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Keywords:

  • Arrhythmias;
  • Atrial tachycardia;
  • Cardiology;
  • Dog

Abstract

  1. Top of page
  2. Abstract
  3. Material and Methods
  4. Results
  5. Discussion
  6. Footnotes
  7. Acknowledgments
  8. References

Background: Focal atrial tachycardia (FAT) is a common supraventricular tachycardia in dogs.

Objective: To evaluate electrophysiologic characteristics and topographic distribution of FAT.

Animals: Sixteen dogs with symptomatic FAT.

Methods: Retrospective case series. Electrophysiological studies were performed to test the inducibility of documented and no documented arrhythmias. Once induced for each dog, FAT was analyzed for electrogenic mechanism, endocardial electrogram, and location.

Results: Nineteen FATs could be studied in 16 dogs, 12 were automatic, 4 nonautomatic, and 3 incessant. Two dogs had >1 focus. Mean atrial cycle length (CL) was 238.2 ± 69.2 (SD) milliseconds, mean ventricular CL of 292.7 ± 72.5 (SD) milliseconds, with atrioventricular block in 6 cases. Mean presystolic atrial activity recorded at the ectopic focus was –39.9 ± 17.7 (SD) milliseconds. Atrial potentials were fragmented in 11 dogs and were low amplitude in 6 dogs. Sixty-three percent of ectopic foci were distributed within the right atrium (5 crista terminalis, 3 triangle of Koch, 2 tricuspid valve annulus, 1 interatrial septum, and 1 right auricle) and 37% in the pulmonary veins (PVs) (4 right superior PV, 2 left superior PV, and 1 right inferior PV). Persistent atrial fibrillation (AF) and paroxysmal AF were triggered by FATs in 7 dogs (2 with multiple ectopic foci and 4 with at least one PV focus).

Conclusion and Clinical Relevance: According to our findings, dogs have a predominance of right-sided FAT. The majority of FATs are automatic and can trigger AF, particularly in the case of PV location.

Abbreviation:
CL

cycle length

CS

coronary sinus

FAT

focal atrial tachycardia

PV

pulmonary veins

RFCA

radiofrequency catheter ablation

SVT

supraventricular tachycardia

TICM

tachycardia-induced cardiomyopathy

Focal atrial tachycardia (FAT) is defined as an atrial activation starting rhythmically at a small area (focus) from which it spreads out centrifugally and without activation over an important portion of the cycle length (CL).1 In people FAT is relatively rare, with a reported prevalence of 0.34% in young asymptomatic patients and 0.46% in symptomatic individuals, with a spontaneous remission rate of 24–63%.2 Sixty-three percent of patients with FAT have left ventricular dysfunction and, of these, 73% have tachycardia-induced cardiomyopathy (TICM).3

FAT exhibits a wide range of electrophysiologic features that reflects at least 3 underlying electrogenic mechanisms: abnormal automaticity, triggered activity, and micro-reentry.4–6 FAT caused by triggered activity and micro-reentry have been also named nonautomatic FAT.7

In people 63% of FATs are right-sided, while the remaining 37% arise from the left atrium wall or tributary veins.8 FAT present a characteristic anatomic distribution with typical clustering around the crista terminalis (21%), the coronary sinus (CS) ostium and body (10%), the para-hissian region (5%), the tricuspid annulus (13–22%), the mitral annulus (28–36%), the pulmonary veins (PVs) (24%), the right interatrial septum (0.8%), the left interatrial septum (2%), and less commonly around the right and left appendages, the superior vena cava and the noncoronary aortic cusp.9–23

Four to 17% of patients with FATs presented >1 focus, and with the most common combinations being 2 sites in the right free wall (29.5%) and right free wall and right septal area (15.9%).24–25 Individuals with multiple ectopic foci revealed cardiovascular comorbidity, shortest tachycardia CL, and lower success rate of radio-frequency catheter ablation (RFCA).25

The aim of our study was to characterize FAT in a group of dogs that underwent detailed endocardial mapping, evaluate the arrhythmic substrate, and analyze the topographic distribution of ectopic foci.

Material and Methods

  1. Top of page
  2. Abstract
  3. Material and Methods
  4. Results
  5. Discussion
  6. Footnotes
  7. Acknowledgments
  8. References

Study Population

The case records of 16 dogs with supraventricular tachycardia (SVT), which had undergone electrophysiologic evaluation at Clinica Veterinaria Malpensa during a research project lasted from January 2005 to August 2008, were retrospectively reviewed. The 16 dogs included 2 Labrador Retrievers, 2 Rottweilers, 2 Boxers, 2 Dogue de Bordeaux, 2 Newfoundlands, 1 mongrel, 1 Pug, 1 Neapolitan Mastiff, 1 Bull Mastiff, 1 Bull Terrier, and 1 Bernese Mountain Dog. Thirteen dogs were males with a median age of 51 months (range 5–156 months) and a mean body weight of 33 ± 17.4 kg (72.6 ± 38.3 lb). Each dog underwent a physical examination, 12-lead surface ECG, thoracic radiographs, standard echocardiography, and electrophysiologic study.

Thirteen dogs were presented for episodic weakness because of SVT, 3 dogs for clinical signs of congestive heart failure. Nine dogs were receiving medical treatment before referral: 2 received metoprolol (0.25 mg/kg [0.11 mg/lb] PO q12 h), 1 quinidine (6 mg/kg [2.7 mg/lb] PO q8 h), 1 amiodarone (10 mg/kg [4.5 mg/lb] PO q12 h), 1 sotalol (0.5 mg/kg [0.22 mg/lb] PO q12 h), 1 propranolol (0.09 mg/kg [0,04 mg/lb] PO q8 h), 1 digoxin (0.0025 mg/kg [0.0011 mg/lb] PO q12 h), 1 amiodarone (10 mg/kg [4.5 mg/lb] PO q12 h) in combination with propranolol (0.09 mg/kg [mg/lb] PO q8 h), and 1 sotalol (0.5 mg/kg [0.22 mg/lb] PO q12 h) in combination with digoxin (0.0025 mg/kg [mg/lb] PO q12 h). At presentation, 4 dogs had an ECG rhythm compatible with persistent atrial fibrillation (AF), 3 dogs with incessant narrow QRS complex tachycardia, and 9 with normal sinus rhythm. Radiographic and echocardiographic findings were unremarkable in 12 dogs; they were diagnostic for TICM in 3 dogs, and for chronic valvular disease in 1 dog.

Interventional Procedure

Electrophysiological studies were performed under general anesthesia as previously described,26 after discontinuing antiarrhythmic drugs for at least 5 drug half-lives.27 Dogs were placed in dorsal recumbency and venous accesses were obtained by modified Seldinger technique. Under fluoroscopic and intracardiac ECG guidance, one multipolar electrode cathetera was inserted through the right external jugular vein into the CS. A 2nd decapolar electrode cathetera was inserted through the right femoral vein and placed around the tricuspid valve annulus to record with the proximal electrodes pairs the potentials of the antero-lateral aspect of the crista terminalis (high right atrium), with the middle pairs the potentials of the middle lateral right atrium (medium right atrium), and with the distal pairs the potentials of the low postero-lateral right atrium (low right atrium) (Fig 1A). A 7-F ablation catheter, 8 mm, with deflectable curveb was advanced through the right femoral vein and placed alternatively at the His bundle, right ventricle and different area of right atrial wall to map endocavitary electrograms and to perform programmed stimulation.

image

Figure 1.  (A) Ventro-dorsal oblique (30° left of the sagittal plane) fluoroscopic view of the thorax of a dog obtained during endocardial mapping of a coronary sinus ostium atrial tachycardia. 1, Coronary sinus decapolar electrode catheter; 2, ablation catheter mapping coronary ostium area; 3, right atrial decapolar electrode catheter. HRA, high right atrium; MRA, middle right atrium; LRA, low right atrium; CSp, coronary sinus proximal; CSd, coronary sinus distal; AT5, coronary sinus ostium. (B) Ventro-dorsal oblique (30° left of the sagittal plane) fluoroscopic view of the thorax of a dog obtained during endocardial mapping of a left superior pulmonary vein atrial tachycardia. 1, Coronary sinus decapolar electrode catheter; 2, ablation catheter mapping left auricle; 3, lasso decapolar circular catheter mapping left superior pulmonary vein. LAu, left appendage; LSPV, left superior pulmonary vein.

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To map left atrial wall or PV ectopic foci, a transeptal puncture was proposed to the owner and performed by the technique introduced in 1960 by Brockenbrough.28 From the right femoral vein, under fluoroscopic guidance, a specially designed guide wirec inserted into the transeptal needled was placed across the fossa ovalis into the left atrium. The movement of the tip of the needle, which resembles a “jump” from the thicker muscular septum to the thin wall of the fossa ovalis, was the indirect radiological sign of the position of the fossa ovalis. Once the wire was into the left atrium, the dedicated needle was pushed across the interatrial septum to produce a larger hole, then an introducer set was left in place and used to guide the mapping and the ablation catheters.28,29 A Lasso cathetere was used to map PV ostia, while an ablation catheterb to map ectopic foci at the left atrial wall, the PVs, and the left appendage (Fig 1B). In case the owner denied the transeptal puncture, left atrial tachycardias, particularly FATs originating from right superior PV, were identified throughout the analysis of double potentials recorded at the high posterior right atrium.22 During tachycardia, if the amplitude of the 1st potential was greater than that of the 2nd potential, this indicated a right posterior atrial focus; in the opposite case a right superior PV focus was diagnosed.22

Twelve leads ECG and intracardiac signals were displayed and analyzed with an EP recorderf at paper speed of 100 or 200 mm/s. The intracardiac electrograms were recorded at filter setting of 50–500 Hz. Pacing was performed using stimuli that were twice diastolic threshold and 2 ms in duration.

During basal state, antegrade and retrograde atrioventricular (AV) conduction times were recorded. Programmed atrial and ventricular stimulation, bursts atrial pacing, and isoproterenol hydrochloride 0.04–0.1 μg/kg/min IV constant rate infusion were used to test inducibility of documented and no documented arrhythmias and to verify arrhythmogenic mechanism.

Entrainment of the tachycardia circuit was used to differentiate reciprocating tachycardia from FAT. After overdrive atrial pacing from the CS area during tachycardia the presence of variable (>10 ms from baseline) ventricular-atrial interval after pacing was considered diagnostic for FAT,4,30 Re-entrant atrial tachycardias were defined by entrainment with concealed fusion. Pacing 10–20 ms faster than the atrial tachycardia at a site with presystolic activity or mid-diastolic potential can entrain a re-entrant tachycardia to the pacing rate without changing the morphology of P wave or the intracardiac electrograms sequence. Pacing in a dead-end site was excluded if the postpacing interval at the termination of concealed entrainment was identical to tachycardia CL.4,31

We defined the electrogenic mechanism as abnormal automaticity in case the tachycardia could be initiated only with isoproterenol infusion, there was no effect of programmed stimulation neither on initiation nor on termination of the tachycardia, and when a transient suppression of the tachycardia with overdrive pacing was obtained. We considered the electrogenic mechanism nonautomatic when the initiation of the tachycardia was reproducible with incremental atrial pacing, programmed atrial pacing, or burst atrial pacing.4,32

The atrial ectopic foci were localized as the site of earliest presystolic activity relative to the onset of the P wave during tachycardia (usually >20–30 ms) where sharp and negative unipolar recording, with QS pattern, appeared4,33 (Fig 2A–D).

image

Figure 2.  Surface and intracardiac ECG obtained from 4 dogs during mapping of a left superior pulmonary vein focus (A), of a coronary sinus ostium focus (B), of a posterior tricuspid valve annulus focus (C), and of a crista terminalis focus (D). Recordings displayed include in all dogs lead I, II, III, V1, V6 of the surface ECG and intracardiac recordings from the distal to the proximal portion of the coronary sinus (CSp and CSd), from the distal to the proximal portion of the different atrial ectopic foci (ABLd and ABLp) and a unipolar recording (unip); and intracardiac recording from the distal to the proximal cristal terminalis area (hrad and hrap) in dog A, from the high right atrial wall, through the medium to the low posterior right atrial wall (HRA1, HRA2, MRA, LRA1) in dog B, and from the distal to the proximal His bundle area (HBED and HBEp) in dogs C and D. Note the presystolic, fractioned potential at atrial potential (A) recorded with the distal pairs of the ablation catheter and sharp and negative with QS morphology of atrial potential of unipolar recording at target area. A, atrial potential; V, ventricular potential; H, His potential.

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When there was difficulty determining the onset of P wave, delivery of a ventricular extra-stimulus permitted advanced ventricular activation and depolarization and the distinction of ectopic P wave.34 Mechanical interruption caused by application of pressure to the focus and the presence of fragmented, long duration, low amplitude electrograms were considered other diagnostic tools for the identification of the site of origin of FAT. Fractioned potential consisted of 3 or more consecutive negative deflections with low peak-to-peak amplitude (Fig 2A–D).35,36

The presence of disorganized atrial activity, characterized by irregular f waves with variable voltage, was considered diagnostic for AF.34 When AF was already present or induced during the study, transthoracic electrical cardioversion with bipolar shock was used to restore sinus rhythm.

Results

  1. Top of page
  2. Abstract
  3. Material and Methods
  4. Results
  5. Discussion
  6. Footnotes
  7. Acknowledgments
  8. References

Nineteen FAT could be studied in 16 dogs, 12 were induced with isoproterenol infusion, 4 with bursts atrial pacing, while 3 were incessant. Two dogs presented >1 focus, the 1st dog had 1 focus along the crista terminalis, the posterior tricuspid valve annulus, and the right superior PV; the 2nd dog had 1 focus in the right superior PV and the right inferior PV. The 4 dogs with persistent AF responded to biphasic electrical cardioversion; sinus rhythm was restored in 3 of these dogs, while the 4th showed sustained focal junctional tachycardia after cardioversion, followed by FAT as soon as isoproterenol infusion was started. According to the induction mode we classified the tachycardia electrogenic mechanism as abnormal automaticity in 12 dogs, and as nonautomatic in 4 dogs.

Induced FAT presented a mean atrial CL of 238.2 ± 69.2 ms (mean ± SD) and a mean ventricular CL of 292.7 ± 72.5 ms (mean ± SD). Six tachycardias were conducted with different degree of AV block (4 with 2 : 1 2nd degree AV block, 1 with 3 : 1 2nd degree AV block, and 1 with variable degree AV block).

To map left-sided FATs transeptal puncture was performed in 3 cases, while endocardial mapping of right posterior atrial wall was performed in 4 cases. During endocardial mapping of ectopic foci mean presystolic atrial activity measured was –39.9 ± 17.7 ms. (mean ± SD), and atrial potentials were fragmented in 11 cases with low amplitude in 6 cases.

Ectopic foci were distributed within the right atrium in 63% of the cases (5 crista terminalis, 3 triangle of Koch, 2 tricuspid valve annulus, 1 interatrial septum, and 1 right auricle) and into the PVs in 37% of cases (4 right superior PV, 2 left superior PV, and 1 right inferior PV) (Fig 3). One dog with persistent AF presented 3 concomitant ectopic foci (1 focus along the crista terminalis, 1 in the posterior tricuspid valve annulus, and 1 in the right superior PV), the remaining 3 dogs had 1 focus at the apex of the triangle of Koch, at the area of the crista terminalis, and left superior PV, respectively.

image

Figure 3.  Gross anatomical section of right and left atrium and tributary veins showing the topographic distribution of 19 atrial ectopic foci (circles) in 16 dogs with symptomatic focal atrial tachycardias. Rau, right auricle; SVC, superior or cranial vena cava; SVCO, superior or cranial vena cava ostium; CT, crista terminalis; IAS, interatrial septum; FO, fossa ovalis; IVCO, inferior or caudal vena cava ostium; CSO, coronary sinus ostium; TV, tricuspid valve leaflet; IVC, inferior or caudal vena cava; LAu, left auricle; LSPV, left superior pulmonary veins; LIPV, left inferior pulmonary veins; RSPV, right superior pulmonary veins; RIPV, right inferior pulmonary veins; MV, mitral valve leaflet; CSB, coronary sinus body.

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Paroxysomal AF was triggered by automatic FATs in 3 cases and by a nonautomatic FAT in 1 case. All these dogs had only documented SVT and atrial foci were located, respectively, into the right superior PV, into the right superior and right inferior PV, at the CS ostium and the posterior tricuspid valve annulus.

Discussion

  1. Top of page
  2. Abstract
  3. Material and Methods
  4. Results
  5. Discussion
  6. Footnotes
  7. Acknowledgments
  8. References

In this study, we analyzed 19 FATs in 16 dogs that underwent electrophysiological examination for documented SVT. Similarly, the 1st onset of clinical signs related to FAT is commonly found in the 1st part of the life in human beings (10 and 40 years), which is consistent with the age of the dogs in this report.37 FATs induced left ventricular dysfunction in 63% of human patients, 73% of which had TICM. In the latter group of patients FATs are caused in 80% of the cases by abnormal automaticity.3 We found TICM in 4 dogs (21%), 2 of which were caused by abnormal automaticity. In our opinion the difference in the occurrence of TICM found in our population of dogs, when compared with human beings, can be because of the small number of dogs studied, because ventricular rate of FATs observed in this study ranged between 164 and 270 bpm and was higher than the one reported in people (130–240 bpm).4,8,36,38–41

The mechanism of FAT can be determined by the induction mode.4–6 Reported incidence of FATs caused by abnormal automaticity in people ranges between 7 and 16%, while nonautomatic FATs ranged between 4 and 20%.4,38,40 The majority of tachycardias (63%) of the present case series were considered automatic because they were inducible only under isoproterenol infusion, while a minority of cases (21%) had a reproducible induction with burst atrial pacing, a characteristic response of both micro-reentry and triggered activity.4 We could not differentiate FATs caused by micro-reentry from tachycardias caused by triggered activity because of the overlap to the response of the entrainment, the lack of the analysis of the monophasic action potential and the difficulty to verify the achievement of a reproducible Cl of atrial pacing before the onset of FAT.4,38,40

In all tachycardias recorded we could exclude atrial macro-reentry because of the presence of an important portion of the CL (isoelectric interval on the surface ECG) without electrical activation, the presence of presystolic atrial activation with often fragmented and low amplitude potentials and the impossibility to entrain the AT from 2 sites >2 cm apart.1,4,33,35

Different degree of AV block, mainly 2 : 1, which did not affect the tachycardia, was found in 6 out of 19 cases. This feature is considered a further diagnostic criterion of FAT in people.40–41

The site of origin of tachycardia was identified through the endocardial mapping of right atrium, left atrium, and tributary veins searching for the site of earliest presystolic activity relative to the onset of the P wave during tachycardia, where sharp and negative unipolar electrograms with QS morphology could be recorded.4,33 In our group of dogs the mean distance between the beginning of atrial activation and the onset of the P wave was –39.9 ± 17.7 ms. The result was similar to the same measure in people (−21 and −51 ms).4,7,15,36,38–43 The presence of negative unipolar recordings with QS configuration was associated with a correct identification of the target site of successful ablation, with a reported acute success rate of 86%.33,40 In our study, all target areas for ablation presented this unipolar deflection morphology.

The areas where FATs arise are characterized by fractioned electrograms that could reflect localized slowing of atrial conduction caused by a poorly coupled automatic focus or small reentrant circuit.15,35,43 We recorded fractioned electrograms in more than half of the tachycardia examined with low peak-to-peak amplitude in 1 of the 3 of them.

We could perform left atrial and PV mapping after transeptal puncture in 3 dogs, while in 4 dogs we identified right PV potentials revealed by double potentials recordable at the high posterior right atrium.22 Tachycardias arising from the posterior wall of the right atrium and right PVs present similar electrophysiologic characteristics because they are anatomically located contiguously to each other. The double potentials are caused by biatrial electrical activation and according to the amplitude of the 1st or 2nd deflection a posterior right atrial or right superior PV focus can be differentiated.22 The limitation of this technique is that the electrophysiologic features of FATs arising from the posterior right atrial wall near the atrial septum and those arising from the right inferior PV are not yet known.

The topographic distribution of atrial ectopic foci found in the present study is similar to the one reported in people, where 63% of the tachycardias arise from the right atrium and 37% from the left atrium.8 In our case series 63% of FAT arose from the right atrium and 37% from the left atrium. In humans, atrial ectopic foci cluster most commonly around the crista terminalis, the tricuspid valve annulus, the CS ostium, peri-nodal area, into the PVs and around the mitral annulus, and less commonly at the right and left interatrial septum, right and left appendages, superior vena cava, and noncoronary aortic cusp.9–23 Similarly, in our study FAT arose from the crista terminalis, the triangle of Koch area, the tricuspid valve annulus, and the PVs, mainly superiors.

In human literature 4–17% of patients with FATs and >1 focus revealed cardiovascular comorbidity, faster tachycardias, and lower RFCA success rate.24–25 We found in 2 dogs multiple foci localized at the right atrial wall and the PV in 1 case and into the right superior and right inferior PVs in the 2nd case. One of these dogs had TICM and persistent AF and the other had an unsuccessful ablation.

Spontaneous initiation of AF by ectopic beats originating in the PVs is described in people.23 The left atrial wall continues into the PVs as muscular sleeves with a mean extent of 13 mm and maximal extent of 25 mm.44 The longest sleeves have been found in the superior PVs, and this anatomic pattern correlates with the relative distribution of the PV foci in people23 and found in dogs in our case series. The ostium and the 1st part of the PVs present a sudden change in fiber orientation with area of slow conduction and fractioned signals.45 In human patients with paroxysmal AF, shorter PV effective and functional refractory periods were noted, that together with a decremental conduction between PVs and left atrium and slow conduction into the PVs facilitated re-entry.46 Several studies have suggested that both abnormal automaticity and triggered activity in the PVs, either alone or in combination with a re-entrant mechanism may play a role in the initiation of AF.47

We identified persistent AF and paroxysmal AF triggered by FATs in 7 dogs, 2 of which had multiple ectopic foci and 4 of which had at least 1 PV focus.

Footnotes

  1. Top of page
  2. Abstract
  3. Material and Methods
  4. Results
  5. Discussion
  6. Footnotes
  7. Acknowledgments
  8. References

aPolaris X, 7F, 2/5/2, Boston Scientific Corp, Genova, Italy

bPolaris C, 4 mm, 7F; Boston Scientific Corp

cTS guidewire, Safe Set, SS120, Mennen Medical, Manta, Genova, Italy

dAngled needle 71 cm, 1.02 mm – St Jude Medical Italia SpA, Agrate Brianza, Milano, Italy

eLasso decapolar circular catheter, Biosense, Webster, Milano, Italy

fEMS, 16 channels, Mennen Medical

Acknowledgments

  1. Top of page
  2. Abstract
  3. Material and Methods
  4. Results
  5. Discussion
  6. Footnotes
  7. Acknowledgments
  8. References

The authors thank Dr Heidi Cooper and Luca Ferasin for reviewing the manuscript and Dr Luca Pirovini for gross pathology specimen.

References

  1. Top of page
  2. Abstract
  3. Material and Methods
  4. Results
  5. Discussion
  6. Footnotes
  7. Acknowledgments
  8. References
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