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Orthodromic incessant atrioventricular reciprocating tachycardia in a dog
Journal of Veterinary Cardiology, Vol. 2, No. 1, May 2000
Orthodromic incessant atrioventricular reciprocating tachycardia in a dog Roberto A. Santilli Dr Med.Vet. D.E.C.V.I.M.-C.A. (Cardiology)* Claudio Bussadori Dr Med.Vet. D.E.C.V.I.M.-C.A. (Cardiology)**
S
U
M
M
A
R
Y
A diagnosis of orthodromic atrioventricular reciprocating tachycardia (OAVRT) was made in a 6-year-old male Boxer based on electrocardiographic and Holter- ECG findings. The surface electrocardiogram showed a narrow-complex tachycardia, with a regular ventricular rhythm ranging from 280 to 300 bpm, QRS alternans, and retrograde P waves present in the late part of ST segment, with a RP’/P’R ratio < 1. The dog was successfully treated short-term with intravenous verapamil, and long-term with procainamide and diltiazem. This report shows the utility of the surface electrocardiogram in the diagnosis of OAVRT with a concealed accessory pathway in the dog, as it was previously reported in human literature.
Introduction Different classifications of supraventricular tachycardia (SVT) have been described: 1) Automatic supraventricular tachycardia, 2) AV-nodal reentrant tachycardia, 3) Orthodromic AV- reciprocating tachycardia (OAVRT) or bypass tract-mediated macroreentrant tachycardia, 4) Intraatrial reentry tachycardia, 5) SA nodal reentry tachycardia, 6) Atrial flutter, 7) Atrial fibrillation. Paroxysmal atrial tachycardia is an old nomenclature which includes types 2, 3, 4, and 5. These types of SVT are on rare occasions accompanied by underlying heart disease both in humans and in dogs1-5. OAVRT is overrepresented in children and infants1-2, in Labrador Retriever (LR) and LR-cross dogs, with an age ranging from 4 months to 2.5 years, and in patients with tricuspid valve dysplasia3-4. Several studies in the human literature showed the sensibility and specificity of surface ECG in differentiating SVT without the use of electrophysiologic studies5.
Case report A 6 year old male Boxer was presented with a history of acute onset of exercise intolerance, weakness, panting, and coughing. The dog had been vaccinated regularly. On admission the dog was alert, mildly tachypnoeic (respiratory rate 45/min), weighing 38 kg; the mucous membranes were pale, capillary refill time was slightly prolonged, jugular pulsations were evident. The arterial pulse was rapid, regular, hypokinetic, with a marked pulse deficit. At
auscultation, a regular and fast rhythm (280-300 bpm) without any heart murmur could be heard., The lung fields presented with rare inspiratory crackles. A complete laboratory work-up, thoracic radiographs, and a 9-lead electrocardiogram (ECG) were performed. Complete blood count, biochemical profile, and urinalysis were within normal limits, thoracic radiographs showed mild generalized cardiomegaly (V.H.S. 11,5), venous congestion, and hilar interstitial infiltrates. On the surface ECG, a narrow-complex tachycardia was seen (Fig. 1-A), the ventricular rhythm was regular and ranged from 280 to 300 bpm, QRS duration was 40 ms, QRS alternans was visible, and retrograde P waves were present in the late part of the ST segment, with a RP’/P’R ratio of 0.8. By means of these electrocardiographic features, an orthodromic AV reciprocating tachycardia with a retrograde conduction macroreentry throughout a concealed accessory AV bypass tract was suspected. These types of SVT are seldom associated with underlying heart disease, but long-standing SVT could induce heart failure due to both systolic and diastolic dysfunction. For this reason, an echocardiographic examination including Doppler was performed to investigate the cardiac status. Initially the patient was stabilised and resolution of pulmonary edema achieved with furosemide (120 mg IV every 2 to 4 hours until respiratory rate decreased) and transdermal nitroglycerin 2% 1 inch
* Clinica Veterinaria Malpensa, Via Verdi, 49 - Samarate Varese - (Italy). ** Clinica Veterinaria Gran Sasso, Milano (Italy).
25
Roberto A. Santilli, Claudio Bussadori
Figure 1 - Lead-II electrocardiograms (paper speed 50 mm/sec; 1cm = 1 mV). A - Rhythm strip during orthodromic incessant atrioventricular reciprocating tachycardia, with a regular ventricular rhythm of 280 bpm, QRS alternans, and retrograde P waves in the late part of ST segment (arrows), with a RP’/P’R ratio < 1. B - Rhythm strip during sinus rhythm obtained after an IV bolus of verapamil 1,9 mg over 4 minutes.
every 6 hours. Echocardiographic scans showed a very rapid ventricular rate, mild dilatation of the left atrium (LA/Aort ic ratio 2,53) and of the right atrium, increased left ventricular end-diastolic (68 mm) and left ventricular end-systolic dimension (54 mm), with a reduced shortening fraction (21 %), and an increase of the EPSS. (12.8 mm). Doppler interrogation showed an aortic and pulmonary flow deficit every other beat, and moderate tricuspid and mitral regurgitation. Peak flow velocity of mitral valve inflow showed a pseudonormalized pattern with a normal E/A ratio (1,25), a decreased systolic fraction (25.2%), and an increased Ar wave (0.45 m/sec.) of pulmonary venous flow. Several vagal maneuvers were ineffective to stop the SVT, therefore verapamil 1.9 mg IV over 4 minutes was given and it rapidly blocked the tachycardia. During sinus rhythm (Fig. 1-B), a ventricular rate was present (100-120 bpm), no signs of ventricular preexcitation were seen, and the QRS complexes were similar to the ones present during the previous SVT bouts. For the following 18 hours the dog remained in the ICU with several recurrences of SVT, furosemide was switched to oral doses of 80 mg twice a day, together with enalapril 20 mg orally once a day. At this time a 24 hour Holter ECG was recorded; it showed 74% of the time sustained SVT alternating with periods of sinus rhythm (Fig. 2). Procainamide retard (750 mg orally three times a day) was added to the furosemide and enalapril, and 26
Figure 2 - 24-hour Holter recording. Notice periods of sinus rhythm in channel 2 (top), alternating with periods of OAVRT in both channels 1 and 2 (bottom).
Journal of Veterinary Cardiology, Vol. 2, No. 1, May 2000
the dog discharged. One week later, the dog was in good physical condition, and the owner hadn’t noticed any recurrence of clinical signs. The ECG demonstrated a normal sinus rhythm, the EchoDoppler examination showed a normalisation of the previously lowered shortening fraction (38%), a reduction of the EPSS (9 mm), while the end-diastolic left ventricular dimension remained slightly enlarged (56 mm), as did the right atrium. Diastolic Doppler parameters at this time were within normal limits, mitral regurgitation had resolved, while low velocity (2,4 m/sec.) tricuspid regurgitation persisted. Furosemide was reduced to 40 mg orally twice a day, while enalapril and procainamide were left at the same dosages, seen that its serum level was within therapeutic range (13.4 ug/ml). Despite normalization of cardiac function, a 24 hour Holter monitoring showed several recurrences of SVT lasting a maximum of 12 minutes. Diltiazem (20 mg orally three times daily) was added, and successfully controlled the tachycardia as proven by a successive Holter monitoring done after 10 days, 1 month, and 4 months. Both furosemide and enalapril were stopped after 10 weeks, since there was no recurrence of left congestive heart failure and normal EchoDoppler findings. At the 7 month recheck, the SVT was still controlled, without evidence of the arrhythmia on Holter recording.
Discussion OAVRT is considered the second most common type of SVT in human beings after AV nodal reentrant tachycardia1-2. Both OAVRT and Wolff-Parkinson-White (WPW) syndrome have a macroreentry circuit constituted by an atrioventricular bypass tract and atrioventricular node, but opposite current directions occur. The circuit used to maintain the macroreentry in OAVRT is a concealed accessory atrioventricular pathway as the retrograde limb, and the AV node as the anterograde limb2-4. In the classic Wolff-Parkinson-White (WPW) syndrome, an accessory AV pathway is capable of anterograde conduction, and signs of ventricular pre-excitation are visible on surface ECG during sinus rhythm. Characteristic electrocardiographic findings of WPW are: short PR interval, slurring of the onset of the QRS complex (delta wave), and alteration of the QRS- ST segment morphology6-7. Four types of AV bypass tracts have been described: 1) Atrioventricular fibers of Kent (WPW syndrome); 2) Atrio-His’ fibers of James (Lown-Ganong-Levine syndrome); 3) Intranodal fibers; 4) Nodoventricular or Mahaim fibers. The Kent fibers are the most common type, and they present rapid conduction velocity with a short refractory period, they block suddenly after a premature stimulus from the His-Purkinje tissue. Therefore they constitute the rapid limb of circuit, while the AV node represents the slow limb 6-7 . Most patients with OAVRT do not show signs of ventricular pre-excita-
tion during sinus rhythm, because the AV bypass tracts are concealed with retrograde conduction3-5. OAVRT is overrepresented in LR 3-4, in which congenital tricuspid dysplasia is also very common8. Because an association of WPW and tricuspid dysplasia has been reported both in man9-10 and dog11, a correlation between these congenital entities has been suspected. OAVRT occurs in dogs during the early months of life (range: 4 months, 2.5 years)3-4. The dog from this report was older, but one can speculate about the existence of a congenital bypass tract, and a progressive increase of length of the paroxysmal SVT during the past years. Biventricular failure was present in this dog, as proven by the presence of jugular pulsations and pulmonary edema. The duration of SVT bouts up to 74 % of a 24-hour period could have induced myocardial failure, but the absence of ascites, usually evident in the majority of cases of tachycardia-induced cardiomyopathy13-14, may suggest early deterioration of cardiac function. The signs of heart failure in this dog were probably not the cause but the consequences of tachyarrhthmias because severe underlying heart disease is rarely found with OAVRT 1,3-4. Experimentally-induced rapid ventricular pacing greater than 200 bpm provokes, instead, myocardial failure within 2 to 6 weeks in dogs12-14. The exact mechanism of myocardial failure is unknown, and although myocardial blood flow reserve is reduced, hypoxia is not considered to be the cause15-16. A decreased number of sarcomeres, with elongation of myocytes, a depletion of glycogen, creatine, phosphocreatine, and ATP stores has been described15-16. It is not still clear if these ultrastructural alterations are the cause or the effect of systolic failure. A reduction of total diastolic filling time during the tachycardia, a shift of the filling from early to late diastole, an alteration of ventricular geometry with asynchronous contraction, and an increase of end-systolic volume could induce concomitant diastolic dysfunction17. Myocardial failure rapidly reverses after cessation of SVT, with a normalization of shortening fraction in 1 - 2 weeks, and a normalisation of the left ventricular diameters in 12 weeks13. The surface ECG has been shown to be the method of choice to classify the different types of SVT in 80% of the cases in man1,5. Atrial flutter or atrial fibrillation and multifocal automatic SVT can easily be detected by this method. Unifocal automatic SVT typically presents with a warm-up phenomenon with acceleration of the ventricular rate after initiation, and depending on autonomic drive, AV conduction disturbances can be present. Interventions that influence AV conduction do not affect the tachycardia itself3-5. Reentrant tachycardia, both intraatrial and SA nodal, present similar AV conduction behavior, but differ from automatic SVT with their paroxysmal characteristics3-5. Automatic and intraatrial SVT have anterograde P waves with different configurations of SA node P waves, and RP’/P’R ratios > 13-5. SA nodal reentry tachycardia is indistin27
Roberto A. Santilli, Claudio Bussadori
guishable from sinus tachycardia, except for paroxysmal initiation and termination3-5. Usually these SVT’s have a ventricular response slower than 200 bpm in man. 5. AV nodal reentrant tachycardia is characterized by the absence of P waves, and the presence of r’ deflection in V1, and pseudo- S waves in lead II, III and aVF, which represent retrograde P waves that distort the normal QRS complex, or a rate-related right ventricular conduction delay 3-5. Sustained AV nodal reentrant tachycardia is usually the fast-slow subtype where the anterograde conduction proceeds across a fast beta limb, while the retrograde conduction proceeds across the slow alpha limb. This is the only case where P waves could be present after the QRS for the delay of the retrograde conduction, but usually in the early portion of ST segment5. The most common type of AV nodal reentrant tachycardia is the slow-fast subtype and the P waves are therefore hidden in the QRS complex5. OAVRT is characterized by a very rapid ventricular response, retrograde P waves in the late part of ST segment, with a RP’/P’R ratio < 1, and the higher incidence of QRS alternans (96%) because of oscillations in the relative refractory period of the specialized conducting system, resulting in an alteration of action potential duration3-5. In the dog of this study, the presence of a fast ventricular rate, QRS alternans, presence of P waves in the late part of ST segment with a R’P/P’R ratio < 1, allowed the diagnosis of OAVRT. Echocardiographic findings during SVT-bouts in this report were similar to the ones reported in the literature12-14, and included reduction of the shortening fraction, increases of the left ventricular dimensions, and of the EPSS. Doppler features revealed, instead, the presence of mitral and tricuspid regurgitation, both probably induced by alteration of ventricular geometry and asynchronous relaxation. Diastolic Doppler parameters of this dog revealed a pseudonormalized pattern with increased left atrial pressure, despite the reduction in preload promoted by diuretic and vasodilator therapy17. With cessation of SVT, the systolic performance of left ventricle improved partially after 1 week, and completely after 11 weeks, as reported in the literature13. Also, diastolic function rapidly resolved due to the prolongation of total diastolic time caused by the interruption of the SVT. Mitral regurgitation resolved, while moderate tricuspid regurgitation persisted despite normalization of cardiac function, and therefore a mild form of tricuspid valve dysplasia was suspected in concomitance with the congenital substrate of OAVRT. The major goal of the treatment of OAVRT is to reduce the tachycardia zone, which represents the range of coupling intervals of premature beats that will initiate reentrant tachycardia, to equalize the conduction time via the two pathways altering normal AV or bypass tracts conduction velocity, and to induce a functional block in one or both limbs of the circuit. Vagal maneuvers, and drugs which increase 28
the refractory period of the AV node (digitalis, calcium blockers, and beta-blockers) reduce the tachycardia zone, blocking the AV node resulting in Wenckebach conduction when the tachycardia begins1,3-4,18. Digitalis usually shortens the bypass tract refractory period, therefore its use alone is controversial, while propranolol and verapamil have variable effect onto accessory pathways1. Class Ia antiarrhythmic drugs such as procainamide has been described to be the drug of choice because they lengthen the retrograde refractory period of accessory pathways, but increase also the anterograde refractory period, the tachycardia zone, and therefore macroreentry could be carried out. The best treatment for OAVRT is therefore a combination of a drug which affects AV nodal refractory period such as diltiazem, with a class Ia agent1,3-4. Class Ic antiarrhythmic agents (flecainide and propafenone), and class III agents (amiodarone and sotalol) could be used alone to control OAVRT1,3-4. In this case we started with procainamide alone to assess its effect, and seeing only moderate resolution, diltiazem was added. The SVT ceased, and complete control of clinical sign of congestion resulted. Holter monitoring was indispensable to assess the control of the arrhythmia. Electrophysiologic studies could have confirmed the diagnosis, demonstrated the location of the bypass tract as described3, and guided a transcatheter radiofrequency ablation of the accessory pathway1920 , but having noticed the long-term successful responsiveness to drug therapy, electrophysiologic testing was not carried out.
Key Terms Supraventricular tachycardia, arrhythmia, dog, AV-bypass tract.
References 1. Chung EK. Tachyarrhythmias in Wolff-ParkinsonWhite syndrome. Antiarrhythmic drug therapy. J Am Med Assoc 1977; 237:376-379. 2. Zipes DP. Specific arrhythmia: Diagnosis and treatment. In: Braunwald E, ed, Heart disease - A Textbook of cardiovascular Medicine, 4th Ed, Philadelphia, PA: W.B. Saunders, 1992:667-725. 3. Atkins CE, Kanter R, Wright K, et al. Orthodromic reciprocating tachycardia and heart failure in a dog with a concealed postero-septal accessory pathway. J Vet Intern Med 1995; 9:43-49. 4. Wright KN, Atkins CE, Kanter R. Supraventricualr tachycardia in four young dogs. J Am Vet Med Assoc 1996; 208:75-79. 5. Kalbfleisch SJ, El-Atassi R, Calkins H, et al. Differentiation of paroxysmal narrow QRS complex tachycardias using the 12-lead electrocardiogram. J Am Coll Cardiol 1993; 21:85-89. 6. Ferrer MI. Preexcitation. Am J Med 1977; 62:715-730.
Journal of Veterinary Cardiology, Vol. 2, No. 1, May 2000 7. Hills BL, Tilley LP. Ventricular preexcitation in seven dogs and nine cats. J Am Vet Med Assoc 1985; 187:1026-1031. 8. Miller MW, Bonagura JD. Congenital heart disease. In Kirk RW, ed. Current Veterinary Therapy. Philadelphia, PA: W.B. Saunders; 1989:224-231. 9. Buja G, Canciani B, Martini B, et al. Coexistence of Kent accessory pathway, enhanced AV node conduction, and various conduction disturbances in a young athlete with tricuspid valve dysplasia. J of Electrocardiol 1991; 24:71-76. 10. Smith WM, Gallegher JJ, Kerr CR, et al. The electrophysiologic basis and management of symptomatic recurrent tachycardia in patients with Ebstein’s anomaly of the tricuspid valve. Am J Cardiol 1981;49:1223-1234. 11. De Madron E, Kadish A, Spear JF. Incessant atrial tachycardia in a dog with tricuspid dysplasia: clinical management and electrophysiology. J Vet Intern Med 1987; 1:163-165 12. Allworth MS, Church DB, Maddison JE, et al. Effect of enalapril in dogs with pacing-induced heart failure. Am J Vet Res 1995; 56:85-94. 13. Shinbane JS, Wood MA, Jensen DN, et al. Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies. J Am Coll Cardiol 1997; 29:709-713.
14. Wilson JR, Douglas P, Hickey WF, et al. Experimental congestive heart failure produced by rapid ventricular pacing in the dog: cardiac effects. Circulation 1987; 75:857-863 15. Spinale FG, Fulbright BM, Mukherjee R, et al. Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy. Circ Res 1992; 71:174-179. 16. Spinale FG, Tanaka R., Crawford FA, et al. Changes in myocardial blood flow during development and recovery form tachycardia-induced cardiomyopathy. Circulation 1992; 85:717-720. 17. Choong CY. Left ventricle V: diastolic function - its principles and evaluation. In Principles and practice of echocardiography, ed. Weyman A.E., Philadelphia: Lea & Febiger; 1994:721-779. 18. Kittleson M, Keen B, Pion P. Verapamil administration for acute termination of supraventricular tachycardia in dogs. J Am Vet Med Assoc 1988; 193:1525-1527. 19. Wright KN, Bright JM, Cox JW, et al. Transcatheter modification of the atrioventricular node in dogs, using radiofrequency energy. Am J Vet Res 1996; 57:229-235. 20. Sherlag 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; 203:1147-1152.
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Orthodromic incessant atrioventricular reciprocating tachycardia in a dog Roberto A. Santilli Dr Med.Vet. D.E.C.V.I.M.-C.A. (Cardiology)* Claudio Bussadori Dr Med.Vet. D.E.C.V.I.M.-C.A. (Cardiology)**
S
U
M
M
A
R
Y
A diagnosis of orthodromic atrioventricular reciprocating tachycardia (OAVRT) was made in a 6-year-old male Boxer based on electrocardiographic and Holter- ECG findings. The surface electrocardiogram showed a narrow-complex tachycardia, with a regular ventricular rhythm ranging from 280 to 300 bpm, QRS alternans, and retrograde P waves present in the late part of ST segment, with a RP’/P’R ratio < 1. The dog was successfully treated short-term with intravenous verapamil, and long-term with procainamide and diltiazem. This report shows the utility of the surface electrocardiogram in the diagnosis of OAVRT with a concealed accessory pathway in the dog, as it was previously reported in human literature.
Introduction Different classifications of supraventricular tachycardia (SVT) have been described: 1) Automatic supraventricular tachycardia, 2) AV-nodal reentrant tachycardia, 3) Orthodromic AV- reciprocating tachycardia (OAVRT) or bypass tract-mediated macroreentrant tachycardia, 4) Intraatrial reentry tachycardia, 5) SA nodal reentry tachycardia, 6) Atrial flutter, 7) Atrial fibrillation. Paroxysmal atrial tachycardia is an old nomenclature which includes types 2, 3, 4, and 5. These types of SVT are on rare occasions accompanied by underlying heart disease both in humans and in dogs1-5. OAVRT is overrepresented in children and infants1-2, in Labrador Retriever (LR) and LR-cross dogs, with an age ranging from 4 months to 2.5 years, and in patients with tricuspid valve dysplasia3-4. Several studies in the human literature showed the sensibility and specificity of surface ECG in differentiating SVT without the use of electrophysiologic studies5.
Case report A 6 year old male Boxer was presented with a history of acute onset of exercise intolerance, weakness, panting, and coughing. The dog had been vaccinated regularly. On admission the dog was alert, mildly tachypnoeic (respiratory rate 45/min), weighing 38 kg; the mucous membranes were pale, capillary refill time was slightly prolonged, jugular pulsations were evident. The arterial pulse was rapid, regular, hypokinetic, with a marked pulse deficit. At
auscultation, a regular and fast rhythm (280-300 bpm) without any heart murmur could be heard., The lung fields presented with rare inspiratory crackles. A complete laboratory work-up, thoracic radiographs, and a 9-lead electrocardiogram (ECG) were performed. Complete blood count, biochemical profile, and urinalysis were within normal limits, thoracic radiographs showed mild generalized cardiomegaly (V.H.S. 11,5), venous congestion, and hilar interstitial infiltrates. On the surface ECG, a narrow-complex tachycardia was seen (Fig. 1-A), the ventricular rhythm was regular and ranged from 280 to 300 bpm, QRS duration was 40 ms, QRS alternans was visible, and retrograde P waves were present in the late part of the ST segment, with a RP’/P’R ratio of 0.8. By means of these electrocardiographic features, an orthodromic AV reciprocating tachycardia with a retrograde conduction macroreentry throughout a concealed accessory AV bypass tract was suspected. These types of SVT are seldom associated with underlying heart disease, but long-standing SVT could induce heart failure due to both systolic and diastolic dysfunction. For this reason, an echocardiographic examination including Doppler was performed to investigate the cardiac status. Initially the patient was stabilised and resolution of pulmonary edema achieved with furosemide (120 mg IV every 2 to 4 hours until respiratory rate decreased) and transdermal nitroglycerin 2% 1 inch
* Clinica Veterinaria Malpensa, Via Verdi, 49 - Samarate Varese - (Italy). ** Clinica Veterinaria Gran Sasso, Milano (Italy).
25
Roberto A. Santilli, Claudio Bussadori
Figure 1 - Lead-II electrocardiograms (paper speed 50 mm/sec; 1cm = 1 mV). A - Rhythm strip during orthodromic incessant atrioventricular reciprocating tachycardia, with a regular ventricular rhythm of 280 bpm, QRS alternans, and retrograde P waves in the late part of ST segment (arrows), with a RP’/P’R ratio < 1. B - Rhythm strip during sinus rhythm obtained after an IV bolus of verapamil 1,9 mg over 4 minutes.
every 6 hours. Echocardiographic scans showed a very rapid ventricular rate, mild dilatation of the left atrium (LA/Aort ic ratio 2,53) and of the right atrium, increased left ventricular end-diastolic (68 mm) and left ventricular end-systolic dimension (54 mm), with a reduced shortening fraction (21 %), and an increase of the EPSS. (12.8 mm). Doppler interrogation showed an aortic and pulmonary flow deficit every other beat, and moderate tricuspid and mitral regurgitation. Peak flow velocity of mitral valve inflow showed a pseudonormalized pattern with a normal E/A ratio (1,25), a decreased systolic fraction (25.2%), and an increased Ar wave (0.45 m/sec.) of pulmonary venous flow. Several vagal maneuvers were ineffective to stop the SVT, therefore verapamil 1.9 mg IV over 4 minutes was given and it rapidly blocked the tachycardia. During sinus rhythm (Fig. 1-B), a ventricular rate was present (100-120 bpm), no signs of ventricular preexcitation were seen, and the QRS complexes were similar to the ones present during the previous SVT bouts. For the following 18 hours the dog remained in the ICU with several recurrences of SVT, furosemide was switched to oral doses of 80 mg twice a day, together with enalapril 20 mg orally once a day. At this time a 24 hour Holter ECG was recorded; it showed 74% of the time sustained SVT alternating with periods of sinus rhythm (Fig. 2). Procainamide retard (750 mg orally three times a day) was added to the furosemide and enalapril, and 26
Figure 2 - 24-hour Holter recording. Notice periods of sinus rhythm in channel 2 (top), alternating with periods of OAVRT in both channels 1 and 2 (bottom).
Journal of Veterinary Cardiology, Vol. 2, No. 1, May 2000
the dog discharged. One week later, the dog was in good physical condition, and the owner hadn’t noticed any recurrence of clinical signs. The ECG demonstrated a normal sinus rhythm, the EchoDoppler examination showed a normalisation of the previously lowered shortening fraction (38%), a reduction of the EPSS (9 mm), while the end-diastolic left ventricular dimension remained slightly enlarged (56 mm), as did the right atrium. Diastolic Doppler parameters at this time were within normal limits, mitral regurgitation had resolved, while low velocity (2,4 m/sec.) tricuspid regurgitation persisted. Furosemide was reduced to 40 mg orally twice a day, while enalapril and procainamide were left at the same dosages, seen that its serum level was within therapeutic range (13.4 ug/ml). Despite normalization of cardiac function, a 24 hour Holter monitoring showed several recurrences of SVT lasting a maximum of 12 minutes. Diltiazem (20 mg orally three times daily) was added, and successfully controlled the tachycardia as proven by a successive Holter monitoring done after 10 days, 1 month, and 4 months. Both furosemide and enalapril were stopped after 10 weeks, since there was no recurrence of left congestive heart failure and normal EchoDoppler findings. At the 7 month recheck, the SVT was still controlled, without evidence of the arrhythmia on Holter recording.
Discussion OAVRT is considered the second most common type of SVT in human beings after AV nodal reentrant tachycardia1-2. Both OAVRT and Wolff-Parkinson-White (WPW) syndrome have a macroreentry circuit constituted by an atrioventricular bypass tract and atrioventricular node, but opposite current directions occur. The circuit used to maintain the macroreentry in OAVRT is a concealed accessory atrioventricular pathway as the retrograde limb, and the AV node as the anterograde limb2-4. In the classic Wolff-Parkinson-White (WPW) syndrome, an accessory AV pathway is capable of anterograde conduction, and signs of ventricular pre-excitation are visible on surface ECG during sinus rhythm. Characteristic electrocardiographic findings of WPW are: short PR interval, slurring of the onset of the QRS complex (delta wave), and alteration of the QRS- ST segment morphology6-7. Four types of AV bypass tracts have been described: 1) Atrioventricular fibers of Kent (WPW syndrome); 2) Atrio-His’ fibers of James (Lown-Ganong-Levine syndrome); 3) Intranodal fibers; 4) Nodoventricular or Mahaim fibers. The Kent fibers are the most common type, and they present rapid conduction velocity with a short refractory period, they block suddenly after a premature stimulus from the His-Purkinje tissue. Therefore they constitute the rapid limb of circuit, while the AV node represents the slow limb 6-7 . Most patients with OAVRT do not show signs of ventricular pre-excita-
tion during sinus rhythm, because the AV bypass tracts are concealed with retrograde conduction3-5. OAVRT is overrepresented in LR 3-4, in which congenital tricuspid dysplasia is also very common8. Because an association of WPW and tricuspid dysplasia has been reported both in man9-10 and dog11, a correlation between these congenital entities has been suspected. OAVRT occurs in dogs during the early months of life (range: 4 months, 2.5 years)3-4. The dog from this report was older, but one can speculate about the existence of a congenital bypass tract, and a progressive increase of length of the paroxysmal SVT during the past years. Biventricular failure was present in this dog, as proven by the presence of jugular pulsations and pulmonary edema. The duration of SVT bouts up to 74 % of a 24-hour period could have induced myocardial failure, but the absence of ascites, usually evident in the majority of cases of tachycardia-induced cardiomyopathy13-14, may suggest early deterioration of cardiac function. The signs of heart failure in this dog were probably not the cause but the consequences of tachyarrhthmias because severe underlying heart disease is rarely found with OAVRT 1,3-4. Experimentally-induced rapid ventricular pacing greater than 200 bpm provokes, instead, myocardial failure within 2 to 6 weeks in dogs12-14. The exact mechanism of myocardial failure is unknown, and although myocardial blood flow reserve is reduced, hypoxia is not considered to be the cause15-16. A decreased number of sarcomeres, with elongation of myocytes, a depletion of glycogen, creatine, phosphocreatine, and ATP stores has been described15-16. It is not still clear if these ultrastructural alterations are the cause or the effect of systolic failure. A reduction of total diastolic filling time during the tachycardia, a shift of the filling from early to late diastole, an alteration of ventricular geometry with asynchronous contraction, and an increase of end-systolic volume could induce concomitant diastolic dysfunction17. Myocardial failure rapidly reverses after cessation of SVT, with a normalization of shortening fraction in 1 - 2 weeks, and a normalisation of the left ventricular diameters in 12 weeks13. The surface ECG has been shown to be the method of choice to classify the different types of SVT in 80% of the cases in man1,5. Atrial flutter or atrial fibrillation and multifocal automatic SVT can easily be detected by this method. Unifocal automatic SVT typically presents with a warm-up phenomenon with acceleration of the ventricular rate after initiation, and depending on autonomic drive, AV conduction disturbances can be present. Interventions that influence AV conduction do not affect the tachycardia itself3-5. Reentrant tachycardia, both intraatrial and SA nodal, present similar AV conduction behavior, but differ from automatic SVT with their paroxysmal characteristics3-5. Automatic and intraatrial SVT have anterograde P waves with different configurations of SA node P waves, and RP’/P’R ratios > 13-5. SA nodal reentry tachycardia is indistin27
Roberto A. Santilli, Claudio Bussadori
guishable from sinus tachycardia, except for paroxysmal initiation and termination3-5. Usually these SVT’s have a ventricular response slower than 200 bpm in man. 5. AV nodal reentrant tachycardia is characterized by the absence of P waves, and the presence of r’ deflection in V1, and pseudo- S waves in lead II, III and aVF, which represent retrograde P waves that distort the normal QRS complex, or a rate-related right ventricular conduction delay 3-5. Sustained AV nodal reentrant tachycardia is usually the fast-slow subtype where the anterograde conduction proceeds across a fast beta limb, while the retrograde conduction proceeds across the slow alpha limb. This is the only case where P waves could be present after the QRS for the delay of the retrograde conduction, but usually in the early portion of ST segment5. The most common type of AV nodal reentrant tachycardia is the slow-fast subtype and the P waves are therefore hidden in the QRS complex5. OAVRT is characterized by a very rapid ventricular response, retrograde P waves in the late part of ST segment, with a RP’/P’R ratio < 1, and the higher incidence of QRS alternans (96%) because of oscillations in the relative refractory period of the specialized conducting system, resulting in an alteration of action potential duration3-5. In the dog of this study, the presence of a fast ventricular rate, QRS alternans, presence of P waves in the late part of ST segment with a R’P/P’R ratio < 1, allowed the diagnosis of OAVRT. Echocardiographic findings during SVT-bouts in this report were similar to the ones reported in the literature12-14, and included reduction of the shortening fraction, increases of the left ventricular dimensions, and of the EPSS. Doppler features revealed, instead, the presence of mitral and tricuspid regurgitation, both probably induced by alteration of ventricular geometry and asynchronous relaxation. Diastolic Doppler parameters of this dog revealed a pseudonormalized pattern with increased left atrial pressure, despite the reduction in preload promoted by diuretic and vasodilator therapy17. With cessation of SVT, the systolic performance of left ventricle improved partially after 1 week, and completely after 11 weeks, as reported in the literature13. Also, diastolic function rapidly resolved due to the prolongation of total diastolic time caused by the interruption of the SVT. Mitral regurgitation resolved, while moderate tricuspid regurgitation persisted despite normalization of cardiac function, and therefore a mild form of tricuspid valve dysplasia was suspected in concomitance with the congenital substrate of OAVRT. The major goal of the treatment of OAVRT is to reduce the tachycardia zone, which represents the range of coupling intervals of premature beats that will initiate reentrant tachycardia, to equalize the conduction time via the two pathways altering normal AV or bypass tracts conduction velocity, and to induce a functional block in one or both limbs of the circuit. Vagal maneuvers, and drugs which increase 28
the refractory period of the AV node (digitalis, calcium blockers, and beta-blockers) reduce the tachycardia zone, blocking the AV node resulting in Wenckebach conduction when the tachycardia begins1,3-4,18. Digitalis usually shortens the bypass tract refractory period, therefore its use alone is controversial, while propranolol and verapamil have variable effect onto accessory pathways1. Class Ia antiarrhythmic drugs such as procainamide has been described to be the drug of choice because they lengthen the retrograde refractory period of accessory pathways, but increase also the anterograde refractory period, the tachycardia zone, and therefore macroreentry could be carried out. The best treatment for OAVRT is therefore a combination of a drug which affects AV nodal refractory period such as diltiazem, with a class Ia agent1,3-4. Class Ic antiarrhythmic agents (flecainide and propafenone), and class III agents (amiodarone and sotalol) could be used alone to control OAVRT1,3-4. In this case we started with procainamide alone to assess its effect, and seeing only moderate resolution, diltiazem was added. The SVT ceased, and complete control of clinical sign of congestion resulted. Holter monitoring was indispensable to assess the control of the arrhythmia. Electrophysiologic studies could have confirmed the diagnosis, demonstrated the location of the bypass tract as described3, and guided a transcatheter radiofrequency ablation of the accessory pathway1920 , but having noticed the long-term successful responsiveness to drug therapy, electrophysiologic testing was not carried out.
Key Terms Supraventricular tachycardia, arrhythmia, dog, AV-bypass tract.
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14. Wilson JR, Douglas P, Hickey WF, et al. Experimental congestive heart failure produced by rapid ventricular pacing in the dog: cardiac effects. Circulation 1987; 75:857-863 15. Spinale FG, Fulbright BM, Mukherjee R, et al. Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy. Circ Res 1992; 71:174-179. 16. Spinale FG, Tanaka R., Crawford FA, et al. Changes in myocardial blood flow during development and recovery form tachycardia-induced cardiomyopathy. Circulation 1992; 85:717-720. 17. Choong CY. Left ventricle V: diastolic function - its principles and evaluation. In Principles and practice of echocardiography, ed. Weyman A.E., Philadelphia: Lea & Febiger; 1994:721-779. 18. Kittleson M, Keen B, Pion P. Verapamil administration for acute termination of supraventricular tachycardia in dogs. J Am Vet Med Assoc 1988; 193:1525-1527. 19. Wright KN, Bright JM, Cox JW, et al. Transcatheter modification of the atrioventricular node in dogs, using radiofrequency energy. Am J Vet Res 1996; 57:229-235. 20. Sherlag 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; 203:1147-1152.
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