapidly becoming the therapy of first choice for most patients with typical atrial flutter. If our results are confirmed by other investigators, early ablation in patients developing atrial flutter after OHT may result in
1. Jacquet L, Ziady G, Stein K, et al. Cardiac rhythm disturbances early after orthotopic heart transplantation: prevalence and clinical importance of the observed abnormalities. J Am Coll Cardiol 1990;16:832–7. 2. Pavri BB, O’Nunain SS, Newell JB, Ruskin JN, William G. Prevalence and prognostic significance of atrial arrhythmias after orthotopic cardiac transplantation. J Am Coll Cardiol 1995;25:1673– 80. 3. Franz MR, Karasik PL, Li C, Moubarak J, Chavez M. Electrical remodeling of the human atrium: similar effects in patients with chronic atrial fibrillation and atrial flutter. J Am Coll Cardiol 1997;30:1785–92. 4. Koller-Strametz J, Wieselthaler G, Kratochwill C, Laufer G, Pacher R, Heinz G. Thromboembolism associated with junctional escape rhythm and atrial standstill after orthotopic heart transplantation. J Heart Lung Transplant 1995;14:999–1002. 5. Jordaens L, Missault L, Germonpre´ E, et al. Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion. Am J Cardiol 1993;71:63–7. 6. Brandt M, Harringer W, Hirt SW, et al. Influence of bicaval anastomoses on late occurrence of atrial arrhythmia after heart transplantation. Ann Thorac Surg 1997;64:70 –2. 7. Heinz G, Hirschl MM, Kratochwill C, et al. Inducible atrial flutter and fibrillation after orthotopic heart transplantation. J Heart Lung Transplant 1993;12:517–21. 8. Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh MD. Activation and entrainment mapping defines the tricuspid annulus as the anterior barrier in typical atrial flutter. Circulation 1996;94:398 – 406. 9. Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter. Activation and entrainment mapping guided by intracardiac echocardiography. Circulation 1995;92:1839 – 48. 10. Shah DC, Jais P, Haissaguerre M, et al. Three-dimensional mapping of the common atrial flutter circuit in the right atrium. Circulation 1997;96:3904 –12. 11. Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996;94:407–24. 12. Arenal A, Almendral J, Munoz R, et al. Mechanism and location of atrial flutter in transplanted hearts: observations during transient entrainment from distant sites. J Am Coll Cardiol 1997;30:539 – 46. 13. Li YG, Gronefeld G, Hohnloser SH. Radiofrequency catheter ablation of atrial flutter after orthotopic heart transplantation. J Cardiovasc Electrophysiol 1996;7:1086 –90. 14. Poty H, Saoudi N, Nair M, Anselme F, Letac B. 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.
Radiofrequency Catheter Ablation of Atrial Flutter After Orthotopic Heart Transplantation: Insights into the Redefined Critical Isthmus Sergio L. Pinski, MD, Audrius J. Bredikis, MD, Elaine Winkel, MD, Richard G. Trohman, MD We report a case of successful radiofrequency catheter ablation of recurrent atrial flutter in a heart transplant recipient and discuss technical aspects of the procedure. A counterclockwise flutter circuit was defined during endocardial mapping of the donor atrium. Termination of atrial flutter was achieved by creating lines of radiofrequency lesions from the tricuspid ring to the suture line between donor and recipient atria. Creation of bidirectional conduction block in the tricuspid ring-suture line isthmus resulted in abolition of atrial flutter. J Heart Lung Transplant 1999;18:292–296.
A
trial arrhythmias, (including atrial fibrillation and atrial flutter), are frequent after orthotopic heart transplantation (OHT).1,2 Recent advances in mapping of cardiac activation and radiofrequency catheter ablation have defined a critical low right atrial isthmus through which typical (counterclockwise or clockwise) atrial flutter routinely traverses. The right atrial anatomy is redefined after OHT. We report a case of successful radiofrequency catheter ablation of recurrent atrial flutter in a heart transplant recipient and discuss technical aspects of the procedure.
CASE REPORT A 47-year-old male with severe heart failure and chronic atrial fibrillation secondary to idiopathic dilated cardiomyopathy underwent OHT with a biatrial anastomosis in November of 1996. His postFrom the Section of Cardiology, Rush-Presbyterian-St. Luke’s Medical Center and Rush Medical College, Chicago, Illinois. Submitted May 19, 1998; accepted August 18, 1998. Reprint requests: Sergio L. Pinski, MD, Rush-Presbyterian-St. Luke’s Medical Center, 1091 Jelke, 1750 West Harrison St, Chicago, IL 60612. Copyright © 1999 by the International Society for Heart and Lung Transplantation. 1053-2498/99/$–see front matter PII S1053-2498(98)00047-3
292
transplantation course was uneventful except for the development of hypertension. On November of 1997, at time of routine surveillance endomyocardial biopsy, he was found to be in atrial flutter with 2:1 atrioventricular block. The surface ECG demonstrated negative flutter waves in inferior leads and positive flutter waves in V1. The arrhythmia was terminated with overdrive atrial pacing. Filling pressures and cardiac output were normal. Coronary angiography and intracoronary ultrasound demonstrated myocardial bridging with mild left anterior descending spasm, moderate intimal thickening with normal endothelial responses to adenosine and nitroglycerin. The endomyocardial biopsy showed mild (ISHLT grade 1A) rejection. An echocardiogram showed normal left ventricular systolic function. He was readmitted a month later with recurrent atrial flutter. The flutter was terminated acutely with intravenous ibutilide. The patient gave informed consent for an ablation procedure.
Electrophysiological Study and Radiofrequency Ablation Technique In the post-absorptive, antiarrhythmic drug-free status, 5 multielectrode catheters were inserted from the right and left femoral veins under fluoroscopic guidance. Conscious sedation was maintained with
The Journal of Heart and Lung Transplantation Volume 18, Number 4
Pinski et al.
293
FIGURE 1 Radiograph of catheter positions in the 45° left anterior oblique projection. The distal (#1) electrode of the tricuspid ring catheter is at the low lateral right atrium in a 7 o’clock position. ABL: ablation; CS: coronary sinus; Rec RA: recipient right atrium. The His bundle catheter is not shown in this picture.
midazolam and fentanyl. Three 6F catheters were positioned into the coronary sinus, in the posterior right atrium to record electrical activity from the recipient atrium, and across the tricuspid valve to record the His bundle electrogram. A 7F steerable (with 2-10-2 mm spacing), duodecapolar catheter (Daig Inc., Minnetonka, Minnesota) was deployed around the tricuspid ring, with the distal pole (#1) at the level of the low lateral right atrium, and the proximal pole (#20) in an 11 o’clock position when viewed in the left anterior oblique projection (Figure 1). Ablation was performed with a 7F quadripolar steerable thermistor catheter with a 4 mm distal tip (Blazer II, EP Technologies, Sunnyvale, California), introduced via a long, preformed intravascular sheath (Daig). Baseline recordings disclosed the recipient atrium to be in a rapid, irregular rhythm compatible with localized atrial fibrillation. The donor atrium was in sinus rhythm with normal conduction intervals (Figure 2). There was atrio-atrial dissociation. Rapid pacing of the donor atrium resulted in the induction of atrial flutter at a cycle length of 238 ms with counterclockwise activation around the tricuspid ring (Figure 3). Pacing during atrial flutter at a cycle
FIGURE 2 Baseline recordings. The recipient right
atrium (Rec RA) is in a rapid irregular rhythm, while the donor atrium is in sinus rhythm with normal intervals. HBE: His bundle electrogram; TR: bipolar electrograms recorded from the tricuspid ring, from the low lateral region (1–2) to the anteroseptal region (19 – 20). CS: bipolar coronary sinus electrograms from distal (1–2) towards its ostium (7– 8).
length of 210 ms from a 6 o’clock position on the tricuspid ring resulted in entrainment with concealed fusion and a postpacing interval equal to the
FIGURE 3 Induced atrial flutter with 2:1 block in the recipient atrium. Note the counterclockwise activation around the tricuspid ring.
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Pinski et al.
flutter cycle length, confirming the participation of the area in the flutter circuit. An anatomical approach was used for ablation of the atrial flutter circuit. The target were the isthmuses between the suture line and the tricuspid ring and coronary sinus ostium. Due to the enlarged right atrium, it was difficult to position the ablation catheter across the tricuspid ring with a standard preformed flutter sheath (SAFL, Daig). The maneuver was more easily accomplished after exchanging this sheath for a SAPD sheath. Starting at the ventricular side of the tricuspid ring at 6 o’clock position, temperature-controlled (65° C) lesions were applied sequentially for 2 minutes each while withdrawing the catheter and sheath towards the inferior vena cava. As the catheter approached the interatrial suture line, atrial fibrillation and atrial flutter were recorded simultaneously (from the recipient and donor atrium, respectively). The operator could also perceive a reproducible ridge when dragging the catheter across the suture line. Radiofrequency lesions were applied on both sides of the suture line to ensure a complete line of block. The line was purposely not continued to the inferior vena cava-right atrium junction, because we hypothesized that the interposed recipient atrium would not participate in the flutter circuit. Atrial flutter was terminated upon completion of an initial line of lesions. However, during pacing from coronary sinus, activation of the lateral right atrium resulted from two wavefronts colliding approximately at the level of electrodes 7– 8 on the tricuspid ring catheter, and indicating residual conduction through our targeted isthmus. It was felt that due to the difficulty in stabilizing the catheter to produce a continuous line of lesions, a gap may have formed. A second, more septallylocated line of radiofrequency lesions was traced from the tricuspid ring to the coronary sinus ostium and continuing to the interatrial suture line. Lesions were applied during pacing from the coronary sinus to monitor the activation sequence of the right atrium. Upon completion of this line, there was a sudden change in activation sequence indicative of conduction block through the isthmus (Figure 4). Pacing from sites medial and lateral to the isthmus confirmed that the block was bidirectional (Figure 5). Atrial flutter was no longer inducible. The patient recovered uneventfully and, after a follow-up of 6 months, remains free of recurrent atrial flutter.
The Journal of Heart and Lung Transplantation April 1999
FIGURE 4 Creation of isthmus block during
radiofrequency energy application during pacing from the coronary sinus ostium at 120 beats per minute. The second beat is the last that conducts through the isthmus. Note the collision in the lateral aspect of the tricuspid ring (TR 7– 8) of clockwise and a counterclockwise waves of activation. The conduction time to the low lateral right atrium (TR 1–2) is 84 ms. Afterwards, conduction occurs only in a counterclockwise fashion, with a conduction time to TR 1–2 of 188 ms.
DISCUSSION Atrial flutter after OHT is frequent and difficult to treat pharmacologically. Restoration and maintenance of sinus rhythm results in a more physiologic rate, prevents atrial electrical remodeling,3 decreases the risk of thromboembolism,4 and restores atrial transport function.5 The standard OHT biatrial anastomosis technique results in alterations in atrial structure and function that may favor the development of reentrant atrial arrhythmias. Brandt et al reported a 40% incidence of atrial flutter or atrial fibrillation during follow-up of heart transplant recipients with right atrial anastomosis. This incidence may be reduced to ,10% by the use of a bicaval anastomosis.6 However, the bicaval anastomosis is technically more demanding, exposes the transplanted heart to a longer ischemic time, and has not been widely adopted. The role of rejection in triggering episodes of atrial flutter in transplant patients is controversial.7 Clinical episodes may occur in patients with no (or minimal) evidence of acute rejection or sinus node dysfunction.
The Journal of Heart and Lung Transplantation Volume 18, Number 4
Pinski et al.
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FIGURE 6 Proposed low right atrial flutter isthmus in
the native (panel A) and transplanted (panel B) hearts. Idealized depiction of the right atrial endocardium is viewed anterior to posterior, through a reflected anterior wall. In the native heart the isthmus is bounded anteriorly by the tricuspid annulus (TA), and posteriorly by the inferior vena cava (IVC), eustachian ridge (ER), and coronary sinus os. In the transplanted heart, the isthmus is bounded anteriorly by the TA, and posteriorly by the suture line. Note the counterclockwise rotation of the impulse in both circuits (arrows). Other anatomical landmarks include the crista terminalis (CT), the fosa ovalis (FO), the right atrial appendage (RAA) and the superior vena cava (SVC).
FIGURE 5 Demonstration of bidirectional isthmus
block. Panel A shows activation around the tricuspid ring during pacing from the coronary sinus os (medial to the area of block). Activation proceeds with a counterclockwise pattern. The low lateral atrium is activated late. Panel B shows activation around the tricuspid ring during pacing from the low lateral right atrium (lateral to the area of block). Activation proceeds with a clockwise pattern. The proximal coronary sinus is activated late.
Typical atrial flutter is a macrorentrant arrhythmia. In the native heart, the circuit is incompletely elucidated, but the tricuspid ring constitutes the anterior barrier.8 A zone of functional block in the posterior right atrium (most likely constituted by the crista terminalis and its continuation the Eustachian ridge9) creates the posterior barrier. The upper turnaround occurs most frequently anteriorly, be-
tween the superior vena cava and the tricuspid ring.10 For the purposes of catheter ablation there is universal activation through a low right atrial isthmus defined by the orifice of the inferior vena cava, the eustachian ridge, the coronary sinus ostium, and the tricuspid annulus. Catheter ablation approaches aimed at creating a line of bidirectional block through this isthmus are curative.11 Recurrences only occur when permanent bidirectional block is not achieved. The flutter circuit in the transplanted heart is not well characterized. The suture line that connects the recipient and donor right atria could in theory create a sufficiently large anatomic obstacle around which macroreentrant excitation could be established, even in the absence of an area of slow conduction. The surgical incision could also be part of the posterior barrier of the circuit. Using entrainment mapping, Arenal et al found evidence suggesting macroreentry around the tricuspid ring in 5 transplant patients with atrial flutter.12 Activation mapping and the results of ablation in our patient suggest that the suture line constitutes the posterior barrier to the circuit (Figure 6). Li et al reported on an OHT patient who underwent successful atrial flutter ablation in the same region, but their approach was largely based on the recording of double
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Pinski et al.
The Journal of Heart and Lung Transplantation April 1999
decreased morbidity, avoidance of hospital readmissions and improved quality of life. REFERENCES
FIGURE 7 Radiograph of catheter positions in the 30° right anterior oblique projection. Note the distance from the inferior vena cava to the most ventricular aspect the isthmus where the ablation (ABL) catheter lays.
potentials and they did not attempt to define the boundaries of an ablated isthmus.13 Several technical aspects of the ablation procedure deserve comment. Due to the enlarged chamber resulting from the anastomosis of recipient and donor right atria, the distance between the inferior vena cava and the tricuspid ring was wider than usual. This could be better appreciated in the right anterior oblique projection (Figure 7), and required the use of a long reach ablation catheter and a preformed sheath not usually used for this indication. It was especially difficult to maintain a stable catheter position to deliver the most ventricular lesions in each line. We found it particularly helpful to identify these sites in sinus rhythm and to apply the lesions during pacing from the coronary sinus.14 It may therefore be optimal to perform the ablation after termination of atrial flutter. The line of lesions should be extended to the donor-recipient atrial suture line, that can be easily identified by recording dissociated electrical activity (from donor and recipient atria) and by tactile perception of a “jump” in the ablation catheter while crossing it. Radiofrequency catheter ablation is rapidly becoming the therapy of first choice for most patients with typical atrial flutter. If our results are confirmed by other investigators, early ablation in patients developing atrial flutter after OHT may result in
1. Jacquet L, Ziady G, Stein K, et al. Cardiac rhythm disturbances early after orthotopic heart transplantation: prevalence and clinical importance of the observed abnormalities. J Am Coll Cardiol 1990;16:832–7. 2. Pavri BB, O’Nunain SS, Newell JB, Ruskin JN, William G. Prevalence and prognostic significance of atrial arrhythmias after orthotopic cardiac transplantation. J Am Coll Cardiol 1995;25:1673– 80. 3. Franz MR, Karasik PL, Li C, Moubarak J, Chavez M. Electrical remodeling of the human atrium: similar effects in patients with chronic atrial fibrillation and atrial flutter. J Am Coll Cardiol 1997;30:1785–92. 4. Koller-Strametz J, Wieselthaler G, Kratochwill C, Laufer G, Pacher R, Heinz G. Thromboembolism associated with junctional escape rhythm and atrial standstill after orthotopic heart transplantation. J Heart Lung Transplant 1995;14:999–1002. 5. Jordaens L, Missault L, Germonpre´ E, et al. Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion. Am J Cardiol 1993;71:63–7. 6. Brandt M, Harringer W, Hirt SW, et al. Influence of bicaval anastomoses on late occurrence of atrial arrhythmia after heart transplantation. Ann Thorac Surg 1997;64:70 –2. 7. Heinz G, Hirschl MM, Kratochwill C, et al. Inducible atrial flutter and fibrillation after orthotopic heart transplantation. J Heart Lung Transplant 1993;12:517–21. 8. Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh MD. Activation and entrainment mapping defines the tricuspid annulus as the anterior barrier in typical atrial flutter. Circulation 1996;94:398 – 406. 9. Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter. Activation and entrainment mapping guided by intracardiac echocardiography. Circulation 1995;92:1839 – 48. 10. Shah DC, Jais P, Haissaguerre M, et al. Three-dimensional mapping of the common atrial flutter circuit in the right atrium. Circulation 1997;96:3904 –12. 11. Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996;94:407–24. 12. Arenal A, Almendral J, Munoz R, et al. Mechanism and location of atrial flutter in transplanted hearts: observations during transient entrainment from distant sites. J Am Coll Cardiol 1997;30:539 – 46. 13. Li YG, Gronefeld G, Hohnloser SH. Radiofrequency catheter ablation of atrial flutter after orthotopic heart transplantation. J Cardiovasc Electrophysiol 1996;7:1086 –90. 14. Poty H, Saoudi N, Nair M, Anselme F, Letac B. 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.