Anatomic distribution and electrophysiologic properties of accessory atrioventricular pathways in dogs

Roberto A. Santilli Clinica Veterinaria Malpensa, Via Marconi, 27, 21017 Samarate, Varese, Italy

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Gianmario Spadacini Università degli Studi dell'Insubria, Facoltà di Medicina, Via Ravasi, 2, 21100 Varese, Italy

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Paolo Moretti Università degli Studi dell'Insubria, Facoltà di Medicina, Via Ravasi, 2, 21100 Varese, Italy

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Manuela Perego Clinica Veterinaria Malpensa, Via Marconi, 27, 21017 Samarate, Varese, Italy

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Alberto Perini Clinica Veterinaria Malpensa, Via Marconi, 27, 21017 Samarate, Varese, Italy

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Serena Crosara Facoltà di Medicina Veterinaria, Dipartimento di Patologia Animale, Via L da Vinci, 44–10095 Grugliasco, Torino, Italy

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Alberto Tarducci Facoltà di Medicina Veterinaria, Dipartimento di Patologia Animale, Via L da Vinci, 44–10095 Grugliasco, Torino, Italy

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Abstract

Objective—To evaluate the anatomic distribution and electrophysiologic properties of accessory pathways (APs) in dogs.

Design—Case series.

Animals—10 dogs with tachyarrhythmias associated with an AP.

Procedures—Each dog underwent electrophysiologic testing to determine the inducibility of documented and undocumented arrhythmias and to identify location, conduction properties, and antegrade and retrograde effective refractory periods of the APs. Radiofrequency catheter ablation was then performed.

Results—15 APs were identified; 7 dogs each had a single AP, and 3 had multiple APs. Fourteen of the 15 APs were right-sided (6 right free wall, 4 posteroseptal, 3 midseptal, and 1 anteroseptal), and 1 was left-sided (left free wall). All APs conducted in an all-or-none fashion. Unidirectional retrograde conduction was observed in 11 APs, and bidirectional conduction was observed in 4. All documented tachyarrhythmias could be induced during electrophysiologic testing; atrial fibrillation was also inducible in 2 dogs. Mean ± SD cycle duration of orthodromic atrioventricular reciprocating tachycardia was 215.80 ± 44.87 milliseconds. Mean shortest R-R interval during atrial fibrillation was 247.33 ± 83.17 milliseconds.

Conclusions and Clinical Relevance—Results suggested that in dogs, most APs are right-sided, had unidirectional retrograde conduction, and are associated with various arrhythmias, including orthodromic atrioventricular reciprocating tachycardia and atrial fibrillation without evidence of pre-excitation.

Abstract

Objective—To evaluate the anatomic distribution and electrophysiologic properties of accessory pathways (APs) in dogs.

Design—Case series.

Animals—10 dogs with tachyarrhythmias associated with an AP.

Procedures—Each dog underwent electrophysiologic testing to determine the inducibility of documented and undocumented arrhythmias and to identify location, conduction properties, and antegrade and retrograde effective refractory periods of the APs. Radiofrequency catheter ablation was then performed.

Results—15 APs were identified; 7 dogs each had a single AP, and 3 had multiple APs. Fourteen of the 15 APs were right-sided (6 right free wall, 4 posteroseptal, 3 midseptal, and 1 anteroseptal), and 1 was left-sided (left free wall). All APs conducted in an all-or-none fashion. Unidirectional retrograde conduction was observed in 11 APs, and bidirectional conduction was observed in 4. All documented tachyarrhythmias could be induced during electrophysiologic testing; atrial fibrillation was also inducible in 2 dogs. Mean ± SD cycle duration of orthodromic atrioventricular reciprocating tachycardia was 215.80 ± 44.87 milliseconds. Mean shortest R-R interval during atrial fibrillation was 247.33 ± 83.17 milliseconds.

Conclusions and Clinical Relevance—Results suggested that in dogs, most APs are right-sided, had unidirectional retrograde conduction, and are associated with various arrhythmias, including orthodromic atrioventricular reciprocating tachycardia and atrial fibrillation without evidence of pre-excitation.

Accessory atrioventricular pathways represent anomalous muscular bundles that directly connect the atrial myocardium to the ventricular myocardium, bypassing the His-Purkinje system.1-4 They are typically classified according to their anatomic position along the atrioventricular groove as left free wall, right free wall, posteroseptal, midseptal, or anteroseptal.5-10 In people, approximately 44% to 70% of APs are classified as left free wall, 5% to 20% are classified as right free wall, 10% to 35% are classified as posteroseptal, 2% to 11% are classified as midseptal, and 4% to 10% are classified as anteroseptal.5-15 Affected individuals may have a single or multiple APs, with 2.4% to 15% of affected individuals reportedly having multiple APs.6,8-10,12-19 Multiple APs are common in human patients with Ebstein anomaly and other congenital heart diseases and are most often confined to the right free wall and posteroseptal area.15,19,20 Patients who have multiple APs have shorter antegrade and retrograde effective refractory periods and are therefore more likely to have atrial tachycardia and atrial fibrillation at faster heart rates.15 In approximately 95% of affected human patients, APs exhibit both antegrade and retrograde conduction with an all-or-none pattern.7,9,11 Antegrade decremental conduction was found to be associated with a right-sided location of the AP in 90% of cases,7,21 whereas in the 5% of patients with retrograde slow conduction, APs were mainly found in the posteroseptal, midseptal, and left free wall areas.7,9,11 Bidirectional AP conduction with overt ECG signs of ventricular pre-excitation has been reported in 53% to 94% of cases,5,8-15 unidirectional retrograde conduction has been reported in 20% to 47% of cases, and unidirectional antegrade conduction has been reported in 0.8% to 6% of cases.5,8,9 At the same or comparable cycle length, the antegrade effective refractory period is usually longer than the retrograde effective refractory period.8,9,15,22 Accessory pathway location was found to influence retrograde effective refractory period,7 with APs located in the left free wall area having shorter retrograde effective refractory periods than APs located in the posteroseptal or right free wall area. Orthodromic atrioventricular reciprocating tachycardia is the most commonly documented and inducible tachyarrhythmia in human patients with APs,7-10,13 particularly when the AP is located in the left free wall, posteroseptal, or anteroseptal area.7 Other tachyarrhythmias reportedly associated with APs include antidromic atrioventricular reciprocating tachycardia,7,10 atrial fibrillation,8-10,13 atrial tachycardia,15 atrial flutter,7 and ventricular fibrillation.7,8

Only a few published reports23-26 document arrhythmias in dogs with APs, although several case reports27-36 describe ventricular pre-excitation and suspected or-thodromic atrioventricular reciprocating tachycardia in affected dogs. Accessory pathways have been described predominantly in young Labrador Retrievers and Boxers with a history of narrow QRS complex tachycardia, causing exercise intolerance, episodic weakness, or heart failure secondary to tachycardia-induced cardiomyopathy.23-26 Nine APs in 7 dogs have been located by means of electrophysiologic testing, with 5 located in the posteroseptal area, 3 located in the right posterior area, and 1 located in the left lateral area. Five APs were concealed, and 2 dogs had multiple APs.23-26 Orthodromic atrioventricular reciprocating tachycardia and atrial fibrillation were the only inducible arrhythmias in these dogs.23-26 Radiofrequency catheter ablation was successfully performed in 6 cases.23,25,26 The purpose of the study reported here was to determine the anatomic distribution and electrophysiologic properties of APs in additional dogs with supraventricular tachycardia.

Materials and Methods

Dogs—Ten dogs with APs causing clinical abnormalities that were examined between January 2004 and June 2006 were included in the study. The 10 dogs included 6 Labrador Retrievers, 2 Boxers, 1 Beagle, and 1 Cavalier King Charles Spaniel. All 10 were male. Mean ± SD age at the time of initial examination was 22.1 ± 16.28 months; mean weight was 27.3 ± 10.5 kg (60.0 ± 23.1 lb). Prior to electrophysiologic testing, all dogs underwent a complete physical examination, 12-lead ECG, thoracic radiography, and 2-dimensional M-mode and Doppler echocardiography. Four of the 10 dogs had a history of periodic weakness, and 2 had a history of syncope. At the time of initial examination, 4 dogs had heart failure (class IIIa). Nine dogs were determined to have narrow QRS complex tachycardia by means of surface ECG or Holter monitoring, and 1 had persistent atrial fibrillation. Three dogs had not received any treatment, 3 were being treated with quinidine (6 mg/kg [2.7 mg/lb], PO, q 8 h), 1 was being treated with amiodarone (10 mg/kg [4.5 mg/lb], PO, q 12 h), 1 was being treated with verapamil (1 mg/kg [0.45 mg/lb], PO, q 8 h), 1 was being treated with diltiazem (0.5 mg/ kg [0.23 mg/lb], PO, q 8 h), and 1 was being treated with sotalol (0.35 mg/kg [0.16 mg/lb], PO, q 8 h). At the time of initial examination, surface electrocardiography revealed that 9 dogs were in sinus rhythm, 3 of which had ECG signs compatible with ventricular pre-excitation (2 fixed and 1 intermittent), and 1 dog was in atrial fibrillation. All 4 dogs with incessant supraventricular tachycardia had echocardiographic signs of biventricular myocardial dysfunction. One dog had residual pulmonic stenosis (1.6 m/s); balloon dilatation valvuloplasty had been done 6 months prior to referral. One dog had tricuspid valve dysplasia.

Electrophysiologic testing—Dogs were anesthetized for electrophysiologic testing as described26; administration of antiarrhythmic drugs was discontinued for at least 5 half-lives prior to electrophysiologic testing. Dogs were placed in dorsal recumbency, and venous access was obtained by use of the modified Seldinger technique. Under fluoroscopic and intracardiac ECG guidance, 2 multipolar electrode catheters were placed in standard positions.23-26 A decapolar cathetera was inserted through the right external jugular vein into the coronary sinus, and a quadripolar catheterb was inserted through the right femoral vein to record His bundle potentials. An ablation catheterc with a deflectable curve that was inserted through the right or left femoral vein and advanced into the right atrium, right ventricular apex, or tricuspid valve annulus was used to perform atrial and ventricular programmed electrical stimulation for unipolar and bipolar endocardial mapping (Figure 1). Surface and intracardiac ECG signals were displayed on a recorderd at a paper speed of 100 or 200 mm/s. Intracardiac ECGs were recorded at filter settings of 50 to 500 Hz. Pacing was performed with stimuli that were twice the diastolic threshold and 2 milliseconds in duration.

Figure 1—
Figure 1—

Ventrodorsal oblique (30° left of sagittal plane) fluoroscopic view of the thorax of a dog obtained during endocardial mapping of a right posteroseptal accessory pathway. A decapolar catheter (1) inserted through the right external jugular vein into the coronary sinus was used to record from the ostium (CSp) to the distal part of the vein (CSd), and a quadripolar catheter (2) inserted through the right femoral vein was used to record His bundle potentials (H). An ablation catheter (3) was inserted through the right femoral vein and advanced to the posteroseptal area of the tricuspid annulus (PS).

Citation: Journal of the American Veterinary Medical Association 231, 3; 10.2460/javma.231.3.393

During electrophysiologic testing, conduction and refractoriness of the AV node and APs were assessed, the anatomic position of APs was localized, and tachycardia mechanisms were identified. Antegrade and retrograde effective refractory periods of the AV node and APs were determined at an atrial or ventricular drive train cycle length slightly less than the native sinus rhythm. The coupling interval of the stimulus was decremented in 10-millisecond steps from 300 milliseconds until the atrial or ventricular refractory period was reached. On the basis of their electrophysiologic properties, APs were classified as having bidirectional, unidirectional antegrade, or unidirectional retrograde conduction and as having decremental or nondecremental conduction. The anatomic location of APs was identified by use of an adapted left anterior oblique fluoroscopic projection and intracardiac ECG guidance while recording bipolar potentials at the earliest site of ventricular activation during antegrade conduction (ie, sinus rhythm or atrial pacing) and at the earliest site of atrial activation during reciprocating tachycardia or ventricular pacing. A sharp, negative, unipolar waveform was used to localize the pole closest to the AP (Figure 2). Left-sided APs were localized by means of epicardial mapping with the coronary sinus catheter, whereas right free wall and septal APs were localized by means of endocardial mapping with the ablation catheter. The disappearance of AP conduction after successful radiofrequency catheter ablation of a particular target was used as further proof of the anatomic location of an AP. On the basis of their position along the atrioventricular groove, APs were classified as left free wall, right free wall, posteroseptal, anteroseptal, or midseptal.

Figure 2—
Figure 2—

Surface and intracardiac ECG recordings obtained from a dog during mapping of the right posteroseptal area of the tricuspid valve annulus. Recordings displayed include leads I, II, III, V1, and V6 of the surface ECG and intracardiac recordings from the distal to proximal portion of the coronary sinus (CSd, CS2, CS3, CS4, and CSp), the distal and proximal portions of the His bundle (Hbed and Hbep), and the distal and proximal portions of the posteroseptal area (Abld and Ablp) and a unipolar recording (Unip). Notice the sequence of ventricular (V) and atrial (A) activation in the various leads during orthodromic atrioventricular reciprocating tachycardia. A shorter ventricular-atrial interval was seen in recordings from the coronary ostium (CSp) and posteroseptal area (Abld), with a sharp, negative deflection in the unipolar recording (A). Findings were diagnostic for eccentric ventricularatrial activation compatible with the presence of a posteroseptal AP. H = His bundle potential.

Citation: Journal of the American Veterinary Medical Association 231, 3; 10.2460/javma.231.3.393

Programmed atrial and ventricular stimulation and rapid atrial pacing were used to test the inducibility of documented and undocumented arrhythmias. Orthodromic atrioventricular reciprocating tachycardia was diagnosed when eccentric ventricular-atrial activation with a fixed ventricular-atrial interval developed after overdrive atrial pacing. If concentric ventricular-atrial activation was present during tachycardia, atrioventricular reciprocating tachycardia was differentiated from atrioventricular nodal reciprocating tachycardia if a single ventricular extrastimulus occurring during the refractory period of the His bundle pre-excited the atrium with an identical activation sequence. Termination of the tachycardia without atrial activation by a ventricular extrastimulus during the His bundle refractory period was also considered diagnostic for orthodromic atrioventricular reciprocating tachycardia. The presence of disorganized atrial activity, characterized by irregular f waves with variable voltage, was considered diagnostic for atrial fibrillation. When atrial fibrillation was already present or induced during the study, antegrade conduction along the AP was assessed and electrical cardioversion with bipolar shock was used to restore sinus rhythm. Data regarding type of sustained arrhythmias that could be induced, cycle length of induced orthodromic reentrant atrioventricular tachycardia, and shortest R-R interval during atrial fibrillation were collected.

Radiofrequency catheter ablation—A thermocouple-tipped steerable 7-F electrodec was used for radio-frequency catheter ablation. Radiofrequency current was generated with a conventional generatore that monitored catheter tip temperature, power output, and impedance. Radiofrequency current was delivered at the atrial or ventricular insertion of an AP at a controlled temperature. Maximum temperature was 65°C, and maximum current was 75 W. Maximal ablation time for a particular target was 60 seconds, but ablation was terminated immediately if there was an increase in impedance or displacement of the catheter. Energy was applied during sinus rhythm in patients with ventricular pre-excitation and during atrioventricular reciprocating tachycardia or ventricular pacing in patients with APs with unidirectional retrograde conduction. The procedure was considered successful if loss of AP conduction lasted for at least 45 minutes after ablation (Figure 3).

Figure 3—
Figure 3—

Surface and intracardiac ECG recordings obtained from a dog during radiofrequency catheter ablation of a right free wall AP (RF). Ablation was performed during a period of orthodromic atrioventricular reciprocating tachycardia (OAVRT). After 3.28 seconds of energy delivery, tachycardia stopped and was replaced by a sinus rhythm. Notice the sequence of ventricular (V) and atrial (A) activation during tachycardia and the abolition of retrograde conduction along the accessory pathways (V not followed by A). See Figure 2 for key.

Citation: Journal of the American Veterinary Medical Association 231, 3; 10.2460/javma.231.3.393

Results

A total of 15 APs were identified in the 10 dogs. Seven dogs had a single AP (right free wall, n = 4; midseptal, 2; and posteroseptal, 1), 1 dog had 2 APs (right free wall and posteroseptal), and 2 dogs had 3 APs each (right free wall, posteroseptal, and anteroseptal in 1 dog; and posteroseptal, midseptal, and left free wall in the other). Overall, 14 of the 15 APs were located around the tricuspid valve annulus, with 6 in the right free wall area, 4 in the posteroseptal area, 3 in the midseptal area, and 1 in the anteroseptal area. Only 1 dog had a left free wall AP (Figure 4).

Figure 4—
Figure 4—

Gross anatomical section at the atrioventricular groove revealing the anatomic distribution of 15 accessory pathways in 10 dogs that underwent radiofrequency catheter ablation for symptomatic tachyarrhythmias. P.T. = Pulmonary trunk. M.V.A. = Mitral valve annulus. T.V.A. = Tricuspid valve annulus. F.O. = Fossa ovalis. C.S. = Coronary sinus ostium.

Citation: Journal of the American Veterinary Medical Association 231, 3; 10.2460/javma.231.3.393

Eleven of the 15 APs had unidirectional retrograde conduction, and 4 had bidirectional conduction. Neither antegrade nor retrograde decremental conduction was identified. Mean ± SD antegrade effective refractory period of the APs was 260 ± 63.77 milliseconds. Retrograde effective refractory period ranged from < 140 to 180 milliseconds.

All 10 dogs had inducible orthodromic atrioventricular reciprocating tachycardia; mean ± SD cycle length was 215.80 ± 44.87 milliseconds. Atrial fibrillation was documented in 1 dog with multiple APs and tachycardia-induced cardiomyopathy and was inducible in 2 dogs with documented narrow QRS complex tachycardia that had midseptal APs and normal atrial size. In 2 dogs, atrial fibrillation was associated with APs with unidirectional retrograde conduction, and in 1, atrial fibrillation was associated with an AP with bidirectional conduction. Atrial fibrillation always showed orthodromic conduction with mean shortest R-R interval of 247.33 ± 83.17 milliseconds. In the dog with documented atrial fibrillation, electrical cardioversion was performed before electrophysiologic testing and 8 times during the procedure because recurrence of the arrhythmia was always triggered by orthodromic atrioventricular reciprocating tachycardia. In the dogs with undocumented but inducible atrial fibrillation, the tachyarrhythmia started during rapid atrial pacing and sinus rhythm was successfully restored by application of a bipolar electrical shock.

Discussion

In affected human patients, APs are most often located in the left free wall and posteroseptal areas,5-15 which differs from the anatomic distribution described in previous reports23-26 of dogs with APs. Most of the APs in these previous reports, as well as in the present study, were located in the right free wall and posteroseptal areas. The cause for this difference in anatomic distribution between humans and dogs is unknown. In human medicine, 2.1% of all APs and 8.9% of right-sided APs are associated with Ebstein anomaly20 and patients with this condition typically have multiple APs located in the right free wall and posteroseptal areas.15,19,20 As was the case in previous reports,23-26 most of the dogs in the present study were Labrador Retrievers and Boxers, and both of these breeds are predisposed to tricuspid valve dysplasia,37 a model of Ebstein anomaly in humans.38,39 Tricuspid valve dysplasia segregates as an autosomal dominant trait with reduced penetrance, and genome-wide linkage analysis of purebred Labrador Retriever kindreds identified a tricuspid valve dysplasia susceptibility locus on canine chromosome 9.38 Considering the prevalence of APs in dogs predisposed to tricuspid valve dysplasia, the similarity of tricuspid valve dysplasia to Ebstein anomaly in humans, and the fact that in human patients with this anomaly, APs are usually distributed in the areas most commonly affected in dogs, one can speculate that minor alterations of the tricuspid valve annulus and mutation of the gene associated with tricuspid valve dysplasia could induce the persistence of anomalous atrioventricular muscular bundles in dogs. Further support for this hypothesis can be found in the fact that 3 of the 10 dogs in the present study had multiple APs, a condition often associated with Ebstein anomaly and other congenital heart diseases in people.15,19,20

Results of the present study highlight 2 other major differences between APs in dogs and APs in humans: the percentage of APs with unidirectional retrograde conduction and the percentage of APs with decremental conduction. In people, most APs have bidirectional nondecremental conduction,5,7-15 although some reports5,8,9 have suggested that 20% to 47% have unidirectional retrograde conduction. Similar to findings in previous reports,23-26 a high prevalence of APs with unidirectional retrograde conduction was found in the present study, emphasizing that ventricular pre-excitation should not be considered a marker of atrioventricular reciprocating tachycardia in dogs. To explain unidirectional retrograde conduction, a theory of impedance mismatch has been postulated.40 According to this theory, an AP that is only a narrow strip generates an insufficient voltage waveform at its insertion site to depolarize the large ventricular muscle mass. The higher prevalence of unidirectional retrograde conduction in dogs versus people could be explained by the small number of dogs examined, differences in AP dimension, differences in the atrial-to-ventricular mass ratio, or differences in intrinsic conduction properties of APs. In human beings, antegrade decremental conduction has often been found to be associated with right-sided APs,7,21 whereas retrograde slow conduction is always confined to APs in the posteroseptal, midseptal, and left free wall areas.7,9,11 Despite the high number of APs identified in these areas in the dogs in the present and previous studies,23-26 slowly conducting APs have not been identified. Considering the low prevalence of APs with decremental properties in people,7,9,11 it is possible that the small number of dogs studied influenced these results.

Both in people8,9,15,22 and in the dogs of the present study, the antegrade effective refractory period at the same cycle length was greater than the retrograde effective refractory period. Mean ± SD antegrade effective refractory period for APs in the present study was 260 ± 63.77 milliseconds, which was similar to the value reported for humans (range, 250 to 313 milliseconds).7-10 Reported retrograde effective refractory periods for APs in human patients range from 190 to 300 milliseconds,7-10 whereas the retrograde effective refractory period for dogs in the present study was shorter (range, < 140 to 180 milliseconds). When measuring retrograde effective refractory period, ventricular refractoriness was often encountered before the retrograde effective refractory period for the AP was reached. The coexistence of very short AP retrograde effective refractory periods in conjunction with atrioventricular node antegrade effective refractory periods of 150 to 300 milliseconds in dogs41 could explain the faster heart rate associated with orthodromic atrioventricular reciprocating tachycardia for dogs in the present report (mean cycle length, 215 ± 44.87 milliseconds), compared with values reported for people (range, 307 to 347 milliseconds).

In the present study and in previous reports,23-26 orthodromic atrioventricular reciprocating tachycardia and atrial fibrillation were the only documented and inducible arrhythmias associated with APs. All APs identified in the present study were capable of maintaining circus-movement tachycardia with different cycle lengths. Atrial fibrillation was documented and inducible in 1 dog and undocumented but inducible in 2 dogs in the present study. In all 3 dogs, orthodromic conduction was present. In human beings, orthodromic atrioventricular reciprocating tachycardia and atrial fibrillation are also the tachycardias most commonly associated with APs.7-10,13 The pathogenesis of atrial fibrillation in patients with APs is not completely understood. Its occurrence correlates with the presence of concomitant atrioventricular reciprocating tachycardia, and often, a transition from reciprocating tachycardia to atrial fibrillation has been observed.42,43 Atrial or ventricular premature beats and rapid atrial pacing have been identified as other possible triggers for atrial fibrillation in patients with APs.7,42,43 In general, people with atrial fibrillation have shorter atrial refractory periods, longer intra-atrial conduction times, and a higher incidence of atrial vulnerability than do people without atrial fibrillation.43 This suggests that atrioventricular reciprocating tachycardia is an important trigger for atrial fibrillation but only when intrinsic atrial abnormalities are present and initiate chaotic atrial activity. Besides triggers and initiators, several perpetuating factors, such as atrial dilatation, anatomic damage to the atrial musculature, and anatomic and electrical remodelling, have been postulated to maintain atrial fibrillation.44 In the present study, this arrhythmia was triggered by atrioventricular reciprocating tachycardia in 1 dog with a documented persistent form, in which tachycardiainduced cardiomyopathy with marked atrial dilatation served as a perpetuator. Two dogs had inducible atrial fibrillation with rapid atrial pacing and normal left atrial size. In these dogs, the paroxysms lasted for > 5 minutes and electrical cardioversion was needed to restore sinus rhythm. A possible explanation for these forms of sustained atrial fibrillation could be the concomitant presence of triggers and initiators.44

The specific role of APs in the initiation or maintenance of atrial fibrillation remains to be elucidated. Various authors have suggested that the inducibility of this tachyarrhythmia and the ability to conduct in an antegrade fashion were related to location of the AP. Anteroseptal APs had a high rate of inducible arrhythmias, compared with right free wall APs.7,45 In the latter, the lower inducibility of atrioventricular reciprocating tachycardia and the longer retrograde effective refractory period, which allows only relatively late ventricular premature beats to be conducted in a retrograde fashion along the AP to the atrium, could explain this difference.7

Finally, branched or multiple APs may provide the potential for complex reentrant circuits, which may result in multiple atrial waveforms during atrioventricular reciprocating tachycardia and induction of atrial fibrillation.15,46 In the present study, atrial fibrillation was present in 1 dog with multiple APs with unidirectional retrograde conduction located in the right free wall, posteroseptal, and anteroseptal areas and in 2 dogs with single midseptal APs, 1 of which had bidirectional conduction. Pre-excited atrial fibrillation was not seen in any of the dogs in the present study. Location of the AP, presence of concealed antegrade or retrograde conduction,47 and long antegrade effective refractory period of the AP could have prevented antegrade propagation of atrial waveforms along APs in our patients.

Other tachyarrhythmias reportedly associated with APs in human beings include antidromic atrioventricular reciprocating tachycardia,7,10 atrial tachycardia,15 atrial flutter,7 and ventricular fibrillation.7,8 None of these arrhythmias were identified in the present study or described in dogs.

In conclusion, our findings suggested that dogs have a predominance of right-sided APs. All APs that were identified had nondecremental conduction, with most having unidirectional retrograde conduction. Associated arrhythmias were orthodromic atrioventricular reciprocating tachycardia and atrial fibrillation. Further studies with large numbers of cases are needed to confirm these data and, given the low prevalence of APs with decremental conduction in human beings, to determine whether APs with decremental conduction occur in dogs.

ABBREVIATIONS

AP

Accessory pathway

a.

Polaris X, 7-F, 2/5/2, Boston Scientific Corp, Genova, Italy.

b.

Explorer 360, 5-F, 5/5/5, Boston Scientific Corp, Genova, Italy.

c.

Polaris C, 4 mm, 7-F, Boston Scientific Corp, Genova, Italy.

d.

EMS, 16 channels, MennenMedical, Manta, Genova, Italy.

e.

EPT 1000 XP, Boston Scientific Corp, Genova, Italy.

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  • 21

    Murdock CJ, Leitch JW & Wee SI, et al. Characteristic of accessory pathways exhibiting decremental conduction. Am J Cardiol 1991;67:506510.

  • 22

    Tonkin AM, Miller HC & Svenson RH, et al. Refractory periods of the accessory pathway in the Wolff-Parkinson-White syndrome. Circulation 1975;52:563569.

    • Search Google Scholar
    • Export Citation
  • 23

    Scherlag BJ, Wang X & Nakagawa H, et al. Radiofrequency ablation of a concealed accessory pathway as treatment for incessant supraventricular tachycardia in a dog. J Am Vet Med Assoc 1993;203:11471152.

    • Search Google Scholar
    • Export Citation
  • 24

    Atkins CE, Kanter R & Wright K, et al. Orthodromic reciprocating tachycardia and heart failure in a dog with a concealed posteroseptal accessory pathway. J Vet Intern Med 1995;9:4349.

    • Search Google Scholar
    • Export Citation
  • 25

    Wright KN, Mehdirad AA & Giacobbe P, et al. Radiofrequency catheter ablation of atrioventricular accessory pathways in 3 dogs with subsequent resolution of tachycardia-induced cardiomyopathy. J Vet Intern Med 1999;13:361371.

    • Search Google Scholar
    • Export Citation
  • 26

    Santilli RA, Spadacini G & Moretti P, et al. Radiofrequency catheter ablation of concealed accessory pathways in two dogs with symptomatic atrioventricular reciprocating tachycardia. J Vet Cardiol 2006;8:157165.

    • Search Google Scholar
    • Export Citation
  • 27

    Patterson DF, Detweiler DK & Hubben K, et al. Spontaneous abnormal cardiac arrhythmias and conduction disturbances in the dog. A clinical and pathologic study of 3,000 dogs. Am J Vet Res 1961;22:355369.

    • Search Google Scholar
    • Export Citation
  • 28

    Hills BL, Tilley LP. Ventricular preexcitation in seven dogs and nine cats. J Am Vet Med Assoc 1985;187:10261031.

  • 29

    Drazner FH. ECG of the month. J Am Vet Med Assoc 1979;175:169170.

  • 30

    Atkins CE, Cali JV, Lombardo PS. ECG of the month. J Am Vet Med Assoc 1994;205:983984.

  • 31

    Wright KN, Atkins CE, Kanter R. Supraventricular tachycardia in four young dogs. J Am Vet Med Assoc 1996;208:7580.

  • 32

    Santilli RA, Bussadori C. Orthodromic incessant atrioventricular reciprocating tachycardia in a dog. J Vet Cardiol 2000;2:2327.

  • 33

    Tidholm A. ECG of the month. J Am Vet Med Assoc 1984;184:154155.

  • 34

    Vit P. ECG of the month. J Am Vet Med Assoc 1985;187:584585.

  • 35

    Miller MW, Bonagura JD, DiBartola SP. ECG of the month. J Am Vet Med Assoc 1988;192:336337.

  • 36

    Lamb WA, Snyder PS. ECG of the month. J Am Vet Med Assoc 1994;204:728730.

  • 37

    Famula TR, Siemens LM & Davidson AP, et al. Evaluation of the genetic basis of tricuspid valve dysplasia in Labrador Retrievers. Am J Vet Res 2002;63:816820.

    • Search Google Scholar
    • Export Citation
  • 38

    Andelfinger G, Wright KN & Lee HS, et al. Canine tricuspid valve malformation, a model of human Ebstein's anomaly, maps to dog chromosome 9. J Med Genet 2003;40:320324.

    • Search Google Scholar
    • Export Citation
  • 39

    Chetboul V, Tran D & Carlos C, et al. Congenital malformations of the tricuspid valve in domestic carnivores: a retrospective study of 50 cases. Schweiz Arch Tierheilkd 2004;146:265275.

    • Search Google Scholar
    • Export Citation
  • 40

    De La Fuente D, Sasyniuk B, Moe GK. Conduction through a narrow isthmus in isolated canine atrial tissue: a model of W-P-W syndrome. Circulation 1971;44:803809.

    • Search Google Scholar
    • Export Citation
  • 41

    Wright KN, Hines DA, Bright JM. Cardiac electrophysiologic measurements in dogs before and after intravenous administration of atropine and propranolol. Am J Vet Res 1996;57:16951701.

    • Search Google Scholar
    • Export Citation
  • 42

    Rinne C, Klein GJ & Sharma AD, et al. Relation between clinical presentation and induced arrhythmias in the Wolff-Parkinson-White syndrome. Am J Cardiol 1987;60:576579.

    • Search Google Scholar
    • Export Citation
  • 43

    Fujimura O, Klein GJ & Yee R, et al. Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway? J Am Coll Cardiol 1990;15:10821086.

    • Search Google Scholar
    • Export Citation
  • 44

    Allessie MA, Konigs K & Kirchhof C, et al. Electrophysiologic mechanism of perpetuation of atrial fibrillation. Am J Cardiol 1996;77:10A23A.

  • 45

    Della Bella P, Brugada P & Talajic M, et al. Atrial fibrillation in patients with an accessory pathway: importance of the conduction properties of the accessory pathway. J Am Coll Cardiol 1991;17:13521356.

    • Search Google Scholar
    • Export Citation
  • 46

    Wathen M, Natale A & Wolfe K, et al. Initiation of atrial fibrillation in the Wolff-Parkinson-White syndrome: the importance of the accessory pathway. Am Heart J 1993;125:753759.

    • Search Google Scholar
    • Export Citation
  • 47

    Svinarich JT, Tai DY & Mickelson J, et al. Electrophysiologic demonstration of concealed conduction in anomalous atrioventricular bypass tracts. J Am Coll Cardiol 1985;5:898903.

    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Ventrodorsal oblique (30° left of sagittal plane) fluoroscopic view of the thorax of a dog obtained during endocardial mapping of a right posteroseptal accessory pathway. A decapolar catheter (1) inserted through the right external jugular vein into the coronary sinus was used to record from the ostium (CSp) to the distal part of the vein (CSd), and a quadripolar catheter (2) inserted through the right femoral vein was used to record His bundle potentials (H). An ablation catheter (3) was inserted through the right femoral vein and advanced to the posteroseptal area of the tricuspid annulus (PS).

  • Figure 2—

    Surface and intracardiac ECG recordings obtained from a dog during mapping of the right posteroseptal area of the tricuspid valve annulus. Recordings displayed include leads I, II, III, V1, and V6 of the surface ECG and intracardiac recordings from the distal to proximal portion of the coronary sinus (CSd, CS2, CS3, CS4, and CSp), the distal and proximal portions of the His bundle (Hbed and Hbep), and the distal and proximal portions of the posteroseptal area (Abld and Ablp) and a unipolar recording (Unip). Notice the sequence of ventricular (V) and atrial (A) activation in the various leads during orthodromic atrioventricular reciprocating tachycardia. A shorter ventricular-atrial interval was seen in recordings from the coronary ostium (CSp) and posteroseptal area (Abld), with a sharp, negative deflection in the unipolar recording (A). Findings were diagnostic for eccentric ventricularatrial activation compatible with the presence of a posteroseptal AP. H = His bundle potential.

  • Figure 3—

    Surface and intracardiac ECG recordings obtained from a dog during radiofrequency catheter ablation of a right free wall AP (RF). Ablation was performed during a period of orthodromic atrioventricular reciprocating tachycardia (OAVRT). After 3.28 seconds of energy delivery, tachycardia stopped and was replaced by a sinus rhythm. Notice the sequence of ventricular (V) and atrial (A) activation during tachycardia and the abolition of retrograde conduction along the accessory pathways (V not followed by A). See Figure 2 for key.

  • Figure 4—

    Gross anatomical section at the atrioventricular groove revealing the anatomic distribution of 15 accessory pathways in 10 dogs that underwent radiofrequency catheter ablation for symptomatic tachyarrhythmias. P.T. = Pulmonary trunk. M.V.A. = Mitral valve annulus. T.V.A. = Tricuspid valve annulus. F.O. = Fossa ovalis. C.S. = Coronary sinus ostium.

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    • Search Google Scholar
    • Export Citation
  • 21

    Murdock CJ, Leitch JW & Wee SI, et al. Characteristic of accessory pathways exhibiting decremental conduction. Am J Cardiol 1991;67:506510.

  • 22

    Tonkin AM, Miller HC & Svenson RH, et al. Refractory periods of the accessory pathway in the Wolff-Parkinson-White syndrome. Circulation 1975;52:563569.

    • Search Google Scholar
    • Export Citation
  • 23

    Scherlag BJ, Wang X & Nakagawa H, et al. Radiofrequency ablation of a concealed accessory pathway as treatment for incessant supraventricular tachycardia in a dog. J Am Vet Med Assoc 1993;203:11471152.

    • Search Google Scholar
    • Export Citation
  • 24

    Atkins CE, Kanter R & Wright K, et al. Orthodromic reciprocating tachycardia and heart failure in a dog with a concealed posteroseptal accessory pathway. J Vet Intern Med 1995;9:4349.

    • Search Google Scholar
    • Export Citation
  • 25

    Wright KN, Mehdirad AA & Giacobbe P, et al. Radiofrequency catheter ablation of atrioventricular accessory pathways in 3 dogs with subsequent resolution of tachycardia-induced cardiomyopathy. J Vet Intern Med 1999;13:361371.

    • Search Google Scholar
    • Export Citation
  • 26

    Santilli RA, Spadacini G & Moretti P, et al. Radiofrequency catheter ablation of concealed accessory pathways in two dogs with symptomatic atrioventricular reciprocating tachycardia. J Vet Cardiol 2006;8:157165.

    • Search Google Scholar
    • Export Citation
  • 27

    Patterson DF, Detweiler DK & Hubben K, et al. Spontaneous abnormal cardiac arrhythmias and conduction disturbances in the dog. A clinical and pathologic study of 3,000 dogs. Am J Vet Res 1961;22:355369.

    • Search Google Scholar
    • Export Citation
  • 28

    Hills BL, Tilley LP. Ventricular preexcitation in seven dogs and nine cats. J Am Vet Med Assoc 1985;187:10261031.

  • 29

    Drazner FH. ECG of the month. J Am Vet Med Assoc 1979;175:169170.

  • 30

    Atkins CE, Cali JV, Lombardo PS. ECG of the month. J Am Vet Med Assoc 1994;205:983984.

  • 31

    Wright KN, Atkins CE, Kanter R. Supraventricular tachycardia in four young dogs. J Am Vet Med Assoc 1996;208:7580.

  • 32

    Santilli RA, Bussadori C. Orthodromic incessant atrioventricular reciprocating tachycardia in a dog. J Vet Cardiol 2000;2:2327.

  • 33

    Tidholm A. ECG of the month. J Am Vet Med Assoc 1984;184:154155.

  • 34

    Vit P. ECG of the month. J Am Vet Med Assoc 1985;187:584585.

  • 35

    Miller MW, Bonagura JD, DiBartola SP. ECG of the month. J Am Vet Med Assoc 1988;192:336337.

  • 36

    Lamb WA, Snyder PS. ECG of the month. J Am Vet Med Assoc 1994;204:728730.

  • 37

    Famula TR, Siemens LM & Davidson AP, et al. Evaluation of the genetic basis of tricuspid valve dysplasia in Labrador Retrievers. Am J Vet Res 2002;63:816820.

    • Search Google Scholar
    • Export Citation
  • 38

    Andelfinger G, Wright KN & Lee HS, et al. Canine tricuspid valve malformation, a model of human Ebstein's anomaly, maps to dog chromosome 9. J Med Genet 2003;40:320324.

    • Search Google Scholar
    • Export Citation
  • 39

    Chetboul V, Tran D & Carlos C, et al. Congenital malformations of the tricuspid valve in domestic carnivores: a retrospective study of 50 cases. Schweiz Arch Tierheilkd 2004;146:265275.

    • Search Google Scholar
    • Export Citation
  • 40

    De La Fuente D, Sasyniuk B, Moe GK. Conduction through a narrow isthmus in isolated canine atrial tissue: a model of W-P-W syndrome. Circulation 1971;44:803809.

    • Search Google Scholar
    • Export Citation
  • 41

    Wright KN, Hines DA, Bright JM. Cardiac electrophysiologic measurements in dogs before and after intravenous administration of atropine and propranolol. Am J Vet Res 1996;57:16951701.

    • Search Google Scholar
    • Export Citation
  • 42

    Rinne C, Klein GJ & Sharma AD, et al. Relation between clinical presentation and induced arrhythmias in the Wolff-Parkinson-White syndrome. Am J Cardiol 1987;60:576579.

    • Search Google Scholar
    • Export Citation
  • 43

    Fujimura O, Klein GJ & Yee R, et al. Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway? J Am Coll Cardiol 1990;15:10821086.

    • Search Google Scholar
    • Export Citation
  • 44

    Allessie MA, Konigs K & Kirchhof C, et al. Electrophysiologic mechanism of perpetuation of atrial fibrillation. Am J Cardiol 1996;77:10A23A.

  • 45

    Della Bella P, Brugada P & Talajic M, et al. Atrial fibrillation in patients with an accessory pathway: importance of the conduction properties of the accessory pathway. J Am Coll Cardiol 1991;17:13521356.

    • Search Google Scholar
    • Export Citation
  • 46

    Wathen M, Natale A & Wolfe K, et al. Initiation of atrial fibrillation in the Wolff-Parkinson-White syndrome: the importance of the accessory pathway. Am Heart J 1993;125:753759.

    • Search Google Scholar
    • Export Citation
  • 47

    Svinarich JT, Tai DY & Mickelson J, et al. Electrophysiologic demonstration of concealed conduction in anomalous atrioventricular bypass tracts. J Am Coll Cardiol 1985;5:898903.

    • Search Google Scholar
    • Export Citation

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