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Alice G. Morey Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO

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Kelly E. Wiggen Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO

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Introduction

A 6-year-old 38.8-kg castrated male Rottweiler was presented to the University of Missouri Veterinary Health Center because of vomiting and labored breathing. The dog had a history of surgical mass removal from the ventral aspect of the neck 5 days before presentation and amputation of the right pelvic limb as a juvenile. On examination, the dog was dull but responsive. Rectal temperature was 37.5 °C, mucous membranes were pale, and capillary refill time was 2 seconds. The heart rate was 260 beats/min. A heart murmur was not appreciated, and heart sounds were decreased. Increased bronchovesicular sounds were present dorsally bilaterally. The left femoral pulse was hypokinetic with pulse deficits. The abdomen was tense on palpation, with pain elicited caudally. Systolic blood pressure was initially 65 mm Hg (Doppler ultrasonographic method) and improved to 90 mm Hg following fluid resuscitation.

Clinicopathologic analysis revealed monocytosis (1,750 monocytes/μL; reference range, 50 to 1,240 monocytes/μL), basophilia (140 basophils/μL; reference range, 0 to 30 basophils/μL), mild hypoglycemia (79 mg/dL; reference range, 81 to 155 mg/dL), metabolic acidosis (bicarbonate, –16 mEq/L; reference range, 17 to 26 mEq/L; anion gap, –23 mEq/L; reference range, 12 to 20 mEq/L), hyponatremia (140 mEq/L; reference range, 145 to 151 mEq/L), hypochloremia (105 mEq/L; reference range, 110 to 117 mEq/L), hyperglobulinemia (4.0 g/dL; reference range, 2.4 to 3.7 g/dL), and hyperphosphatemia (5.1 mEq/L; reference range, 2.3 to 5.0 mEq/L). Thoracic radiography revealed a diffuse interstitial pattern and possible sternal lymphadenopathy; mild pleural effusion was identified on thoracic-focused assessment for triage. On analysis, the pleural effusion was consistent with a neutrophilic to mixed-cell exudate (specific gravity, 1.023; PCV, < 2%; total protein, 3.2 g/dL), without neoplastic cells or microorganisms. Abdominal radiography revealed small-volume pneumoperitoneum. Abdominal ultrasonography showed mild abdominal effusion, gall bladder wall edema, splenic nodules, and mildly enlarged abdominal lymph nodes (approx diameter, 8 mm). Analysis of the abdominal effusion yielded a mixed-cell, high-protein transudate (specific gravity, 1.030; PCV, < 2%; total protein, 4.9 g/dL), without neoplastic cells or microorganisms.

Echocardiography revealed an infiltrative mass lesion within the left ventricular (LV) free wall extending from the papillary muscle to the mitral valve annulus and a large, heterogenous intrathoracic mass that extended cranially and caudally around the heart. Left ventricular and left atrial dimensions were normal (LV internal end-diastolic dimension, 42.6 mm [normalized = 1.34]; LV internal end-systolic dimension, 30.5 mm [normalized = 0.73]; left atrial diameter, 41.3 mm [normalized = 1.33]1), with trace mitral regurgitation. A 10-lead ECG tracing was obtained (Figure 1).

Figure 1
Figure 1

Ten-lead ECG tracing from a 6-year-old Rottweiler that was evaluated because of vomiting and labored breathing. The heart rate is 250 beats/min. The QRS complexes are wide and bizarre (100 milliseconds), which is highlighted in the precordial leads (V2, V3, and V4). No P waves are discernible throughout the tracing. Biphasic T waves are present in leads II, III, aVF, and aVL, which appear as pseudo P waves (arrows). The precordial leads display discordance with the limb leads, which aids in differentiating this arrhythmia as ventricular tachycardia. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 15; 10.2460/javma.21.05.0263

ECG Interpretation

The 10-lead ECG tracing revealed an incessant tachycardia with a mean ventricular response rate of 250 beats/min (Figure 1). The QRS complexes were wide and bizarre with prolonged duration (100 milliseconds; reference range,2 < 70 milliseconds), highlighted on the left precordial leads (V2, V3, and V4). There were no visible P waves in any leads. The R-wave peak time in lead II was prolonged (50 milliseconds; mesomorphic reference range3 in lead II, 30 milliseconds). The waveform preceding each QRS complex in leads II, III, aVL, and aVF was a biphasic T wave, as determined from the left precordial leads, rather than a P wave. The rhythm diagnosis was sustained monomorphic ventricular tachycardia (VT).

Four lidocaine boluses (total dose, 8 mg/kg, IV) followed by a lidocaine constant rate infusion (50 μg/kg/min, IV) were administered to the dog without response. A bolus of amiodarone hydrochloride (3 mg/kg, IV) was administered, and approximately 2 to 3 minutes of sinus rhythm was achieved before VT resumed. Thoracic CT and fine-needle aspiration of the masses were declined, and euthanasia was elected.

A necropsy was performed, and findings were consistent with a cranial mediastinal mass, nodules in multiple organs (lungs, kidneys, and heart), and an infiltrative adrenal mass. The gross appearance of the nodules was similar to that of the cranial mediastinal mass, and the histologic characteristics of the neoplastic cells were suggestive of a round cell tumor with histiocytic sarcoma as the top differential. However, results of immunohistochemical staining for CD204 and IBA were negative. Neoplastic cells were also negative for cytokeratin, ruling out an epithelial neoplasm. Results of subsequent staining were negative for CD79a but positive for CD3, confirming T-cell lymphoma. The left adrenal gland had multifocal, tan-to-white nodules associated with the cortex and medulla on cross section; invasion of neoplastic adrenal medullary cells into the adrenal cortex was present, consistent with a pheochromocytoma.

Discussion

This case described sustained VT in a dog with infiltrative LV myocardial disease and a pheochromocytoma. The utility of a 10-lead ECG is highlighted, given that a 6-lead ECG may have led to a misdiagnosis of supraventricular tachycardia (SVT) owing to the unusual appearance of the QRS complexes and T waves in the limb leads.

Ventricular tachycardia, SVT conducted with a bundle branch block, and SVT conducted via an accessory pathway are potential differential diagnoses for wide-complex tachycardias.4 There are several ways to differentiate VT from SVT. In this case, the ECG highlighted a discordance between the limb leads and the left precordial leads (V2, V3, and V4), a morphologic pattern present with VT but not with SVT conducted with aberrancy or with pre-excitation SVT. In this case, leads II, III, and aVF were positively deflected, whereas leads V2, V3, and V4 were negatively deflected. Typically, SVT conducted with a classic left or right bundle branch block should display limb lead and left precordial lead concordance,4 which was not present in this dog. An SVT conducted via an accessory pathway could also be ruled out because an accessory pathway should cause ventricular activation from base to apex, resulting in the widest, most-positive QRS complexes in the left precordial leads4; in this patient, they were negatively deflected. Another defining feature used to diagnose VT is the presence of atrioventricular dissociation, which confirms a ventricular rhythm that is independent of the supraventricular structures. Although not present in this ECG, signs of atrioventricular dissociation include P waves with a sinus axis that are unrelated to the QRS complexes, fusion beats, and capture beats.4 Finally, R-peak time (also known as intrinsicoid deflection) is used to differentiate wide-complex tachycardias in humans, and reference ranges have recently been described in dogs. The R-peak time is from the onset of the QRS complex to the peak of the R wave and corresponds to ventricular depolarization from the endocardium to the epicardium; an R-peak time of 30 milliseconds in lead II is considered normal in mesomorphic dogs.3,5 In this patient, the R-peak time was approximately 50 milliseconds. A previous report6 of humans suggested that an R-peak time > 50 milliseconds in lead II may aid in differentiating VT from SVT. Although this method has not been validated in dogs, the R-peak time in this patient (50 milliseconds) supported VT as the rhythm diagnosis.

Given the postmortem findings, either the infiltrative LV mass or the pheochromocytoma could have been the reason for this patient developing refractory VT. Generally, arrhythmogenic mechanisms include altered automaticity, triggered activity, and reentry.7 In this case, the infiltrative LV mass may have acted as an anatomic substrate that perpetuated monomorphic VT via reentry. However, if this were the case, it is unclear why a right bundle branch block pattern was not more obvious. It is also possible that neoplastic cells may have extended further into the myocardium than was apparent on echocardiography, leading to VT with atypical QRS complex morphology in the limb leads secondary to an unusual reentrant circuit. Triggers and modulating factors are required for initiation and maintenance of arrhythmias, and in this dog, hypoxia of the myocardium surrounding the tumor could have increased the occurrence of early after-depolarizations, which can precipitate VT that is subsequently sustained by reentry.8 Cardiac lymphoma is uncommon, and in this patient, the tumor would be considered stage V, substage b.9 In a previous case series10 of dogs with cardiac lymphoma, refractory ventricular arrhythmias were not reported. However, all dogs in that report were presented with pericardial effusion, and overt mass-like lesions affecting the heart were not reported.

Pheochromocytomas are the most common tumor originating from the adrenal medulla in dogs,11 and this neoplasm also likely contributed to the patient’s refractory arrhythmia. Functional pheochromocytomas produce excessive circulating catecholamines, especially epinephrine, which may lead to triggered activity such as delayed after-depolarizations.12 Excessive catecholamines are also proarrhythmic by causing an increase in automaticity and conduction velocity and increasing the permeability of the myocardial cells. This can increase intracellular calcium release from the sarcoplasmic reticulum, which propagates an influx of sodium into the myocyte, resulting in triggered activity.11,13 Additionally, excessive catecholamines can cause profound coronary vasoconstriction and subsequent myocardial ischemia,14,15 which could allow for propagation of a reentrant arrhythmia.4 Previously, 3 of 9 dogs were described to have arrhythmias secondary to a pheochromocytoma, with only 1 displaying a ventricular arrhythmia; however, all dogs showed histologic evidence of cardiomyocyte necrosis with contraction band formation, cellular degeneration, myocyte fibrosis, and myocarditis.15 Although histologic evidence of cardiomyocyte necrosis was not reported in this patient, acute alterations in myocardial permeability and alterations in intracellular calcium cycling secondary to the pheochromocytoma may have also played a role in propagation of the arrhythmia.16

Acknowledgments

No third-party funding or support was received in connection with this case or the writing or publication of the manuscript. The authors declare that there were no conflicts of interest.

References

  • 1.

    Visser LC, Ciccozzi MM, Sintov DJ, Sharpe AN. Echocardiographic quantitation of left heart function in 122 healthy dogs: a prospective study proposing reference intervals and assessing repeatability. J Vet Intern Med. 2019;33(5):19091920.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2.

    Santilli R, Möise NS, Pariaut R, Perego M. Formation and interpretation of the electrocardiographic waves. In: Electrocardiography of the Dog and Cat: Diagnosis of Arrhythmias. 2nd ed. Edra; 2018:3569.

    • Search Google Scholar
    • Export Citation
  • 3.

    Mateos Pañero M, Battaia S, Ramera L, Perego M, Santilli RA. R-peak time in clinically healthy dogs with different thoracic conformations. Vet J. 2021;268:105592. doi:10.1016/j.tvjl.2020.105592

    • Search Google Scholar
    • Export Citation
  • 4.

    Santilli RA, Möise NS, Pariaut R, Perego M. Ventricular arrhythmias. In: Electrocardiography of the Dog and Cat: Diagnosis of Arrhythmias. 2nd ed. Edra; 2018:203238.

    • Search Google Scholar
    • Export Citation
  • 5.

    Deng J, Chen T, Zeng C, et al. R-wave peak time at lead II in Chinese healthy adults. BMC Cardiovasc Disord. 2016;16:88. doi:10.1186/s12872-016-0258-7

    • Search Google Scholar
    • Export Citation
  • 6.

    Pava LF, Perafán P, Badiel M, et al. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm. 2010;7(7):922926.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7.

    Marriott HJ, Conover MB. Arrhythmogenic mechanisms and their modulation. Advanced Concepts in Arrhythmias. 3rd ed. Mosby; 1998:4768.

  • 8.

    Santilli RA, Möise NS, Pariaut R, Perego M. Background to the diagnosis of arrhythmias. In: Electrocardiography of the Dog and Cat: Diagnosis of Arrhythmias. 2nd ed. Edra; 2018:93129.

    • Search Google Scholar
    • Export Citation
  • 9.

    Treggiari E, Pedro B, Dukes-McEwan J, Gelzer AR, Blackwood L. A descriptive review of cardiac tumours in dogs and cats. Vet Comp Oncol. 2017;15(2):273288.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 10.

    MacGregor JM, Faria MLE, Moore AS, Tobias AH, Brown DJ, de Morais HS. Cardiac lymphoma and pericardial effusion in dogs: 12 cases (1994–2004). J Am Vet Med Assoc. 2005;227(9):14491453.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11.

    Ettinger SJ, Feldman EC, Côté E. Pheochromocytoma. Textbook of Veterinary Internal Medicine. 8th ed. Elsevier; 2017:18381843.

  • 12.

    Atkins CE. Cardiac manifestations of systemic and metabolic disease. In: Fox PR, Sisson DD, Möise NS, eds. Textbook of Canine and Feline Cardiology: Principles and Clinical Practice. 2nd ed. Saunders; 1999:761784.

    • Search Google Scholar
    • Export Citation
  • 13.

    Ahmed MA, Abdullah AS, Kiernan TJ. Phaeochromocytoma presenting with ST segment elevation myocardial infarction. BMJ Case Rep. 2016;2016:bcr2015214134. doi:10.1136/bcr-2015-214134

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14.

    Maher ER Jr, McNiel EA. Pheochromocytoma in dogs and cats. Vet Clin North Am Small Anim Pract. 1997;27(2):359380.

  • 15.

    Edmondson EF, Bright JM, Halsey CH, Ehrhart EJ. Pathologic and cardiovascular characterization of pheochromocytoma-associated cardiomyopathy in dogs. Vet Pathol. 2015;52(2):338343.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16.

    Gu YW, Poste J, Kunal M, Schwarcz M, Weiss I. Cardiovascular manifestations of pheochromocytoma. Cardiol Rev. 2017;25(5):215222.

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