Introduction
A 13-year-old 6.1-kg neutered female Lhasa Apso was referred to a veterinary teaching hospital for investigation of dyspnea and episodes of syncope over the preceding 7 days. The patient’s history included weight loss, inappetence, coughing, and fatigue of 3 months’ duration. The referring veterinarian had previously made a diagnosis of stage D myxomatous mitral valve disease, and the dog had been treated with furosemide, benazepril, spironolactone, pimobendan, and sildenafil for 1 year. Physical examination of the dog revealed a respiratory rate of 60 breaths/min, heart rate of 120 beats/min, systolic blood pressure of 110 mm Hg, pale mucous membranes, capillary refill time of 2 seconds, and rectal temperature of 39.0 °C. Cardiac auscultation revealed a grade 6/6 holosystolic murmur over the left and right cardiac apex, and bilateral pulmonary crackles were noted on pulmonary auscultation. The dog was hospitalized and provided with lactated Ringer solution (240 mL/24 h, IV) and oxygen therapy. Furosemide was administered (bolus of 4 mg/kg, IV; followed by repeated doses of 3 mg/kg, IV, q 12 h) along with pimobendan (0.3 mg/kg, PO, q 8 h), sildenafil (0.75 mg/kg, PO, q 8 h), benazepril (0.42 mg/kg, PO, q 24 h), spironolactone (3.12 mg/kg, PO, q 24 h), and amoxicillin–clavulanic acid (8.3 mg/kg, PO, q 12 h).
Blood samples were collected for laboratory analyses. Results of a CBC were within reference intervals. The only abnormalities identified by serum biochemical analysis were high concentrations of creatinine (2.2 mg/dL; reference range, 0.5 to 1.5 mg/dL) and BUN (181.4 mg/dL; reference range, 21 to 60 mg/dL) and a high activity of alkaline phosphatase (352.5 U/L; reference range, 20 to 156 U/L). Generalized cardiomegaly was evident on thoracic radiographic views, along with marked left atrium enlargement, bulging of the left heart border, and areas of pulmonary opacification suggestive of pulmonary edema. Two-dimensional echocardiography revealed thickened mitral and tricuspid valve leaflets, mitral valve prolapse, severely high left atrium-to-aorta ratio (2.9; reference limit, 1.4), and dilation of the pulmonary veins. The Doppler ultrasonographic examination findings confirmed mitral and tricuspid valve insufficiency, a high ratio of early-to-late transmitral flow peak velocities (2.7; reference range, 1.18 to 1.89), decreased ratio of early-to-late diastolic mitral annular motion (0.7; reference limit, > 1), and an increased E-to-isovolumic relaxation time ratio (3.6; values associated with myxomatous mitral valve disease are typically < 2.5), which suggested increased filling pressures. Systolic pulmonary artery pressure was 55 mm Hg, indicating moderate pulmonary hypertension. Subsequently, an ECG was recorded, and because of documented alterations, 24-hour Holter monitoring of the dog was requested.
ECG Interpretation
Ten-lead ECG revealed sinus rhythm, a mean heart rate of 142 beats/min, and an electrical axis of +60° (reference range, +40° to +100°). However, there was an increase in both amplitude (0.41 mV; reference range, ≤ 0.40 mV) and duration (47 milliseconds; reference range, ≤ 40 milliseconds) of P waves, which suggested biatrial overload or atrial conduction delay attributable to atrial fibrosis (Figure 1). The 24-hour Holter examination revealed maximum, mean, and minimum heart rates of 255, 138, and 56 beats/min, respectively. There was a total of 31,353 supraventricular events, including 179 isolated atrial ectopic beats and 319 episodes of supraventricular tachycardia (SVT). Also, 23 polymorphic isolated ventricular ectopic beats (VEBs) as well as a single sinus arrest event of 2.3 seconds’ duration were documented. There were long-lasting episodes of SVT characterized by narrow QRS complexes and regular R-R intervals accompanied by a VEB that did not alter the course of the SVT (Figure 2). The longest supraventricular event was sustained SVT of 42 minutes’ duration (heart rate, 210 to 255 beats/min) with narrow QRS complexes, regular R-R intervals, short RP intervals (60 milliseconds), long PR intervals (210 milliseconds), and a small RP:PR ratio (0.28). This SVT ended spontaneously and was followed by a pause, after which a P wave emerged followed by a wide and bizarre QRS complex with a negative T wave (PR interval, 120 milliseconds). Next, a narrow QRS complex was recorded, and sinus rhythm resumed. All following sinus beats also had a PR interval of 120 milliseconds (Figure 3). Unfortunately, the dog died 1 day after the Holter examination.
Portions of an initial 10-lead ECG recorded from a Lhasa Apso that was evaluated because of a 7-day period of dyspnea and episodes of syncope. The dog had a history of weight loss, inappetence, coughing, and fatigue of 3 months’ duration; stage D myxomatous mitral valve disease had previously been diagnosed. In these traces, there is sinus rhythm and a mean electrical axis +60°. The amplitude (0.41 mV; reference interval, ≤ 0.40 mV) and duration (47 milliseconds; reference interval, ≤ 45 milliseconds) of the P waves suggest biatrial overload or atrial conduction delay due to atrial fibrosis. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 259, 7; 10.2460/javma.259.7.732
Tracings obtained during 24-hour, 3-channel (C1, C2, and C3) Holter monitoring of the dog. Notice the episode of supraventricular tachycardia (SVT; 190 to 218 beats/min), which was not altered by the occurrence of an isolated ventricular ectopic beat (asterisk).
Citation: Journal of the American Veterinary Medical Association 259, 7; 10.2460/javma.259.7.732
Two-minute period of the 24-hour Holter recording. Notice that after a long-lasting episode of sustained SVT (210 to 255 beats/min), a beat with a wide QRS complex (asterisk) occurs and sinus rhythm resumes (dagger).
Citation: Journal of the American Veterinary Medical Association 259, 7; 10.2460/javma.259.7.732
Discussion
Supraventricular tachycardia encompasses a group of arrhythmias involving at least 1 supraventricular anatomic structure in their circuit, such as the atrium (focal atrial tachycardia [FAT]) and the atrioventricular junction (atrioventricular reciprocating tachycardia). In the case of atrioventricular reciprocating tachycardias, not only a supraventricular structure but also an extra nodal accessory pathway and the ventricular myocardium are involved.1,2 Orthodromic atrioventricular reciprocating tachycardia (OAVRT) and FAT in dogs have been reported.3,4 During the Holter monitoring of the dog of the present report, the longest duration of SVT (42 minutes) had ECG characteristics compatible with the presence of a retrograde atrioventricular conduction pathway, as in instances of OAVRT. Orthodromic atrioventricular reciprocating tachycardia develops when an electrical impulse circles antegrade through the atrioventricular node, activates the ventricles, and conducts retrogradely through the accessory pathway.5 Electrocardiographic characteristics of OAVRT are sudden initiation and termination of the tachycardia, narrow QRS complexes, a ventricular rate between 190 and 300 beats/min, and regular R-R intervals.2 This arrhythmia has been described in various dog breeds, including Labrador Retriever,6,7 Beagle,8 Boxer,9 English Bulldog,10,11 Dalmatian,12 and Brittany.10
In a previous study, Santilli et al1 established criteria to differentiate OAVRT from FAT in dogs on the basis of the analysis of 12-lead ECG traces. Those criteria are heart rate, presence of QRS alternans, superior P-wave axis in the frontal plane during tachycardia, RP interval, RP:PR ratio, and presence of repolarization anomalies. The fact that the dog of the present report had SVT recorded only during the period of Holter monitoring limited the interpretation of some ECG features. However, the dog’s heart rate, RP interval, RP:PR ratio, and cycle duration were more characteristic of OAVRT than FAT. Compared with findings for dogs with FAT, dogs with OAVRT usually have lower heart rates (OAVRT, 190 to 300 beats/min; FAT, 210 to 330 beats/min), a shorter RP interval (OAVRT, 68.2 to 101.8 milliseconds; FAT, 119.8 to 194.4 milliseconds), and a lower RP:PR ratio (OAVRT, 0.41 to 0.78 milliseconds; FAT, 0.93 to 1.97). In addition, irregularity of cycle duration is uncommon in dogs with OAVRT and more common in dogs with FAT.1 Furthermore, tachycardias in dogs with OAVRT may be ended by a ventricular premature beat that interrupts the reentry circuit,2 which is compatible with one of the differential diagnoses considered at the end of 42-minute-long period of SVT recorded by the Holter monitor for the dog of the present report.
For the dog of the present report, the wide and bizarre QRS complex at the end of the longest-lasting period of SVT was preceded by a P wave and had a PR interval of similar duration to those of sinus beats (Figure 3). The aberrant intraventricular conduction and fusion beat were proposed mechanisms for this ECG event (Figure 4). In medicine, a wide QRS complex at the end of paroxysmal SVT is not a rare phenomenon. It has been associated with ATP administration, esophageal pacing, calcium channel antagonist administration, vagal maneuvers, and administration of class Ia or Ic antiarrhythmic drugs.13 However, the wide QRS complex developed spontaneously in this dog.
Ladder diagram constructed from a portion of the 24-hour Holter recording in Figure 3 to illustrate 2 possible interpretations for the ventricular beat with a wide QRS complex at the end of the SVT. The SVT characteristics are compatible with orthodromic atrioventricular reciprocating tachycardia (OVART), and the 2 possible ventricular beat interpretations include a fusion beat and aberrant intraventricular conduction. As such, there are 2 possible combinations: OVART with an aberrant intraventricular conduction (1) or OVART with a fusion beat (2). In each ladder diagram, the upper zone represents atrial activation (A), the middle zone represents atrioventricular conduction (AV), and the lower zone represents ventricular activation (V). See Figure 3 for key.
Citation: Journal of the American Veterinary Medical Association 259, 7; 10.2460/javma.259.7.732
Fusion beats may occur in instances of ventricular parasystole, which is the state where 2 independent pacemakers compete for the activation of the ventricular myocardium.14 The Holter examination of the dog of the present report revealed some VEBs that did not modify the course of SVT and had highly variable coupling intervals, which are characteristics of parasystole.14 On the other hand, the lack of compensatory pause after the wide QRS complex documented for this dog is a feature of aberrant conduction. Aberrant conduction is a functional block of the ventricular conduction system that is usually preceded by a sudden change in heart frequency.15
Despite the fact that the dog of the present report underwent neither ECG nor a 24-hour Holter evaluation before the onset of cardiac disease, it was likely that SVT developed mainly as a consequence of marked left atrial dilation (LA:Ao ratio, 2.9) and postcapillary pulmonary hypertension. In fact, 65% of dogs with SVT have evidence of structural heart disease,16 whereas the prevalence is much lower in human patients.5
In ECG recordings, right and left atrial depolarization activity is represented by the P wave. Changes in the duration and amplitude of P waves may suggest changes in atrial pressure or volume overload.10 The dog of the present report had both increased P-wave duration and amplitude, which correlated with left atrial enlargement and tricuspid valve regurgitation with pulmonary hypertension, respectively. Nonetheless, depolarization delay secondary to atrial fibrosis may also explain an increase in P-wave measurements.17 Dogs with chronic postcapillary pulmonary hypertension develop myocardial atrophy and fibrosis and intramural artery narrowing, factors that predispose affected animals to the development of ventricular arrhythmias.18 Although the clinical course and final outcome vary for each patient, dogs with clinical signs of heart failure generally have a worse prognosis and increased risk of cardiac-related death secondary to development of severe left-sided chamber enlargement, congestive heart failure, and life-threatening arrhythmias.8,19,20
References
- 1. ↑
Santilli RA, Perego M, Crosara S, et al. Utility of 12‐lead electrocardiogram for differentiating paroxysmal supraventricular tachycardias in dogs. J Vet Intern Med 2008;22:915–923.
- 2. ↑
Santilli R, Moïse NS, Pariaut R, et al. Supraventricular tachycardias. In: Santilli R, Moïse NS, Pariaut R, et al, eds. Electrocardiography of the dog and cat: diagnosis of arrhythmias. 2nd ed. Trento, Italy: Edra SpA, 2019;145–189.
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Santilli RA, Perego M, Perini A, et al. Electrophysiologic characteristics and topographic distribution of focal atrial tachycardias in dogs. J Vet Intern Med 2010;24:539–545.
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Wright KN, Connor CE, Irvin HM, et al. Atrioventricular accessory pathways in 89 dogs: clinical features and outcome after radiofrequency catheter ablation. J Vet Intern Med 2018;32:1517–1529.
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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;9:43–49.
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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;8:157–165.
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Santilli RA, Bussadori C. Orthodromic incessant atrioventricular reciprocating tachycardia in a dog. J Vet Cardiol 2000;2:25–29.
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Santilli RA, Caivano D, Pariaut R, et al. Low-energy ablation of anteroseptal accessory pathways in two dogs. J Vet Cardiol 2018;20:285–293.
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Santilli RA, Diana A, Baron Toaldo M. Orthodromic atrioventricular reciprocating tachycardia conducted with intraventricular conduction disturbance mimicking ventricular tachycardia in an English Bulldog. J Vet Cardiol 2012;14:363–370.
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Sousa MG, Lucina SB, Carareto R. Orthodromic atrioventricular reciprocating tachycardia in a Dalmatian. Open J Vet Med 2018;8:1–8.
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Endoh Y, Atarashi H, Hayakawa H, et al. Clinical significance of wide QRS complexes at the termination of paroxysmal supraventricular tachycardias. J Nippon Med Sch 2002;69:525–533.
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Santilli R, Moïse NS, Pariaut R, et al. Conduction disorders. In: Santilli R, Moïse NS, Pariaut R, et al, eds. Electrocardiography of the dog and cat: diagnosis of arrhythmias. 2nd ed. Trento, Italy: Edra SpA, 2019;259–292.
- 16. ↑
Finster ST, DeFrancesco TC, Atkins CE, et al. Supraventricular tachycardia in dogs: 65 cases (1990–2007). J Vet Emerg Crit Care (San Antonio) 2008;18:503–510.
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Santilli R, Moïse NS, Pariaut R, et al. Formation and interpretation of the electrocardiographic waves. In: Santilli R, Moïse NS, Pariaut R, et al, eds. Electrocardiography of the dog and cat: diagnosis of arrhythmias. 2nd ed. Trento, Italy: Edra SpA, 2019;35–70.
- 18. ↑
Falk T, Jönsson L, Olsen LH, et al. Associations between cardiac pathology and clinical, echocardiographic and electrocardiographic findings in dogs with chronic congestive heart failure. Vet J 2010;185:68–74.
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Borgarelli M, Crosara S, Lamb K, et al. Survival characteristics and prognostic variables of dogs with preclinical chronic degenerative mitral valve disease attributable to myxomatous degeneration. J Vet Intern Med 2012;26:69–75.
- 20. ↑
Oliveira MS, Muzzi RAL, Araújo RB, et al. Heart rate variability and arrhythmias evaluated with Holter in dogs with degenerative mitral valve disease. Arq Bras Med Vet Zootec 2014;66:425–432.
