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Giovanni Romito Department of Veterinary Medical Sciences, Alma Mater Studiorum - University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia, Italy.

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Marco Baron Toaldo Department of Veterinary Medical Sciences, Alma Mater Studiorum - University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia, Italy.

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Alessia Diana Department of Veterinary Medical Sciences, Alma Mater Studiorum - University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia, Italy.

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Mario Cipone Department of Veterinary Medical Sciences, Alma Mater Studiorum - University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia, Italy.

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A 7-year-old 23-kg (51-lb) sexually intact male English Bulldog was evaluated at the Cardiology Unit of the Veterinary Teaching Hospital of the University of Bologna because of recurrent ascites secondary to right congestive heart failure and ventricular arrhythmias. A presumptive diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC)1 had been made a few months prior on the basis of findings of echocardiography, electrocardiography, and 24-hour Holter monitoring. The dog was currently being treated with torsemidea (0.2 mg/kg [0.09 mg/lb], PO, q 12 h), benazepril hydrochlorideb (0.5 mg/kg [0.23 mg/lb], PO, q 24 h), spironolactonec (1 mg/kg [0.45 mg/lb], PO, q 24 h), hydrochlorothiazided (1 mg/kg, PO, q 24 h), and amiodarone hydrochlorided (maintenance dose, 15 mg/kg [6.8 mg/lb], PO, q 12 h). On physical evaluation, the dog was bright, alert, and responsive. Mucous membranes were pink, and capillary refill time was 2 seconds. The mean heart rate was approximately 120 beats/min, and no femoral pulse irregularities were detected. Auscultation of the lungs revealed no detectable abnormalities. Abdominal distension was evident, and a fluid wave was palpable during abdominal ballottement. Transthoracic echocardiography was performed with an ultrasound unite equipped with a 5- to 1-MHz phased array transducer and with continuous ECG monitoring. Two-dimensional, M-mode, and Doppler echocardiography revealed biatrial and right ventricular dilation, impaired ventricular systolic function, and moderate tricuspid valve regurgitation. Moreover, a dyskinetic right ventricular outflow tract with evidence of segmental aneurysm was identified. During echocardiographic examination, rhythm abnormalities occurred; therefore, a 12-lead surface ECG (6 peripheral standard leads and 6 precordial leads as previously described2) was subsequently performed (Figures 1 and 2).

Figure 1—
Figure 1—

Initial 12-lead ECG tracing obtained from an English Bulldog that was evaluated because of recurrent ascites secondary to right congestive heart failure and ventricular arrhythmias. A few months prior, a presumptive diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC) had been made. Notice the mildly variable and short PQ intervals (from 0.04 to 0.06 seconds) that precede wide QRS complexes (duration, 0.1 seconds). The QRS complexes are predominantly positive in caudoventral and precordial leads, but negative in leads I, aVL, and aVR. There is slurring at the onset of each R wave that mimics a pseudo-delta wave (arrow). The first 4 P waves are marked (asterisk). Paper speed = 50 mm/s; 1 cm = 2 mV.

Citation: Journal of the American Veterinary Medical Association 247, 5; 10.2460/javma.247.5.484

ECG Interpretation

The first 12-lead surface ECG tracing (Figure 1) revealed a regular rhythm with a mean heart rate of 120 beats/min. The P waves had a normal axis (63°; reference range,3 −18° to 90°) and amplitude (0.25 mV; upper reference limit,4 < 0.4 mV), but their duration was slightly prolonged (0.05 seconds; upper reference limit,4 < 0.04 seconds). Short and mildly variable PR intervals (0.04 to 0.06 seconds; reference range,4 0.06 to 0.13 seconds) were followed by wide QRS complexes (0.1 seconds; upper reference limit,4 < 0.06 seconds) with a notch at the onset of each R wave (R-wave amplitude, 2 mV; upper reference limit,4 < 2.5 mV) that in positive leads had a slurred upslope. Moreover, QRS complexes were predominantly positive in caudoventral and precordial leads, but negative in leads I, aVL, and aVR (mean electrical axis, 100°; reference range,4 40° to 110°). Precordial concordance was present, such that the polarity of the QRS complexes was the same (positive) for all the precordial leads. At this point, the 2 differential diagnoses were accelerated idioventricular rhythm (AIVR) with left bundle branch block (LBBB) morphology coupled to isorhythmic atrioventricular dissociation (IAVD), with synchronization type 25 or sinus rhythm associated with ventricular preexcitation (VP).6

In the second ECG tracing (a direct continuation of the first ECG strip; Figure 2), a premature ventricular complex (VPC) with right bundle branch block morphology (negative in the caudoventral leads and positive in leads I, V4, V5, and V6) abruptly interrupted the aforementioned rhythm. Subsequently, a postextrasystolic pause occurred, followed by restoration of normal sinus rhythm. However, no notable change in heart rate was detected between the first and second tracings. Accurate examination of the last 6 beats revealed normalization of PQ intervals (duration, 0.1 seconds); moreover, remarkable changes in the QRS-complex shape (lack of notched morphology), duration (0.06 seconds), amplitude (1 mV), and mean electrical axis (90°) were evident.

Figure 2—
Figure 2—

A second 12-lead ECG tracing representing the direct continuation of the ECG strip in Figure 1. Notice the abrupt end of the ectopic rhythm owing to the occurrence of a ventricular premature complex (VPC) with right bundle branch block morphology (asterisk). This VPC is followed by a postextrasystolic pause. Restoration of sinus rhythm subsequently occurs (arrow) with normalization of the PQ intervals as well as remarkable changes in QRS-complex duration, shape, amplitude, and mean electrical axis. Paper speed = 50 mm/s; 1 cm = 2 mV.

Citation: Journal of the American Veterinary Medical Association 247, 5; 10.2460/javma.247.5.484

Discussion

Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac disease characterized by abnormalities of right ventricular structure and function that result from myocyte loss with fatty or fibrofatty replacement.7 In people, pathogenic mutation of desmosomal proteins has been detected in up to 50% of affected individuals.7 In dogs with ARVC, similar gene mutations have not been identified but lower expressions of cardiac ryanodine receptors, myocardial calstabin-2, and connexion 43 junction protein as well as mutation of striatin have been demonstrated.8 As a consequence, myocyte depolarization and repolarization abnormalities may occur, thereby promoting either ventricular or, less commonly, supraventricular arrhythmias.7–9 In humans, ARVC most frequently affects the right ventricle, but it can also involve the left side of the heart. When the right ventricle is affected, the cardiomyopathy can either be diffuse or segmental, involving the subtricuspid valve region, right ventricular apex, or outflow tract.7 Interestingly, the segmental form of ARVC affecting the right ventricular outflow tract in an English Bulldog has been described.10 Moreover, characteristic clinical features of ARVC have been reported for several dogs of the same breed, suggesting a possible breed predisposition for the disease, as observed in Boxers.8

In the dog of the present report, several ECG features were identified as follows: a regular rhythm with mean ventricular rate of 120 beats/min, mildly variable and short PR intervals, and wide QRS complexes with notched R waves and normal mean electrical axis. Explanations for these findings include AIVR with LBBB morphology coupled to IAVD with synchronization type 25 and sinus rhythm associated with VP.6 Control of the atria and ventricles by independent pacemakers defines atrioventricular (AV) dissociation.11–13 The term isorhythmic is additionally used when rates of the independent pacemakers approximate each other over relatively long periods, despite different influences acting on each.11–13 Because the sinus node has the fastest inherent automaticity (compared with other cardiac tissues that have inherent automaticity) under normal conditions, a subsidiary pacemaker (either junctional or ventricular) becomes apparent only when the sinus rate slows, the junctional or ventricular rate accelerates, or the AV conduction is disturbed or when these events occur simultaneously in some combination. This phenomenon is called synchronization, and it develops when separate and distinct cellular elements that have no anatomic continuity and possess inherently different rhythms are placed in contact with each other; subsequently, they can begin to discharge impulses simultaneously at a common rate.14 The term synchronization is used when the hook-up between cardiac elements is relatively long; when the phenomenon lasts for only a few beats, the term accrochage has been proposed.14

In humans and dogs, IAVD has been previously reported in cases of third-degree AV block, junctional tachycardia, and AIVR.5,11–13 During IAVD, P waves may oscillate gradually back and forth across the QRS complexes, thereby resulting in rhythmic PQ-interval fluctuations (ie, synchronization type 1), or, conversely, may be coupled to correspondent QRS complexes at constant or almost constant PQ intervals with P waves always preceding R waves (ie, synchronization type 2).5 Different theories have been proposed to explain synchronization type 1, including cyclic fluctuations of arterial blood pressure and mechanical stretching of the sinus node.5,13 The mechanism of synchronization type 2 has not been conclusively established.5,13

The presence of highly similar atrial and ventricular rates with P waves preceding QRS complexes at fixed or mildly variable and short PQ intervals can lead to erroneous diagnosis of VP, suggestive of the presence of an accessory pathway (AP) with an antegrade conduction property.6,15 Ventricular pre-excitation is an ECG phenomenon in which a supraventricular impulse travels over an AP and activates a portion or the entire ventricular muscle earlier than would be expected if the impulse travelled via the normal AV conduction system.6 Because the physiological AV conduction delay is bypassed, the ventricle is prematurely activated, resulting in a shortened PR interval.6 Moreover, the QRS complexes are often widened and characterized by a slurring at the onset of R waves (known as a delta wave), which is a result of summation of 2 fronts of ventricular excitation (the earliest activation front, which initiates the delta waves, travels over the AP; the other travels throughout the AV node in a normal manner).6 Correct identification of VP may be often difficult because of the wide range of VP patterns, including intermittent VP and preexcitation alternans that may be easily mistaken for frequent VPCs and ventricular bigeminy, respectively.6 Similarly, if VP persists for several beats, the rhythm can be misdiagnosed as an AIVR.6 On the other hand, late-coupled VPCs can sometimes mimic VP, especially when intraventricular conduction disturbances occur and result in notched R waves (thereby creating pseudo-delta waves).6

Definitive distinction of ectopic rhythms with IAVD from VP may be extremely challenging without electrophysiologic examination6,15; nevertheless, a scrupulous analysis of surface ECG tracings (taking into account all findings recorded either during arrhythmia and sinus rhythm) has a key role in diagnosis. In the case described in the present report, AIVR with LBBB morphology was strongly hypothesized to be the underlying rhythm disorder for several reasons. First, ventricular arrhythmias with LBBB morphology (suggesting a right ventricular origin) represent the ECG hallmark of ARVC, being identified in > 80% of dogs with definitive histologic diagnosis.8 Second, the presence of precordial concordance strongly suggested the ventricular origin of the QRS complexes. However, a few exceptions may exist, for example when tachycardia involves a left posterior AP for the AV conduction.16 Third, simultaneous existence of ARVC and AP-mediated rhythm disturbances represents an exceptionally rare condition in people17 and, to the authors’ knowledge, has not been described for veterinary patients. Fourth, variations in PQ-interval durations are usual in cases of IAVD,5,6 whereas the classic ECG pattern of VP has fixed PQ intervals.6 Lastly, remarkable modifications in QRS complexes were identified after restoration of sinus rhythm in the dog of this report. Such changes represent a typical finding of ventricular arrhythmias alternating with sinus beats. This ECG pattern would be unlikely in cases of intermittent VP during which QRS complex morphology and duration are expected to change (because of the delta wave's intermittent occurrence and disappearance), but QRS complex amplitude and mean electrical axis are less commonly affected.6

In the present report, an intriguing case of ARVC with somewhat confusing ECG characteristics in an English Bulldog has been described. This case highlights the fact that an ECG pattern of short PQ intervals followed by widened QRS complexes with notched R waves may not always indicate VP.5,6 In such circumstances, less common differential diagnoses, including AIVR with IAVD, should be also considered.

a.

Torasemide, Germed Pharma S.p.A., Cinisello Balsamo, Italy.

b.

Fortekor, Novartis Animal Health S.p.A., Origgio, Italy.

c.

Aldactazide, SPA - Società Prodotti Antibiotici S.p.A., Milan, Italy.

d.

Amiodarone, Mylan S.p.A., Milan, Italy.

e.

iU22 ultrasound system, Philips Medical Systems S.p.A., Monza, Italy.

References

  • 1. Meurs KM. Boxer dog cardiomyopathy: an update. Vet Clin North Am Small Anim Pract 2004; 34: 12351244.

  • 2. Kraus MS, Moïse NS, Rishniw M, et al. Morphology of ventricular arrhythmias in the boxer as measured by 12-lead electrocardiography with pace-mapping comparison. J Vet Intern Med 2002; 16: 153158.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3. Santilli RA, Perego M. Genesi e interpretazione delle onde elettrocardiografiche. In: Elettrocardiografia del cane e del gatto. Milan: Elsevier Inc, 2009; 3946.

    • Search Google Scholar
    • Export Citation
  • 4. Tilley LP. Analysis of canine P-QRS-T deflections. In: Tilley LP, ed. Essentials of canine and feline electrocardiography: interpretation and treatment. 2nd ed. Philadelphia: Lea & Febiger, Lea & Febiger; 58.

    • Search Google Scholar
    • Export Citation
  • 5. Perego M, Ramera L, Santilli RA. Isorhythmic atrioventricular dissociation in Labrador Retrievers. J Vet Intern Med 2012; 26: 320325.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6. Issa ZF, Miller JM, Zipes DP. Atrioventricular reentrant tachycardia. In: Issa ZF, Miller JM, Zipes DP, eds. Clinical arrhythmology and electrophysiology: a companion to Braunwald's heart disease. 2nd ed. Philadelphia: Elsevier Inc, Elsevier Inc; 411467.

    • Search Google Scholar
    • Export Citation
  • 7. Saguner AM, Brunckhorst C, Duru F. Arrhythmogenic right ventricular cardiomyopathy: a paradigm shift from right to biventricular disease. World J Cardiol 2014; 6: 154174.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Santilli RA, Bontempi LV, Perego M. Ventricular tachycardia in English bulldogs with localized right ventricular outflow tract enlargement. J Small Anim Pract 2011; 52: 574580.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Palermo V, Stafford Johnson MJ, Sala E, et al. Cardiomyopathy in Boxer dogs: a retrospective study of the clinical presentation, diagnostic findings and survival. J Vet Cardiol 2011; 13: 4555.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10. Santilli RA, Bontempi LV, Perego M, et al. Outflow tract segmental arrhythmogenic right ventricular cardiomyopathy in an English Bulldog. J Vet Cardiol 2009; 11: 4751.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11. Waldo AL, Vitikainen KJ, Harris PD, et al. The mechanism of synchronization in isorhythmic A-V dissociation: some observations on the morphology and polarity of the P wave during retrograde capture of atria. Circulation 1968; 38: 880898.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. Levy MN, Zieske H. Mechanism of synchronization in isorhythmic dissociation. I. Experiments on dogs. Circ Res 1970; 27: 429443.

  • 13. Levy MN, Edflstein J. The mechanism of synchronization in isorhythmic A-V dissociation. II. Clinical studies. Circulation 1970; 42: 689699.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14. Marriott HJ. Atrioventricular synchronization and accrochage. Circulation 1956; 14: 3843.

  • 15. Tϋrkoğlu C, Aliyev F, Çeliker C, et al. Diagnostic trilemma: isorhythmic AV dissociation mimicking intermittent preexcitation and acute inferior myocardial infarction. J Interv Card Electrophysiol 2008; 22: 4547.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16. Santilli RA, Diana A, Baron Toaldo M. Orthodromic atrioventricular reciprocating tachycardia with intraventricular conduction disturbance mimicking ventricular tachycardia in an English Bulldog. J Vet Cardiol 2012; 14: 363370.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17. Frais MA, Manyari DE, Duff HJ, et al. Coexistent arrhythmogenic right ventricular dysplasia and Wolff-Parkinson-White syndrome. Am J Cardiol 1984; 53: 632634.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Initial 12-lead ECG tracing obtained from an English Bulldog that was evaluated because of recurrent ascites secondary to right congestive heart failure and ventricular arrhythmias. A few months prior, a presumptive diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC) had been made. Notice the mildly variable and short PQ intervals (from 0.04 to 0.06 seconds) that precede wide QRS complexes (duration, 0.1 seconds). The QRS complexes are predominantly positive in caudoventral and precordial leads, but negative in leads I, aVL, and aVR. There is slurring at the onset of each R wave that mimics a pseudo-delta wave (arrow). The first 4 P waves are marked (asterisk). Paper speed = 50 mm/s; 1 cm = 2 mV.

  • Figure 2—

    A second 12-lead ECG tracing representing the direct continuation of the ECG strip in Figure 1. Notice the abrupt end of the ectopic rhythm owing to the occurrence of a ventricular premature complex (VPC) with right bundle branch block morphology (asterisk). This VPC is followed by a postextrasystolic pause. Restoration of sinus rhythm subsequently occurs (arrow) with normalization of the PQ intervals as well as remarkable changes in QRS-complex duration, shape, amplitude, and mean electrical axis. Paper speed = 50 mm/s; 1 cm = 2 mV.

  • 1. Meurs KM. Boxer dog cardiomyopathy: an update. Vet Clin North Am Small Anim Pract 2004; 34: 12351244.

  • 2. Kraus MS, Moïse NS, Rishniw M, et al. Morphology of ventricular arrhythmias in the boxer as measured by 12-lead electrocardiography with pace-mapping comparison. J Vet Intern Med 2002; 16: 153158.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3. Santilli RA, Perego M. Genesi e interpretazione delle onde elettrocardiografiche. In: Elettrocardiografia del cane e del gatto. Milan: Elsevier Inc, 2009; 3946.

    • Search Google Scholar
    • Export Citation
  • 4. Tilley LP. Analysis of canine P-QRS-T deflections. In: Tilley LP, ed. Essentials of canine and feline electrocardiography: interpretation and treatment. 2nd ed. Philadelphia: Lea & Febiger, Lea & Febiger; 58.

    • Search Google Scholar
    • Export Citation
  • 5. Perego M, Ramera L, Santilli RA. Isorhythmic atrioventricular dissociation in Labrador Retrievers. J Vet Intern Med 2012; 26: 320325.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6. Issa ZF, Miller JM, Zipes DP. Atrioventricular reentrant tachycardia. In: Issa ZF, Miller JM, Zipes DP, eds. Clinical arrhythmology and electrophysiology: a companion to Braunwald's heart disease. 2nd ed. Philadelphia: Elsevier Inc, Elsevier Inc; 411467.

    • Search Google Scholar
    • Export Citation
  • 7. Saguner AM, Brunckhorst C, Duru F. Arrhythmogenic right ventricular cardiomyopathy: a paradigm shift from right to biventricular disease. World J Cardiol 2014; 6: 154174.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Santilli RA, Bontempi LV, Perego M. Ventricular tachycardia in English bulldogs with localized right ventricular outflow tract enlargement. J Small Anim Pract 2011; 52: 574580.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Palermo V, Stafford Johnson MJ, Sala E, et al. Cardiomyopathy in Boxer dogs: a retrospective study of the clinical presentation, diagnostic findings and survival. J Vet Cardiol 2011; 13: 4555.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10. Santilli RA, Bontempi LV, Perego M, et al. Outflow tract segmental arrhythmogenic right ventricular cardiomyopathy in an English Bulldog. J Vet Cardiol 2009; 11: 4751.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11. Waldo AL, Vitikainen KJ, Harris PD, et al. The mechanism of synchronization in isorhythmic A-V dissociation: some observations on the morphology and polarity of the P wave during retrograde capture of atria. Circulation 1968; 38: 880898.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. Levy MN, Zieske H. Mechanism of synchronization in isorhythmic dissociation. I. Experiments on dogs. Circ Res 1970; 27: 429443.

  • 13. Levy MN, Edflstein J. The mechanism of synchronization in isorhythmic A-V dissociation. II. Clinical studies. Circulation 1970; 42: 689699.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14. Marriott HJ. Atrioventricular synchronization and accrochage. Circulation 1956; 14: 3843.

  • 15. Tϋrkoğlu C, Aliyev F, Çeliker C, et al. Diagnostic trilemma: isorhythmic AV dissociation mimicking intermittent preexcitation and acute inferior myocardial infarction. J Interv Card Electrophysiol 2008; 22: 4547.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16. Santilli RA, Diana A, Baron Toaldo M. Orthodromic atrioventricular reciprocating tachycardia with intraventricular conduction disturbance mimicking ventricular tachycardia in an English Bulldog. J Vet Cardiol 2012; 14: 363370.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17. Frais MA, Manyari DE, Duff HJ, et al. Coexistent arrhythmogenic right ventricular dysplasia and Wolff-Parkinson-White syndrome. Am J Cardiol 1984; 53: 632634.

    • Crossref
    • Search Google Scholar
    • Export Citation

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