ECG of the Month

Tommaso Vezzosi 1Department of Veterinary Sciences, University of Pisa, 56122 Pisa, Italy.

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Oriol Domenech 2Dipartimento di Cardiologica, Istituto Veterinario di Novara, 28060 Novara, Italy.

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Chiara Cipollini 1Department of Veterinary Sciences, University of Pisa, 56122 Pisa, Italy.

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Carlo Cantile 1Department of Veterinary Sciences, University of Pisa, 56122 Pisa, Italy.

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Etienne Côté 3Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE CIA 4P3, Canada.

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Rosalba Tognetti 1Department of Veterinary Sciences, University of Pisa, 56122 Pisa, Italy.

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A 13-year-old 4.2-kg (9.2-lb) spayed female Maine Coon cat was referred to the Veterinary Teaching Hospital of the University of Pisa for cardiovascular evaluation after an acute episode of dyspnea associated with suspected cardiogenic pulmonary edema. The cat was initially treated with furosemide by the referring veterinarian. On physical examination, the cat had dull mentation and was paraparetic. The respiratory rate was 36 breaths/min, and the heart rate was 180 beats/min. Femoral pulse quality was weak bilaterally. Cardiac auscultation revealed no murmur or gallop sounds. Lung auscultation revealed no detectable abnormalities. The cat's rectal temperature was 37.1°C (98.8°F).

The initial diagnostic workup included a CBC, serum biochemical panel, thoracic radiography, echocardiography, and abdominal ultrasonography (including evaluation of the terminal portion of the aorta). Electrocardiography was also performed. The results of the CBC were within reference intervals. The serum biochemical panel revealed high creatinine concentration (4.8 mg/dL; reference interval, 0.7 to 1.7 mg/dL), high urea concentration (263 mg/dL; reference interval, 20 to 65 mg/dL), hypoalbuminemia (1.8 g/dL; reference interval, 2.8 to 4 g/dL), hyponatremia (145 mEq/L; reference interval, 153 to 162 mEq/L), and hyperkalemia (6.6 mEq/L; reference interval, 3.6 to 5.8 mEq/L). Thoracic radiography revealed cardiomegaly without evidence of pulmonary edema or pleural effusion. Echocardiographically, there was severe diffuse thickening of the left ventricle with heterogeneous echogenicity of the myocardium, severe left atrial enlargement, spontaneous echocardiographic contrast in the left auricle associated with blood stasis, and mild pericardial effusion. Abdominal ultrasonography revealed bilateral kidney enlargement with increased cortical echogenicity, loss of corticomedullary differentiation, and retroperitoneal effusion. The right adrenal gland was enlarged and had heterogeneous echogenicity. Two-dimensional and Doppler ultrasonographic examination of the terminal portion of the aorta revealed no abnormalities. Six-lead surface ECG was performed (Figure 1).

Figure 1—
Figure 1—

Six-lead ECG recording obtained from a Maine Coon cat that was evaluated after an acute episode of dyspnea associated with suspected cardiogenic pulmonary edema. The main rhythm is regular, with an instantaneous ventricular rate of 176 beats/min. This is faster than the atrial rate (171 beats/min; arrows). All of the QRS complexes have a bizarre morphology consistent with a ventricular origin, and all are narrow except for those marked with an asterisk. The P waves (arrows) occur with a regular P-P interval. The P waves are found mainly in the ST segment and occasionally before QRS complexes when preceded by premature ventricular complexes of a morphology that is different (asterisks) from the morphology of the premature ventricular complexes making up the rest of the rhythm. These findings are indicative of accelerated idioventricular rhythm with atrioventricular dissociation. The 2 premature ventricular complexes that are of a different morphology (asterisks) than the others are followed by postextrasystolic pauses that cause a variation of the regular R-R intervals. This momentary change in rate further illustrates the regularity of the P-P interval and the lack of association between P waves and QRS complexes throughout this tracing. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 255, 11; 10.2460/javma.255.11.1234

ECG Interpretation

Six-lead surface ECG revealed that the main rhythm was regular and the heart rate was 176 beats/min. Most QRS complexes were narrow (duration, 40 milliseconds; reference interval, ≤ 40 milliseconds), and all had a bizarre morphology. This morphology suggested a ventricular origin or an intraventricular conduction disturbance; the lack of a P wave preceding each QRS complex at a fixed PR interval indicated that all QRS complexes were of ventricular origin. Two complexes on the ECG recording were even more premature and of a very different morphology than the rest. These features indicated that those 2 complexes were also premature ventricular complexes, but they originated from a location in the ventricles that differed from that of the QRS complexes making up the rest of the ventricular rhythm in this tracing. Each of these 2 wider and more bizarre-appearing premature complexes was followed by a postextrasystolic pause, which caused an instantaneous variation of the R-R interval but not of the P-P interval. The P waves were mainly found in the ST segment; occasionally, the P wave was visible before the next QRS complex if a premature ventricular complex had just occurred, but in these instances, the PR interval was not constant. The atrial rate (171 beats/min) was constant and slightly lower than the ventricular rate (176 beats/min). Together, these findings indicated atrioventricular dissociation. The ECG diagnosis was accelerated idioventricular rhythm with 2 additional premature ventricular complexes.

Discussion

Accelerated idioventricular rhythm consists of 4 or more QRS complexes of ventricular origin that occur consecutively with a heart rate less than the defined cutoff for ventricular tachycardia (which for cats is 240 beats/min).1 In the ECG recording obtained from the cat of the present report, accelerated idioventricular rhythm was apparent for the duration of the tracing, with 2 premature ventricular complexes of a different morphology. Ventricular rhythms at heart rates < 120 beats/min may be considered ventricular escape rhythms in cats.1,2 Ventricular ectopic beats typically have a wide and bizarre morphology. However, ventricular beats originating from near the bundle of His (the para-Hisian area) are characterized by narrow QRS complexes.3 In the cat of the present report, the QRS complexes had bizarre morphology but a normal QRS duration, suggestive of an accelerated idioventricular rhythm originating from the para-Hisian area. Moreover, atrioventricular dissociation was evident because the cat's ventricular rate was slightly faster than its atrial rate. For the cat of the present report, the P waves were mainly found in the ST segment with little variation in their position because the ventricular rate coincidentally was only slightly higher than the atrial rate. This type of atrioventricular dissociation, wherein atria and ventricles are driven by independent pacemakers at equal or nearly equal rates, is termed isorhythmic atrioventricular dissociation.4–6 The lack of relationship between atrial and ventricular activity was further emphasized by the occurrence of 2 premature ventricular complexes that were seemingly from different foci of origin, compared with that of the others, after which the relationship between P waves and QRS complexes was different but the P-P interval remained unchanged. A reasonable explanation was that the premature ventricular complexes depolarized the ectopic focus of the accelerated idioventricular rhythm, leading to a transient prolongation of the R-R interval of the underlying main ventricular rhythm. After that, the ectopic focus of the accelerated idioventricular rhythm recovered the preceding depolarization rate and the position of the P waves progressively moved again into the ST segment. The lack of variation in the P-P interval indicated no detectable influence of ectopic ventricular activity on the atria through ventriculo-atrial retrograde conduction.7

In the case described in the present report, the owners elected for the cat to be euthanized because of its severe clinical condition. The cat was premedicated with ketamine and butorphanol, and then an injectable euthanasia solution of embutramide, mebezonium iodide, and tetracaine hydrochloride was administered IV. Necropsy revealed small-cell multicentric lymphoma that had affected the heart, kidneys, adrenal glands, spinal cord, and brain. In the heart, a heavy neoplastic infiltration of the interventricular septum was detected, which could have been responsible for a para-Hisian origin of the ectopic ventricular rhythm. In humans, cardiac involvement with malignant lymphoma has been described in as many as 25% of 196 autopsies8 of patients with Hodgkin disease (n = 75), lymphosarcoma (32), reticulum cell sarcoma (22), mycosis fungoides (51), and undifferentiated types of lymphoma (16).

Both ventricular arrhythmias and atrioventricular blocks associated with cardiac lymphoma in human patients have been reported.9–12 In dogs with lymphoma, myocardial involvement has been described only rarely.13,14 One of the largest retrospective studies15 of secondary heart tumors in cats found carcinoma to be the most common tumor type (3/8 cats with heart metastases), followed by mammary gland tumors and lymphoma (2 cases each), and then lung primary tumor (1 case). Third-degree atrioventricular block associated with cardiac lymphoma in dogs and cats has rarely been reported.16,17

Acknowledgments

The authors thank Damiano Frangioni for technical assistance.

References

  • 1. Côté E, Meurs KM, MacDonald KA, et al. Arrhythmias and other electrocardiographic abnormalities. In: Feline cardiology. Chichester, England: John Wiley & Sons Ltd, 2011;213253.

    • Search Google Scholar
    • Export Citation
  • 2. Kellum HB, Stepien RL. Third-degree atrioventricular block in 21 cats (1997-2004). J Vet Intern Med 2006;20:97103.

  • 3. Ban JE, Cheng YL, Park HC, et al. Idiopathic ventricular arrhythmia originating from the para-Hisian area: prevalence, electrocardiographic and electrophysiological characteristic. J Arrhythmia 2014;30:4854.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4. Shipley EA, Saunders AB. ECG of the Month. Sinus arrhythmia. J Am Vet Med Assoc 2008;233:714715.

  • 5. Perego M, Ramera R, Santilli RA. Isorhythmic atrioventricular dissociation in Labrador Retrievers. J Vet Intern Med 2012;26:320325.

  • 6. Pereira NJ, Glaus T, Matos JN. ECG of the Month. Isorhythmic atrioventricular dissociation during hypothermia. J Am Vet Med Assoc 2014;244:13841386.

    • Search Google Scholar
    • Export Citation
  • 7. Kistin AD, Landowne M. Retrograde conduction from premature ventricular contractions, a common occurrence in the human heart. Circulation 1951;3:738751.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Roberts WC, Glancy DL, DeVita VT. Heart in malignant lymphoma (Hodgkin's disease, lymphosarcoma, reticulum cell sarcoma and mycosis fungoides): a study of 196 autopsy cases. Am J Cardiol 1968;22:85107.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Cho JG, Ahn YK, Cho SK, et al. A case of secondary myocardial lymphoma presenting with ventricular tachycardia. Korean Med Sci 2002;17:549551.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10. Nakabayashi K, Sugiura R, Oka T, et al. Catheter ablation targeting Purkinje potentials controller ventricular fibrillation in a patient with a malignant lymphoma occurring in the ventricular septum. BMJ Case Rep 2015;2015:brc2014209026.

    • Search Google Scholar
    • Export Citation
  • 11. Montiel V, Maziers N, Dereme T. Primary cardiac lymphoma and complete atrio-ventricular block: case report and review of the literature. Acta Cardiol 2007;62:5558.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. Miguel CE, Bestetti RB. Primary cardiac lymphoma. Int J Cardiol 2011;149:358363.

  • 13. MacGregor JM, Faria ML, Moore AS, et al. Cardiac lymphoma and pericardial effusion in dogs: 12 cases (1994-2004). J Am Vet Med Assoc 2005;227:14491453.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14. Walter JH, Rudolph R. Systemic, metastatic, eu- and heterotope tumours of the heart in necropsied dogs. Zentralbl Veterinarmed A 1996;43:3145.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15. Aupperle H, Marz I, Ellenberger C, et al. Primary and secondary heart tumours in dogs and cats. J Comp Pathol 2007;136:1826.

  • 16. Tilley LP. Feline third-degree AV block (complete block). In: Tilley LP, ed. Essentials of canine and feline electrocardiography: interpretation and treatment. 3rd ed. Philadelphia: Lea & Febiger, 1992;234235.

    • Search Google Scholar
    • Export Citation
  • 17. Stern JA, Tobias JR, Keene BW. Complete atrioventricular block secondary to cardiac lymphoma in a dog. J Vet Cardiol 2012;14:537539.

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