Journal of Veterinary Cardiology (2014) 16, 9e17
www.elsevier.com/locate/jvc
Radiofrequency catheter ablation of atypical atrial flutter in dogs Roberto A. Santilli, Dr. Med. Vet., PhD a,*, Lucia Ramera, Dr. Med. Vet. a, Manuela Perego, Dr. Med. Vet. a, Paolo Moretti, MD b, Giammario Spadacini, MD b a b
Clinica Veterinaria Malpensa, Viale Marconi, 27, 21017 Samarate Varese, Italy Humanitas Mater Domini, Via Gerenzano, 2, 21053 Castellanza Varese, Italy
Received 23 April 2013; received in revised form 15 October 2013; accepted 21 October 2013
KEYWORDS Electrophysiology; Supraventricular tachycardia; Arrhythmias
Abstract Five dogs were presented to our institution for fatigue caused by an incessant supraventricular tachycardia. In all dogs, an ECG on admission showed a narrow QRS complex tachycardia with a median ventricular cycle length of 220 ms (range 180e360 ms), and a positive atrial depolarization identifiable in the ST segment following the previous QRS complex. There was a 1:1 atrioventricular conduction ratio in all but one dog, which presented with 2:1 atrioventricular block. Electrophysiologic studies identified the underlying arrhythmogenic mechanism as a right atrial macro-reentrant tachycardia with two distinct isthmic areas: right septal (RS) in three dogs and right atrial free wall (RAFW) in two dogs. Linear radiofrequency catheter ablation was performed during tachycardia in all dogs at the identified isthmic area, which acutely blocked the macroreentrant circuit. At 18-month follow-up, 3 dogs (1 with RAFW isthmus and 2 with RS isthmus) showed no recurrence of the arrhythmia on Holter monitoring. One dog with RS isthmus showed recurrence of the supraventricular tachycardia 15 days post-ablation, and 1 dog with RAFW isthmus presented with persistent atrial fibrillation 2 months post-ablation. ª 2013 Elsevier B.V. All rights reserved.
* Corresponding author. E-mail addresses: [email protected], rasantil@ tin.it (R.A. Santilli).
Five dogs (3 Bernese dogs, 1 dogue de Bordeaux and 1 Irish setter), 3 females and 2 males, with a median age of 90 months (range 9e132 months) and a median body weight of 48 kg (range 32e59 kg) (Table 1) were presented to our
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Abbreviations AFL AV CS CTI HRA LRA LLR MRA MRT RA RAFW RS SVT ULR
atrial flutter atrioventricular coronary sinus cavo-tricuspid isthmus high right atrium low right atrium lower loop reentry middle right atrium macroreentrant tachycardia right atrium right atrial free wall right septal supraventricular tachycardia upper loop reentry
institution for incessant supraventricular tachycardia (SVT), profound weakness and dysorexia of 5e8-day duration. Three out of 5 dogs were treated with sotalol (2 mg/kg PO q12 h) with no response to medical treatment. At admission all dogs were depressed, showed mild weight loss, rapid heart rate and had pulse deficits. Thoracic radiographs displayed cardiomegaly in 2 out of 5 dogs with no signs of congestion. Echocardiography revealed reduced left ventricular volume with Table 1
pseudohypertrophy and mildly depressed systolic function in 2 out of 3 Bernese dogs and left atrial and ventricular dilation with volume overload and severely depressed systolic function in the remaining dogs (Table 1).1,2 In all dogs, 12-lead ECG showed a narrow QRS complex tachycardia (median QRS duration 40 ms, range 40e60 ms) with a median ventricular cycle length of 220 ms (range 180e360 ms). Atrial depolarization was visible in the preceding ST segment as a positive wave in the inferior leads (II, III, aVF) with a median voltage of 0.25 mV (range 0.15e0.4 mV), a median duration of 40 ms (range 35e60 ms) and a median axis on the frontal plane of 74 (range 63e90 ) (Table 1). In all dogs an isoelectric line was present between consecutive atrial depolarizations. The atrioventricular (AV) conduction ratio was 1:1 in all but one dog in which it was 2:1 (Fig. 1). An electrophysiologic (EP) study was performed in all dogs to characterize the electrogenic mechanism and ablate the arrhythmic substrate.
Electrophysiology studies and ablation procedures The electrophysiology studies were performed under general anesthesia with dogs prepared as
Signalment, echocardiographic and electrocardiographic findings in 5 dogs with atypical atrial flutter.
Signalment Breed Gender Age (months) Body weight (Kg) Echocardiography LVEDD (mm) LVESD (mm) 2D-EF (%) LA/Ao Surface ECG QRS duration (ms) Atrial CL (ms) Ventricular CL (ms) F wave amplitude (mV) F wave duration (ms) F wave axis (degree) AV conduction ratio Intracardiac ECG Atrial CL (ms) Ventricular CL (ms) AV conduction ratio AFL Isthmus
Dog A
Dog B
Dog C
Dog D
Dog E
Bernese Female 60 48
Bernese Female 90 59
Bernese Female 96 51
Dogue de Bordeaux Male 9 46
Irish setter Male 132 32
36.88 23.09 45.66 1.57
42.75 25.36 38.52 1.65
34.09 21.04 51.82 1.56
54.56 34.02 30.72 3.2
46.63 32.95 25.94 1.88
50 220 220 0.2 40 63 1:1
40 200 200 0.25 60 74 1:1
40 180 180 0.4 60 90 1:1
60 180 360 0.15 35 84 2:1
40 220 220 0.25 40 72 1:1
230 230 1:1 Right septal
220 220 1:1 Right septal
240 240 1:1 Right septal
180 360 2:1 RA free wall
300 300 1:1 RA free wall
LVEDD, left ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; EF, ejection fraction; LA, left atrium; Ao, aorta; CL, cycle lenght; AV, atrioventricular; AFL, atrial flutter; RA, right atrial.
Atypical atrial flutter in dogs
11
Figure 1 Twelve-lead surface ECG in 5 dogs with right atrial macroreentrant tachycardia (A, B, C right septal atrial flutter; D, E right atrial free wall atrial flutter). Notice in all dogs narrow QRS complex (median duration 40 ms, range 40e60 ms), a median ventricular cycle length of 220 ms (range 180e340 ms), a positive atrial activation (F) in the previous ST segment in the inferior leads (II, III, aVF) with a median voltage of 0.25 mV (range 0.15e0.4 mV), a median duration of 40 ms (range 35e60 ms) and an average axis on the frontal plane of 74 (range 63e84 ). In all cases isoelectric line was present between consecutive atrial depolarization. In dogs A, B, C, E, 1:1 AV conduction was present; in dog D, 2:1 AV conduction can be noted. In this latter case, the F wave located in the previous ST segment conducts to the ventricles. The location of the F waves was confirmed by atrial activation mapping. (Paper speed 50 mm/s e amplitude 5 mm/1 mV).
previously reported.3e5 Three vascular accesses were obtained using a modified Seldinger technique in each dog: one in the right jugular vein and two in the right femoral vein. A decapolar catheterc was advanced along the right jugular vein into the coronary sinus (CS).3,4 A second decapolar catheterc was inserted into the right femoral vein and positioned along the right atrial (RA) lateral wall to record potentials from the antero-lateral aspect of the crista terminalis (HRA) with the proximal pair of electrodes, the mid-lateral right atrial (MRA) potentials with the middle pair and the low posterior-lateral right atrial (LRA) potentials with the distal pair.5,6 Finally, a 7-Fr, 4-mm ablation catheterd with steerable tip was inserted along the right femoral vein and positioned alternatively at the His bundle, right ventricle and isthmic areas to map local electrograms and perform electrical stimulations.5,6 At baseline all dogs showed incessant tachycardia with a median atrial cycle length of 230 ms (range 180e300 ms) and a ventricular cycle length of 240 ms (range 220e360 ms) (Table 1). All dogs had a 1:1 AV conduction ratio, except one, which c
Polaris X, 7 Fr, Boston Scientfic Corp., Genova, Italy. Std CrV Blazer II HTD, 4 mm, 7 Fr; Boston Scientific Corp., Genova, Italy. d
presented with 2:1 AV block. Intracardiac atrial depolarization potentials coincided in each patient with the positive atrial waves superimposed to the preceding ST segment on the surface ECG. In all dogs, a diagnosis of macroreentrant right atrial tachycardia was made based on the following: 1) atrial activation within the RA for the tachycardia cycle length, 2) a return cycle after entrainment less than 30 ms longer than the tachycardia cycle length identified the pacing site as a critical component of that tachycardia circuit, and 3) entrainment in 2 opposite quadrants within the RA, each with return cycle lengths within 20 ms of the tachycardia cycle length.7 To evaluate the location of critical isthmic areas, potential targets of ablation, initially the cavo-tricuspid isthmus (CTI) was mapped during LRA pacing paying attention to the presence of concealed entrainment. The maneuver revealed overt fusion with acceleration of the tachycardia cycle length and the pacing cycle length, and changes in both the sequence of atrial activation and the morphology of the surface and endocardial electrograms. Once CTI-dependent atrial flutter (AF) was ruled out, different tests were performed to demonstrate a critical isthmus, its extent, the presence of bystander sites and possibly barriers bordering the isthmus.6e8 In
12 addition to the presence of mid-diastolic potentials, these tests included concealed entrainment with a post-pacing interval within 30 ms longer than the tachycardia cycle length, stimulus timed within 30 ms of activation time; the presence of double potentials was used to demonstrate either functional or fixed lines of block and the presence of electrically silent area.6e8 In the Bernese dogs the critical isthmus was localized in the middle portion of the right interatrial septum with an inferior-to-superior activation of the area and a counterclockwise activation pattern (left anterior 30 fluoroscopic view) (Fig. 2).5 In the other 2 dogs the critical isthmus was localized in the midlateral right atrial free wall (RAFW), an area characterized by fractionated electrograms with an inferior-to-superior activation of the area itself and a later activation of the CS (Fig. 3). Split potentials were recorded in 3 out of 5 dogs along the crista terminalis but none of them were middiastolic or close to the area of concealed entrainment. In all dogs a diagnosis of atypical right AF was reached. Radiofrequency catheter ablation was performed at controlled temperature with a thermo-
R.A. Santilli et al. coupled steerable 7-Fr, 4-mm catheterd at the right septal (RS) and RAFW isthmus. Maximal catheter tip temperature and power output were set respectively at 65 C and 75 W. Linear lesions of the isthmus areas were obtained with several applications of 45 s duration with no recurrence of the macroreentrant tachycardia (MRT) with programmed atrial pacing noticed within the following 20 min6 Isthmic ablation was performed during tachycardia in all dogs with an electro-anatomic approach aiming at either mid- or late-diastolic atrial potentials, concealed entrainment and eventual fractionated electrograms. Radiofrequency energy was delivered during tachycardia twice on average (range 1e4) in each dog (45.2 W, 62.4 C, 113.2 U) at the area of the right interatrial septum for the length of the dipole in the Bernese dogs and sequentially from the caudal vena cava ostium superiorly to the midlateral RAFW fractionated electrograms in the remaining dogs. Acute termination of the macroreentrant atrial tachycardia occurred within an average of 17.2 s (range 10e25 s) in each dog and persisted until the end of the procedure (Fig. 4). Radiofrequency ablation was considered successful in
Figure 2 Surface and intracardiac ECG obtained in one of the Bernese dogs during endocardial mapping and concealed entrainment of a right septal atrial flutter. Recording displayed includes lead I, II, III, aVF, V1, V6 of the surface ECG and intracardiac recording from the high right atrial wall, through the medium to the low posterior right atrial wall (HRA, MRA, LRA), from the distal to the proximal portions of the right septal isthmic area (ABLd and ABLp) and from the distal to the proximal portion of the coronary sinus (CSd and CSp). Note the counterclockwise activation pattern moving from the isthmic area (ABLd), where mid-diastolic electrograms were recorded, to the HRA, MRA, LRA and the CSd. The atrial cycle length during atrial flutter was 237 ms, an atrial extrastimulus was introduced from the ABLd and accelerated the tachycardia cycle length (215 ms), with the same sequence of activation on intracardiac recording and no change of atrial morphology on surface ECG. After the pacing tachycardia cycle length returned to its original value. (Paper speed 300 mm/s e amplitude 22.8 mV/cm).
Atypical atrial flutter in dogs
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Figure 3 Surface and intracardiac ECG obtained in the Irish Setter during endocardial mapping and concealed entrainment of a right atrial free wall atrial flutter. Recording displayed includes lead I, II, III, aVF, V1, V6 of the surface ECG and intracardiac recording from the high right atrial wall, through the medium to the low posterior right atrial wall (HRA, MRA, LRA), from the distal to the proximal portions of the right atrial free wall isthmic area (ABLd and ABLp) and from the distal to the proximal portion of the coronary sinus (CSd and CSp). Note the inferior-tosuperior activation of the right atrial free wall moving from the isthmic area (ABLd), where mid-diastolic, delayed and fractioned electrograms were recorded to LRA, MRA, HRA and CSd. The atrial cycle length during atrial flutter was 167 ms with a 2:1 conduction ratio, an atrial extrastimulus was introduced from the ABLd and accelerated the tachycardia cycle length (145 ms), with the same sequence of activation on intracardiac recording and no change of atrial morphology on surface ECG. After the pacing tachycardia cycle length returned to its original value. (Paper speed 300 mm/s e amplitude 22.8 mV/cm).
case of termination and subsequent noninducibility of the arrhythmia with programmed atrial stimulation.
congestive heart failure after 12 months and were treated with furosemide (2 mg/kg PO q12 h), pimobendan (0.25 mg/kg PO q12 h) and enalapril (0.5 mg/kg PO q12 h).
Follow-up Discussion An ECG 15 days after the procedure and Holter monitoring at 2, 6 and 18-month intervals were performed in all dogs. At 18-month follow-up, 3 dogs (1 with RAFW isthmus and 2 with RS isthmus) showed no recurrence of the arrhythmia on Holter monitoring. One dog with RS isthmus showed recurrence of the SVT 15 days post-ablation, and one with RAFW isthmus presented with persistent atrial fibrillation 2 months post-ablation. The dog with recurrence of the AFL is now partially controlled with diltiazem extended release (3 mg/kg PO q12 h) and presented a progressive loss of systolic function, while the dog with persistent atrial fibrillation is well controlled with a combination of digoxin and diltiazem extended release (0.0055 mg/kg PO q12 h and 3 mg/kg PO q12 h, respectively) and no further deterioration of left ventricular systolic function. Both dogs developed
In the present study we were able to demonstrate the existence of atypical AFL in dogs with 2 different critical isthmus areas located over the RAFW and the RS, and show that definitive ablation of the circuit is possible in most cases. The term AFL has been used in human medicine to define an electrocardiographic pattern of regular tachycardia with rate >240 bpm, atrial depolarizations with a classical “saw tooth” pattern in leads II, III and/or aVF and absence of an isoelectric baseline between consecutive atrial waves in at least 1 lead.9 Further studies pointed out that neither rate nor lack of isoelectric baseline should be considered specific of any tachycardia mechanism,10e12 and that the sequence of left atrial activation and interatrial connections play a major role in F wave morphology during flutter.13,14
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R.A. Santilli et al.
Figure 4 Surface and intracardiac ECG obtained in one of the Bernese dogs during radiofrequency catheter ablation of a right septal atrial flutter. Recording displayed includes lead I, II, III, aVR, aVL, aVF, V1, V6 of the surface ECG and intracardiac recording from the high right atrial wall, through the medium to the low posterior right atrial wall (HRA, MRA, LRA), from the distal to the proximal portions of the right septal isthmic area (ABLd and ABLp) and from the distal to the proximal portion of the coronary sinus (CSd and CSp). A linear lesion with the length of the dipole was performed along the isthmic area during tachycardia and 20 s after the beginning of the second radiofrequency application (arrow) the tachycardia stopped and sinus rhythm resumed. (Paper speed 50 mm/s e amplitude 22.8 mV/cm).
For these reasons in 2001 the ESC/NASPE expert consensus proposed a new classification of AFLs and regular atrial tachycardias based on mechanism of arrhythmia and isthmus dependence rather than surface ECG features. In this classification the term MRT refers to all reentrant tachycardias with a large central obstacle, including typical AFL and other macroreentrant circuits in either the right or left atrium.11 In more detail, AFL are classified as typical, when CTI-dependent, regardless of the ECG pattern, and atypical when a non-CTIdependent circuit is documented. Typical AFLs have been classified, based on the direction of atrial activation within their circuit, as typical and reverse typical. During typical AFL the wavefront travels counterclockwise around the tricuspid valve annulus (90% of patients), in the LAO fluoroscopic view, whereas during reverse typical AFL it travels clockwise (10% of cases).11e16 Three unusual forms of typical CTI-dependent AFLs have also been reported in human: lower loop reentry (LLR), double wave reentry, and sub-eustachian
isthmus short circuit.17e21 In LLR an early breakthrough over the caudal portion of the crista terminalis is present, with simultaneous conduction along the lateral wall and the septum as well conduction over the CTI toward the ostium of the CS.18e21 Double wave reentry is a transient arrhythmia characterized by two wavefronts within the flutter circuit, usually present in patients with CTI-dependent AFL, and that rapidly reverts to single wave typical AFL.19,20 This circuit has been documented in 25%e50% of human patients with typical AFL and is characterized by early activation of the region of the coronary sinus with a breakthrough over the eustachian ridge, posterior to the ostium of the coronary sinus.22 Both typical and typical reverse CTI-dependent AFLs, confirmed by detailed endocardial mapping, have been reported in the dog.6 The term atypical AFL is used to describe non-CTIdependent MRT, usually more rapid and irregular, with variable flutter wave morphology, and often proven to be prefibrillatory.11,17,21,23e31 In humans
Atypical atrial flutter in dogs these types of MRT can be secondary to surgical lesions from previous atriotomy, septal prostethic patch, suture line or secondary to radiofrequency catheter ablation (right atrial scar related MRT or lesion MRT and pulmonary vein-related AFL).17,21,23,25,26,29,30 Alternatively they can be supported by electrically silent areas of atrial myocardium, presumably due to fibrosis or infiltration, located either in the right or left atrium.17,21,24e28,30,31 Atypical left AFL circuits involve circulation of a wavefront around unexcitable areas over the posterior left atrial wall, around the pulmonary veins, the mitral annulus (left atrial MRTs),10,11,25,26,30 or over the left atrial septum (left septal AFL).27,30 The prevalence of non scar-related atypical right AFLs is approximately 8% and this type of arrhythmia includes upper loop reentry tachycardia (ULR), RAFW atypical AFL, and unstable complex circuits of the RAFW.17,21,24e26,28,30,31 The ULR affects the upper portion of the right atrium with a clockwise circuit breaking over the lateral or anterolateral annulus with impulse collision in the isthmus, which can be identified between the superior vena cava and the fossa ovalis.17,25,26,30 In RAFW atypical AFL the impulse rotates around low-voltage areas inducing conduction delay frequently localized in the antero-infero-lateral aspect of the right atrial free wall.17,24e26,28,30,31 A final variant of atypical AFL was described by Wells et al. based on flutter rate, stable intracardiac electrogram and morphology, and the possibility of transient entrainment and labeled as type II.32 According to this classification typical or type I AFL display an excitable gap, while atypical or type II AFL present shorter cycle length with no gap. Type II AFL cannot be entrained, are transient and common under vagal stimulation, transitioning spontaneously to baseline flutter or fibrillation.33 Detailed endocardial mapping and entrainment response in the dogs herein reported showed two right atrial macro-reentrant circuits around electrically silent areas with two critical isthmus areas different from the CTI and located over the RAFW in 2 dogs, and the right atrial septum in 3 dogs, similar to what has been reported in human patients.17,24e28,30,31 The right posterior free wall is a well-recognized arrhythmogenic substrate in patients with AFL since it includes a line of transverse conduction block adjacent to the crista terminalis. In patients with AFL the area of the crista terminalis is usually larger and the effective refractory period of this region is longer and site-specific compared to normal patients.34 Activation mapping of the RAFW in the dogs described in our study demonstrated the presence of an electrically silent area characterized by low
15 amplitude and fractionated and/or delayed components as described in human patients without a history of atriotomy as well as in sterile pericarditis and models of atrial enlargement.24,28,31,35e37 In human patients, RAFW atypical AFL is commonly associated with sinus node dysfunction since the electrically silent areas involve large portions of the atrial wall including the sinus node (local right atrial cardiomyopathy).28 None of the dogs with RAFW atypical AFL herein reported showed evidence of sinus node dysfunction. The right atrial septum is another arrhythmogenic site in human patients with AFL since it displays a lower mean bipolar voltage and both longitudinal and transverse conduction velocity delays compared to normal patients.38 The atrial septum has a bilaminate muscle structure constituting the thin membranous primary atrial septum that may contribute to the protection and maintenance of septal flutters.27 Concealed entrainment techniques are widely used to localize the critical isthmus both in human and in dogs with CTI-dependent AFL.6e8,16 Atypical MRT circuits are more difficult to map since there is not a fixed location for the circuit or its critical isthmus.17,24e26,30,31 In our case series the AFL circuits were stable and concealed entrainment could be achieved at the RA midseptal area in 3 dogs and along the right atrial free wall in 2 dogs. Post-pacing interval and stimulus time measurements permitted us to exclude bystander sites.8 Atypical AFLs have been associated with different structural heart diseases such as coronary artery disease, idiopathic dilated cardiomyopathy and valvular heart disease, but have also been mapped in a small number of human patients with no underlying heart disease.24,31 Conversely, in the case of left septal atrial flutter, 65% of the patients showed no concurrent heart disease.27 Similarly in our dogs, right septal AFLs were not associated with cardiac disease, while RAFW AFLs were associated with chamber dilation and ventricular dysfunction. In these cases, although tachycardia-induced cardiomyopathy must be considered, the etiology of the cardiac disease could not be completely elucidated. The surface electrocardiogram may be used to predict the type of AFL in human patients.39,40 Typical CTI-dependent AFL, double wave reentry and ULR are characterized by negative F waves in the inferior leads and positive in V1, while typical reverse AFL shows positive F waves in the inferior leads. Atypical AFL presents a highly variable flutter wave morphology and may appear as typical reverse AFL, resembling typical or focal AFL.39 A broad-based upright V1 is highly predictive of a left-sided flutter, while when V1 has an initial
16 isoelectric or inverted component followed by an upright component, this is consistent with right flutter.39 Unfortunately, considering the variability of chest conformation in the dog, the precordial lead criteria for AFL diagnosis cannot be applied in this species. Septal flutter circuits usually show large, positive F waves in V1 with almost flat F waves in other leads.27,40 In dogs seen clinically and in experimental models, CTI-dependent AFL circuits showed a saw-tooth pattern in the inferior leads in cases of typical or counterclockwise rotation, and positive deflection in inferior leads in case of typical reverse or clockwise rotation.6 In the dogs reported here, both macro-reentrant circuits showed large and positive F waves in the inferior leads as previously described in dogs with typical reverse AFL,6 with a tendency for a greater isoelectric interval, which might reflect wide areas of slow conduction or electrically silent.37 Reported success rate of radiofrequency catheter ablation of atypical AFLs in human is usually lower than that in case of CTI-dependent circuits, ranging from 67% to 73%, and deterioration into atrial fibrillation was observed.24,27,31 In the dogs reported here, complete resolution of the arrhythmias was achieved in 3 cases, while the remaining 2 cases (1 with RS and 1 with RAFW) showed recurrence of the arrhythmia and development of persistent atrial fibrillation, respectively. One of the possible causes for this failure is the anatomy of the critical isthmuses that, unlike the CTI, are not completely protected by anatomical barriers and therefore linear lesions performed with ablation may not completely interrupt the circuits. The major limitation of the present study is the impossibility to map instantaneously the entire circuit of the flutters since we used only 2 decapolar catheters, 1 in the CS and 1 along the RAFW. Other parts of the RA, such as the interatrial septum, the tricuspid valve annulus and the Hissian area were mapped alternatively with the ablation catheter. The use of more decapolar catheters would have allowed the assessment of the complete activation of the right atrial myocardium as performed in human cases and in experimental models.17,24e26,30,31,37 Furthermore the execution of a transeptal puncture with the positioning of a decapolar catheter into the left atrium, the use of a Halo catheter around the tricuspid annulus, and of a crista catheter placed in the posterior RA along the crista terminalis or the use of contact and noncontact electroanatomic mapping, would have permitted to better analyze atrial activations and rotation pattern of the flutter waves.5,41,42 Based on the results of our report, we conclude that atypical right AFL may occasionally occur in
R.A. Santilli et al. dogs. Endocardial mapping and entrainment techniques allowed us to identify 2 RA macroreentrant circuits not yet reported in the dog, that could be definitively abolished with RFCA in most of our cases.
Conflict of interest The authors have no conflicts of interest.
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14. Tadanobu I, Kaneko Y, Nakajima T, Saito A, Ota M, Kato T, Iijima T, Tamura M, Kobayashi H, Ito T, Manita M, Kurabayashi M. Typical atrial flutter with atypical flutter wave morphology due to abnormal interatrial conduction. Cardiol J 2011;18:450e453. 15. Cosı´o FG, Lo ´pez-Gil M, Arribas F, Gonzales HD. Mechanisms of induction of typical and reversed atrial flutter. J Cardiovasc Electrophysiol 1998;9:281e291. 16. 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;94:398e406. 17. Yang Y, Cheng J, Bochoeyer A, Hamdam MH, Kowal RC, Page R, Lee JR, Steiner PR, Saxon LA, Lesh MD, Modin GW, Schinman MM. Atypical right atrial flutter patterns. Circulation 2001;103:3092e3098. 18. Cheng J, Cabeen WR, Scheinman MM. Right atrial flutter due to lower loop reentry: mechanism and anatomic substrates. Circulation 1999;99:1700e1705. 19. Kalman JM, Olgin JE, Saxon LA, Lee RJ, Scheinman MM, Lesh MD. Electrocardiographic and electrophysiologic characterization of atypical atrial flutter in man: use of activation and entrainment mapping and implication for catheter ablation. J Cardiovasc Electrophysiol 1997;8: 121e144. 20. Cheng J, Scheinman MM. Characteristics of double-wave reentry induced by programmed stimulation in patients with typical atrial flutter. Circulation 1998;97:1589e1596. 21. Scheinman MM, Cheng J, Yang Y. Mechanisms and clinical implications of atypical atrial flutter. J Cardiovasc Electrophysiol 1999;10:1153e1157. 22. Nakagawa H, Lazzara R, Khastgir T, Beckman KJ, McClelland JH, Imai S, Pitha JV, Becker AE, Rome M, Neuhauser J, Wang X, Calame JD, Goudeau MD, Jackman WM. Role of the tricuspid annulus and the Eustachian valve/ridge on atrial flutter: relevance to catheter ablation of septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996;94:407e424. 23. Kalman JM, VanHare GF, Olgin JE, Saxon LA, Stark SI, Lesh MD. Ablation of ‘incisional’ reentrant atrial tachycardia complicating surgery for congenital heart disease. Use of entrainment to define a critical isthmus of conduction. Circulation 1996;93:502e512. 24. Kall JG, Rubenstein DS, Kopp DE, Burke MC, Verdino RJ, Lin AC, Johnson CT, Cooke PA, Wang ZG, Fumo M, Wilber DJ. Atypical atrial flutter originating in the right atrial free wall. Circulation 2000;101:270e279. 25. Ricard P, Imianitoff M, Yaı¨ci K, Coutelour JM, Bergonzi M, Rinaldi JP, Saoudi N. Atypical atrial flutters. Europace 2002; 4:229e239. 26. Cosı´o FG, Martı´n-Pen ˜ato A, Pastor A, Nunez A, Goicolea A. Atypical flutter: a review. Pacing Clin Electrophysiol 2003; 26:2157e2169. 27. Marrouche NF, Natale A, Wazni O, Cheng J, Yang Y, Pollack H, Verma A, Ursell P, Schinman MM. Left septal atrial flutter: electrophysiology, anatomy and results of ablation. Circulation 2004;109:2440e2447. 28. Stevenson I, Kistler P, Spense S, Vohra J, Sparks P, Morton J, Kalman J. Scar-related right atrial macroreentrant tachycardia in patients without prior atrial surgery:
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electroanatomic characterization and ablation outcome. Ht Rhythm 2005;2:594e601. Cummings JE, Schweikert R, Saliba W, Hao S, Martin DO, Marrouche NF, Burkhardt JD, Kilicaslan F, Verma A, Beheiry S, Belden RN, Natale A. Left atrial flutter following pulmonary vein XXX isolation with radiofrequency energy: linear lesion or repeat isolation. J Cardiovasc Electrophysiol 2005;16:293e297. Tai CT, Chen SA. Electrophysiological mechanisms of atrial flutter. Indian Pacing Electrophysiol J 2006;6:119e132. Satomi K, Chun J, Tilz R, Bansch D, Ernst S, Antz M, Schmidt B, Kuck KH, Ouyang F. Catheter ablation of multiple unstable macroreentrant tachycardia within the right atrium free wall in patients without previous cardiac surgery. Circ Arrhythm Electrophysiol 2010;3:24e31. Wells JL, McLean WAH, James TN, Waldo AL. Characterization of atrial flutter. Studies in a man after open heart surgery using fixed atrial electrodes. Circulation 1979;60:665e673. Allesie MA, Lammers WJ, Bonke IM, Hollen J. Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog. Circulation 1984;70: 123e135. Okumura Y, Watanabe I, Ashino S, Kofune M, Ohkubo K, Takagi Y, Kawauchi K, Yamada T, Hashimoto K, Shindo A, Sugimura H, Nakai T, Saito S. Electrophysiologic and anatomical characteristics of the right posterior wall in patients with and without atrial flutter. Analysis by intracardiac echocardiography. Circ J 2007;71:636e642. Uno K, Kumagai K, Khrestian CM, Waldo AL. New insights regarding the atrial flutter reentrant circuit: studies in the canine sterile pericarditis model. Circulation 1999;100: 1354e1360. Boyden PA. Activation sequence during atrial flutter in dogs with surgical induced right atrial enlargement. Circ Res 1998;62:569e608. Schoels W, Offner B, Brachmann J, Kuebler W, El-Sherif N. Circus movement atrial flutter in the canine sterile pericarditis model. Relation of characteristics of the surface electrocardiogram and conduction properties of the reentrant pathway. J Am Coll Cardiol 1994;23:799e808. Yamaguchi N, Kumagai K, Fukuda K, Wakayama Y, Sugai Y, Hirose M, Shimokawa H. Electrophysiological properties of the right atrial septum in patients with atrial tachyarrhythmias. Tohoku J Exp Med 2008;215:13e22. Medi C, Kalman JM. Prediction of the atrial flutter circuit location from the surface electrocardiogram. Europace 2008;10:786e796. Bochoeyer A, yang Y, Cheng J, Lee RJ, Keung EC, Marrouche NF, Natale A, Scheinman MM. Surface electrocardiographic characteristics of right and left atrial flutter. Circulation 2003;108:60e66. Ching-Tai Tai CT, Liu TY, Lee PC, Lin YJ, Chang MS, Chen SA. Non-contact mapping to guide radiofrequency ablation of atypical right atrial flutter. J Am Coll Cardiol 2004;44: 1080e1086. Duru F, Hindricks G, Kottkamp H. Atypical left atrial flutter after intraoperative radiofrequency ablation of chronic atrial fibrillation: successful ablation using threedimensional electroanatomic mapping. J Cardiovasc Electrophysiol 2001;12:602e605.
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Radiofrequency catheter ablation of atypical atrial flutter in dogs Roberto A. Santilli, Dr. Med. Vet., PhD a,*, Lucia Ramera, Dr. Med. Vet. a, Manuela Perego, Dr. Med. Vet. a, Paolo Moretti, MD b, Giammario Spadacini, MD b a b
Clinica Veterinaria Malpensa, Viale Marconi, 27, 21017 Samarate Varese, Italy Humanitas Mater Domini, Via Gerenzano, 2, 21053 Castellanza Varese, Italy
Received 23 April 2013; received in revised form 15 October 2013; accepted 21 October 2013
KEYWORDS Electrophysiology; Supraventricular tachycardia; Arrhythmias
Abstract Five dogs were presented to our institution for fatigue caused by an incessant supraventricular tachycardia. In all dogs, an ECG on admission showed a narrow QRS complex tachycardia with a median ventricular cycle length of 220 ms (range 180e360 ms), and a positive atrial depolarization identifiable in the ST segment following the previous QRS complex. There was a 1:1 atrioventricular conduction ratio in all but one dog, which presented with 2:1 atrioventricular block. Electrophysiologic studies identified the underlying arrhythmogenic mechanism as a right atrial macro-reentrant tachycardia with two distinct isthmic areas: right septal (RS) in three dogs and right atrial free wall (RAFW) in two dogs. Linear radiofrequency catheter ablation was performed during tachycardia in all dogs at the identified isthmic area, which acutely blocked the macroreentrant circuit. At 18-month follow-up, 3 dogs (1 with RAFW isthmus and 2 with RS isthmus) showed no recurrence of the arrhythmia on Holter monitoring. One dog with RS isthmus showed recurrence of the supraventricular tachycardia 15 days post-ablation, and 1 dog with RAFW isthmus presented with persistent atrial fibrillation 2 months post-ablation. ª 2013 Elsevier B.V. All rights reserved.
* Corresponding author. E-mail addresses: [email protected], rasantil@ tin.it (R.A. Santilli).
Five dogs (3 Bernese dogs, 1 dogue de Bordeaux and 1 Irish setter), 3 females and 2 males, with a median age of 90 months (range 9e132 months) and a median body weight of 48 kg (range 32e59 kg) (Table 1) were presented to our
1760-2734/$ - see front matter ª 2013 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.jvc.2013.10.002
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Abbreviations AFL AV CS CTI HRA LRA LLR MRA MRT RA RAFW RS SVT ULR
atrial flutter atrioventricular coronary sinus cavo-tricuspid isthmus high right atrium low right atrium lower loop reentry middle right atrium macroreentrant tachycardia right atrium right atrial free wall right septal supraventricular tachycardia upper loop reentry
institution for incessant supraventricular tachycardia (SVT), profound weakness and dysorexia of 5e8-day duration. Three out of 5 dogs were treated with sotalol (2 mg/kg PO q12 h) with no response to medical treatment. At admission all dogs were depressed, showed mild weight loss, rapid heart rate and had pulse deficits. Thoracic radiographs displayed cardiomegaly in 2 out of 5 dogs with no signs of congestion. Echocardiography revealed reduced left ventricular volume with Table 1
pseudohypertrophy and mildly depressed systolic function in 2 out of 3 Bernese dogs and left atrial and ventricular dilation with volume overload and severely depressed systolic function in the remaining dogs (Table 1).1,2 In all dogs, 12-lead ECG showed a narrow QRS complex tachycardia (median QRS duration 40 ms, range 40e60 ms) with a median ventricular cycle length of 220 ms (range 180e360 ms). Atrial depolarization was visible in the preceding ST segment as a positive wave in the inferior leads (II, III, aVF) with a median voltage of 0.25 mV (range 0.15e0.4 mV), a median duration of 40 ms (range 35e60 ms) and a median axis on the frontal plane of 74 (range 63e90 ) (Table 1). In all dogs an isoelectric line was present between consecutive atrial depolarizations. The atrioventricular (AV) conduction ratio was 1:1 in all but one dog in which it was 2:1 (Fig. 1). An electrophysiologic (EP) study was performed in all dogs to characterize the electrogenic mechanism and ablate the arrhythmic substrate.
Electrophysiology studies and ablation procedures The electrophysiology studies were performed under general anesthesia with dogs prepared as
Signalment, echocardiographic and electrocardiographic findings in 5 dogs with atypical atrial flutter.
Signalment Breed Gender Age (months) Body weight (Kg) Echocardiography LVEDD (mm) LVESD (mm) 2D-EF (%) LA/Ao Surface ECG QRS duration (ms) Atrial CL (ms) Ventricular CL (ms) F wave amplitude (mV) F wave duration (ms) F wave axis (degree) AV conduction ratio Intracardiac ECG Atrial CL (ms) Ventricular CL (ms) AV conduction ratio AFL Isthmus
Dog A
Dog B
Dog C
Dog D
Dog E
Bernese Female 60 48
Bernese Female 90 59
Bernese Female 96 51
Dogue de Bordeaux Male 9 46
Irish setter Male 132 32
36.88 23.09 45.66 1.57
42.75 25.36 38.52 1.65
34.09 21.04 51.82 1.56
54.56 34.02 30.72 3.2
46.63 32.95 25.94 1.88
50 220 220 0.2 40 63 1:1
40 200 200 0.25 60 74 1:1
40 180 180 0.4 60 90 1:1
60 180 360 0.15 35 84 2:1
40 220 220 0.25 40 72 1:1
230 230 1:1 Right septal
220 220 1:1 Right septal
240 240 1:1 Right septal
180 360 2:1 RA free wall
300 300 1:1 RA free wall
LVEDD, left ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; EF, ejection fraction; LA, left atrium; Ao, aorta; CL, cycle lenght; AV, atrioventricular; AFL, atrial flutter; RA, right atrial.
Atypical atrial flutter in dogs
11
Figure 1 Twelve-lead surface ECG in 5 dogs with right atrial macroreentrant tachycardia (A, B, C right septal atrial flutter; D, E right atrial free wall atrial flutter). Notice in all dogs narrow QRS complex (median duration 40 ms, range 40e60 ms), a median ventricular cycle length of 220 ms (range 180e340 ms), a positive atrial activation (F) in the previous ST segment in the inferior leads (II, III, aVF) with a median voltage of 0.25 mV (range 0.15e0.4 mV), a median duration of 40 ms (range 35e60 ms) and an average axis on the frontal plane of 74 (range 63e84 ). In all cases isoelectric line was present between consecutive atrial depolarization. In dogs A, B, C, E, 1:1 AV conduction was present; in dog D, 2:1 AV conduction can be noted. In this latter case, the F wave located in the previous ST segment conducts to the ventricles. The location of the F waves was confirmed by atrial activation mapping. (Paper speed 50 mm/s e amplitude 5 mm/1 mV).
previously reported.3e5 Three vascular accesses were obtained using a modified Seldinger technique in each dog: one in the right jugular vein and two in the right femoral vein. A decapolar catheterc was advanced along the right jugular vein into the coronary sinus (CS).3,4 A second decapolar catheterc was inserted into the right femoral vein and positioned along the right atrial (RA) lateral wall to record potentials from the antero-lateral aspect of the crista terminalis (HRA) with the proximal pair of electrodes, the mid-lateral right atrial (MRA) potentials with the middle pair and the low posterior-lateral right atrial (LRA) potentials with the distal pair.5,6 Finally, a 7-Fr, 4-mm ablation catheterd with steerable tip was inserted along the right femoral vein and positioned alternatively at the His bundle, right ventricle and isthmic areas to map local electrograms and perform electrical stimulations.5,6 At baseline all dogs showed incessant tachycardia with a median atrial cycle length of 230 ms (range 180e300 ms) and a ventricular cycle length of 240 ms (range 220e360 ms) (Table 1). All dogs had a 1:1 AV conduction ratio, except one, which c
Polaris X, 7 Fr, Boston Scientfic Corp., Genova, Italy. Std CrV Blazer II HTD, 4 mm, 7 Fr; Boston Scientific Corp., Genova, Italy. d
presented with 2:1 AV block. Intracardiac atrial depolarization potentials coincided in each patient with the positive atrial waves superimposed to the preceding ST segment on the surface ECG. In all dogs, a diagnosis of macroreentrant right atrial tachycardia was made based on the following: 1) atrial activation within the RA for the tachycardia cycle length, 2) a return cycle after entrainment less than 30 ms longer than the tachycardia cycle length identified the pacing site as a critical component of that tachycardia circuit, and 3) entrainment in 2 opposite quadrants within the RA, each with return cycle lengths within 20 ms of the tachycardia cycle length.7 To evaluate the location of critical isthmic areas, potential targets of ablation, initially the cavo-tricuspid isthmus (CTI) was mapped during LRA pacing paying attention to the presence of concealed entrainment. The maneuver revealed overt fusion with acceleration of the tachycardia cycle length and the pacing cycle length, and changes in both the sequence of atrial activation and the morphology of the surface and endocardial electrograms. Once CTI-dependent atrial flutter (AF) was ruled out, different tests were performed to demonstrate a critical isthmus, its extent, the presence of bystander sites and possibly barriers bordering the isthmus.6e8 In
12 addition to the presence of mid-diastolic potentials, these tests included concealed entrainment with a post-pacing interval within 30 ms longer than the tachycardia cycle length, stimulus timed within 30 ms of activation time; the presence of double potentials was used to demonstrate either functional or fixed lines of block and the presence of electrically silent area.6e8 In the Bernese dogs the critical isthmus was localized in the middle portion of the right interatrial septum with an inferior-to-superior activation of the area and a counterclockwise activation pattern (left anterior 30 fluoroscopic view) (Fig. 2).5 In the other 2 dogs the critical isthmus was localized in the midlateral right atrial free wall (RAFW), an area characterized by fractionated electrograms with an inferior-to-superior activation of the area itself and a later activation of the CS (Fig. 3). Split potentials were recorded in 3 out of 5 dogs along the crista terminalis but none of them were middiastolic or close to the area of concealed entrainment. In all dogs a diagnosis of atypical right AF was reached. Radiofrequency catheter ablation was performed at controlled temperature with a thermo-
R.A. Santilli et al. coupled steerable 7-Fr, 4-mm catheterd at the right septal (RS) and RAFW isthmus. Maximal catheter tip temperature and power output were set respectively at 65 C and 75 W. Linear lesions of the isthmus areas were obtained with several applications of 45 s duration with no recurrence of the macroreentrant tachycardia (MRT) with programmed atrial pacing noticed within the following 20 min6 Isthmic ablation was performed during tachycardia in all dogs with an electro-anatomic approach aiming at either mid- or late-diastolic atrial potentials, concealed entrainment and eventual fractionated electrograms. Radiofrequency energy was delivered during tachycardia twice on average (range 1e4) in each dog (45.2 W, 62.4 C, 113.2 U) at the area of the right interatrial septum for the length of the dipole in the Bernese dogs and sequentially from the caudal vena cava ostium superiorly to the midlateral RAFW fractionated electrograms in the remaining dogs. Acute termination of the macroreentrant atrial tachycardia occurred within an average of 17.2 s (range 10e25 s) in each dog and persisted until the end of the procedure (Fig. 4). Radiofrequency ablation was considered successful in
Figure 2 Surface and intracardiac ECG obtained in one of the Bernese dogs during endocardial mapping and concealed entrainment of a right septal atrial flutter. Recording displayed includes lead I, II, III, aVF, V1, V6 of the surface ECG and intracardiac recording from the high right atrial wall, through the medium to the low posterior right atrial wall (HRA, MRA, LRA), from the distal to the proximal portions of the right septal isthmic area (ABLd and ABLp) and from the distal to the proximal portion of the coronary sinus (CSd and CSp). Note the counterclockwise activation pattern moving from the isthmic area (ABLd), where mid-diastolic electrograms were recorded, to the HRA, MRA, LRA and the CSd. The atrial cycle length during atrial flutter was 237 ms, an atrial extrastimulus was introduced from the ABLd and accelerated the tachycardia cycle length (215 ms), with the same sequence of activation on intracardiac recording and no change of atrial morphology on surface ECG. After the pacing tachycardia cycle length returned to its original value. (Paper speed 300 mm/s e amplitude 22.8 mV/cm).
Atypical atrial flutter in dogs
13
Figure 3 Surface and intracardiac ECG obtained in the Irish Setter during endocardial mapping and concealed entrainment of a right atrial free wall atrial flutter. Recording displayed includes lead I, II, III, aVF, V1, V6 of the surface ECG and intracardiac recording from the high right atrial wall, through the medium to the low posterior right atrial wall (HRA, MRA, LRA), from the distal to the proximal portions of the right atrial free wall isthmic area (ABLd and ABLp) and from the distal to the proximal portion of the coronary sinus (CSd and CSp). Note the inferior-tosuperior activation of the right atrial free wall moving from the isthmic area (ABLd), where mid-diastolic, delayed and fractioned electrograms were recorded to LRA, MRA, HRA and CSd. The atrial cycle length during atrial flutter was 167 ms with a 2:1 conduction ratio, an atrial extrastimulus was introduced from the ABLd and accelerated the tachycardia cycle length (145 ms), with the same sequence of activation on intracardiac recording and no change of atrial morphology on surface ECG. After the pacing tachycardia cycle length returned to its original value. (Paper speed 300 mm/s e amplitude 22.8 mV/cm).
case of termination and subsequent noninducibility of the arrhythmia with programmed atrial stimulation.
congestive heart failure after 12 months and were treated with furosemide (2 mg/kg PO q12 h), pimobendan (0.25 mg/kg PO q12 h) and enalapril (0.5 mg/kg PO q12 h).
Follow-up Discussion An ECG 15 days after the procedure and Holter monitoring at 2, 6 and 18-month intervals were performed in all dogs. At 18-month follow-up, 3 dogs (1 with RAFW isthmus and 2 with RS isthmus) showed no recurrence of the arrhythmia on Holter monitoring. One dog with RS isthmus showed recurrence of the SVT 15 days post-ablation, and one with RAFW isthmus presented with persistent atrial fibrillation 2 months post-ablation. The dog with recurrence of the AFL is now partially controlled with diltiazem extended release (3 mg/kg PO q12 h) and presented a progressive loss of systolic function, while the dog with persistent atrial fibrillation is well controlled with a combination of digoxin and diltiazem extended release (0.0055 mg/kg PO q12 h and 3 mg/kg PO q12 h, respectively) and no further deterioration of left ventricular systolic function. Both dogs developed
In the present study we were able to demonstrate the existence of atypical AFL in dogs with 2 different critical isthmus areas located over the RAFW and the RS, and show that definitive ablation of the circuit is possible in most cases. The term AFL has been used in human medicine to define an electrocardiographic pattern of regular tachycardia with rate >240 bpm, atrial depolarizations with a classical “saw tooth” pattern in leads II, III and/or aVF and absence of an isoelectric baseline between consecutive atrial waves in at least 1 lead.9 Further studies pointed out that neither rate nor lack of isoelectric baseline should be considered specific of any tachycardia mechanism,10e12 and that the sequence of left atrial activation and interatrial connections play a major role in F wave morphology during flutter.13,14
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R.A. Santilli et al.
Figure 4 Surface and intracardiac ECG obtained in one of the Bernese dogs during radiofrequency catheter ablation of a right septal atrial flutter. Recording displayed includes lead I, II, III, aVR, aVL, aVF, V1, V6 of the surface ECG and intracardiac recording from the high right atrial wall, through the medium to the low posterior right atrial wall (HRA, MRA, LRA), from the distal to the proximal portions of the right septal isthmic area (ABLd and ABLp) and from the distal to the proximal portion of the coronary sinus (CSd and CSp). A linear lesion with the length of the dipole was performed along the isthmic area during tachycardia and 20 s after the beginning of the second radiofrequency application (arrow) the tachycardia stopped and sinus rhythm resumed. (Paper speed 50 mm/s e amplitude 22.8 mV/cm).
For these reasons in 2001 the ESC/NASPE expert consensus proposed a new classification of AFLs and regular atrial tachycardias based on mechanism of arrhythmia and isthmus dependence rather than surface ECG features. In this classification the term MRT refers to all reentrant tachycardias with a large central obstacle, including typical AFL and other macroreentrant circuits in either the right or left atrium.11 In more detail, AFL are classified as typical, when CTI-dependent, regardless of the ECG pattern, and atypical when a non-CTIdependent circuit is documented. Typical AFLs have been classified, based on the direction of atrial activation within their circuit, as typical and reverse typical. During typical AFL the wavefront travels counterclockwise around the tricuspid valve annulus (90% of patients), in the LAO fluoroscopic view, whereas during reverse typical AFL it travels clockwise (10% of cases).11e16 Three unusual forms of typical CTI-dependent AFLs have also been reported in human: lower loop reentry (LLR), double wave reentry, and sub-eustachian
isthmus short circuit.17e21 In LLR an early breakthrough over the caudal portion of the crista terminalis is present, with simultaneous conduction along the lateral wall and the septum as well conduction over the CTI toward the ostium of the CS.18e21 Double wave reentry is a transient arrhythmia characterized by two wavefronts within the flutter circuit, usually present in patients with CTI-dependent AFL, and that rapidly reverts to single wave typical AFL.19,20 This circuit has been documented in 25%e50% of human patients with typical AFL and is characterized by early activation of the region of the coronary sinus with a breakthrough over the eustachian ridge, posterior to the ostium of the coronary sinus.22 Both typical and typical reverse CTI-dependent AFLs, confirmed by detailed endocardial mapping, have been reported in the dog.6 The term atypical AFL is used to describe non-CTIdependent MRT, usually more rapid and irregular, with variable flutter wave morphology, and often proven to be prefibrillatory.11,17,21,23e31 In humans
Atypical atrial flutter in dogs these types of MRT can be secondary to surgical lesions from previous atriotomy, septal prostethic patch, suture line or secondary to radiofrequency catheter ablation (right atrial scar related MRT or lesion MRT and pulmonary vein-related AFL).17,21,23,25,26,29,30 Alternatively they can be supported by electrically silent areas of atrial myocardium, presumably due to fibrosis or infiltration, located either in the right or left atrium.17,21,24e28,30,31 Atypical left AFL circuits involve circulation of a wavefront around unexcitable areas over the posterior left atrial wall, around the pulmonary veins, the mitral annulus (left atrial MRTs),10,11,25,26,30 or over the left atrial septum (left septal AFL).27,30 The prevalence of non scar-related atypical right AFLs is approximately 8% and this type of arrhythmia includes upper loop reentry tachycardia (ULR), RAFW atypical AFL, and unstable complex circuits of the RAFW.17,21,24e26,28,30,31 The ULR affects the upper portion of the right atrium with a clockwise circuit breaking over the lateral or anterolateral annulus with impulse collision in the isthmus, which can be identified between the superior vena cava and the fossa ovalis.17,25,26,30 In RAFW atypical AFL the impulse rotates around low-voltage areas inducing conduction delay frequently localized in the antero-infero-lateral aspect of the right atrial free wall.17,24e26,28,30,31 A final variant of atypical AFL was described by Wells et al. based on flutter rate, stable intracardiac electrogram and morphology, and the possibility of transient entrainment and labeled as type II.32 According to this classification typical or type I AFL display an excitable gap, while atypical or type II AFL present shorter cycle length with no gap. Type II AFL cannot be entrained, are transient and common under vagal stimulation, transitioning spontaneously to baseline flutter or fibrillation.33 Detailed endocardial mapping and entrainment response in the dogs herein reported showed two right atrial macro-reentrant circuits around electrically silent areas with two critical isthmus areas different from the CTI and located over the RAFW in 2 dogs, and the right atrial septum in 3 dogs, similar to what has been reported in human patients.17,24e28,30,31 The right posterior free wall is a well-recognized arrhythmogenic substrate in patients with AFL since it includes a line of transverse conduction block adjacent to the crista terminalis. In patients with AFL the area of the crista terminalis is usually larger and the effective refractory period of this region is longer and site-specific compared to normal patients.34 Activation mapping of the RAFW in the dogs described in our study demonstrated the presence of an electrically silent area characterized by low
15 amplitude and fractionated and/or delayed components as described in human patients without a history of atriotomy as well as in sterile pericarditis and models of atrial enlargement.24,28,31,35e37 In human patients, RAFW atypical AFL is commonly associated with sinus node dysfunction since the electrically silent areas involve large portions of the atrial wall including the sinus node (local right atrial cardiomyopathy).28 None of the dogs with RAFW atypical AFL herein reported showed evidence of sinus node dysfunction. The right atrial septum is another arrhythmogenic site in human patients with AFL since it displays a lower mean bipolar voltage and both longitudinal and transverse conduction velocity delays compared to normal patients.38 The atrial septum has a bilaminate muscle structure constituting the thin membranous primary atrial septum that may contribute to the protection and maintenance of septal flutters.27 Concealed entrainment techniques are widely used to localize the critical isthmus both in human and in dogs with CTI-dependent AFL.6e8,16 Atypical MRT circuits are more difficult to map since there is not a fixed location for the circuit or its critical isthmus.17,24e26,30,31 In our case series the AFL circuits were stable and concealed entrainment could be achieved at the RA midseptal area in 3 dogs and along the right atrial free wall in 2 dogs. Post-pacing interval and stimulus time measurements permitted us to exclude bystander sites.8 Atypical AFLs have been associated with different structural heart diseases such as coronary artery disease, idiopathic dilated cardiomyopathy and valvular heart disease, but have also been mapped in a small number of human patients with no underlying heart disease.24,31 Conversely, in the case of left septal atrial flutter, 65% of the patients showed no concurrent heart disease.27 Similarly in our dogs, right septal AFLs were not associated with cardiac disease, while RAFW AFLs were associated with chamber dilation and ventricular dysfunction. In these cases, although tachycardia-induced cardiomyopathy must be considered, the etiology of the cardiac disease could not be completely elucidated. The surface electrocardiogram may be used to predict the type of AFL in human patients.39,40 Typical CTI-dependent AFL, double wave reentry and ULR are characterized by negative F waves in the inferior leads and positive in V1, while typical reverse AFL shows positive F waves in the inferior leads. Atypical AFL presents a highly variable flutter wave morphology and may appear as typical reverse AFL, resembling typical or focal AFL.39 A broad-based upright V1 is highly predictive of a left-sided flutter, while when V1 has an initial
16 isoelectric or inverted component followed by an upright component, this is consistent with right flutter.39 Unfortunately, considering the variability of chest conformation in the dog, the precordial lead criteria for AFL diagnosis cannot be applied in this species. Septal flutter circuits usually show large, positive F waves in V1 with almost flat F waves in other leads.27,40 In dogs seen clinically and in experimental models, CTI-dependent AFL circuits showed a saw-tooth pattern in the inferior leads in cases of typical or counterclockwise rotation, and positive deflection in inferior leads in case of typical reverse or clockwise rotation.6 In the dogs reported here, both macro-reentrant circuits showed large and positive F waves in the inferior leads as previously described in dogs with typical reverse AFL,6 with a tendency for a greater isoelectric interval, which might reflect wide areas of slow conduction or electrically silent.37 Reported success rate of radiofrequency catheter ablation of atypical AFLs in human is usually lower than that in case of CTI-dependent circuits, ranging from 67% to 73%, and deterioration into atrial fibrillation was observed.24,27,31 In the dogs reported here, complete resolution of the arrhythmias was achieved in 3 cases, while the remaining 2 cases (1 with RS and 1 with RAFW) showed recurrence of the arrhythmia and development of persistent atrial fibrillation, respectively. One of the possible causes for this failure is the anatomy of the critical isthmuses that, unlike the CTI, are not completely protected by anatomical barriers and therefore linear lesions performed with ablation may not completely interrupt the circuits. The major limitation of the present study is the impossibility to map instantaneously the entire circuit of the flutters since we used only 2 decapolar catheters, 1 in the CS and 1 along the RAFW. Other parts of the RA, such as the interatrial septum, the tricuspid valve annulus and the Hissian area were mapped alternatively with the ablation catheter. The use of more decapolar catheters would have allowed the assessment of the complete activation of the right atrial myocardium as performed in human cases and in experimental models.17,24e26,30,31,37 Furthermore the execution of a transeptal puncture with the positioning of a decapolar catheter into the left atrium, the use of a Halo catheter around the tricuspid annulus, and of a crista catheter placed in the posterior RA along the crista terminalis or the use of contact and noncontact electroanatomic mapping, would have permitted to better analyze atrial activations and rotation pattern of the flutter waves.5,41,42 Based on the results of our report, we conclude that atypical right AFL may occasionally occur in
R.A. Santilli et al. dogs. Endocardial mapping and entrainment techniques allowed us to identify 2 RA macroreentrant circuits not yet reported in the dog, that could be definitively abolished with RFCA in most of our cases.
Conflict of interest The authors have no conflicts of interest.
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