Canis ISSN: 2398-2942

Arrhythmogenic right ventricular cardiomyopathy (ARVC) in the Boxer

Synonym(s): Boxer cardiomyopathy, arrhythmogenic cardiomyopathy, familial ventricular arrhythmia (FVA of Boxers)

Contributor(s): Dan Ohad, Alan Spier

Introduction

  • Boxer cardiomyopathy is an inherited myocardial abnormality of Boxer dogs characterized by the presence of ventricular arrhythmias.
  • Affected dogs are predisposed to the development of clinical signs including syncope, sudden death and, rarely, congestive heart failure.
  • The disease exhibits many clinical, pathologic, and genetic features of arrhythmogenic right ventricular cardiomyopathy (ARVC) in humans.
Print off the owner factsheet Boxer cardiomyopathy (arrhythmogenic right ventricular cardiomyopathy (AVRC)) Boxer cardiomyopathy (arrhythmogenic right ventricular cardiomyopathy (AVRC)) to give to your client.

Pathogenesis

Etiology

  • The etiology of ARVC in Boxers is most likely genetic, and has been demonstrated to be inherited as an autosomal dominant trait. The actual genetic abnormality is, as of yet, unidentified. Efforts are ongoing to determine the actual gene(s) responsible for the disease.

Predisposing factors

General

  • As a genetic disease, the single most important disposing factor is a family history of disease.
  • Given the apparent heterogeneous manifestation of the disease, not all animals with ARVC are overtly affected. Silent carriers are easily missed which precludes readily identifying individual animals that should be excluded from breeding programs. Consequently, a family history of disease may exist and not be recognized by either the breeder of the veterinarian.

Pathophysiology

  • The underlying cardiac abnormalities associated with disease are unknown, but may be related to cellular calcium dynamics.
  • Histologically, affected dogs have a fibrofatty myocardial infiltration that appears to originate in the right ventricle and interventricular septum, with left ventricular involvement occurring later in the course of disease.
  • This pattern is consistent with the clinical manifestation of disease in that ventricular arrhythmias of right ventricular origin are most commonly seen, with abnormal left ventricular morphology and impaired function seen less commonly and in more severe cases (Type III dogs).

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Baumwart R D, Meurs K M, Atkins C E, Bonagura J D, DeFrancesco T C, Keene B W, Koplitz S, Luis Fuentes V, Miller M W, Rausch W & Spier A (2005) Clinical, echocardiographic, and electrocardiograhic abnormalities in Boxers with cardiomyopathy and left ventricular systolic dysfunction: 48 cases (1985-2003). JAVMA 226, 1102-1104 PubMed.
  • Basso C, Fox P R, Meurs K M et al (2004) Arrhythmogenic right ventricular cardiomyopathy causing sudden death in boxer dogs: a new animal model of human disease. Circulation 109 (9), 1180-1185 PubMed.
  • Meurs K M, Spier A W, Wright N A et al (2002) Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers. J Am Vet Med Assoc 221 (4), 522-527 PubMed.
  • Meurs K M, Spier A W, Wright N A et al (2001) Comparison of in-hospital versus 24-hour ambulatory electrocardiography for detection of ventricular premature complexes in mature Boxers. J Am Vet Med Assoc 218 (2), 222-224 PubMed.
  • Meurs K M, Spier A W, Miller M W et al (1999) Familial ventricular arrhythmias in Boxers. J Vet Intern Med 13 (5), 437-439 PubMed.
  • Harpster N K (1991) Boxer cardiomyopathy. A review of the long term benefits of antiarrhythmic therapy. Vet Clin North Am Small Anim Pract 21 (5), 989-1004 PubMed.

Other sources of information

  • Prosek R et al (2006) Comparison of sotalol and mexiletine versus stand alone sotalol in treatment of boxer dogs with ventricular arrhythmias. JVIM 20(3), 748 (abstract).
  • Harpster N K (1983) Boxer cardiomyopathy. In: Kirk RW, ed. Current Veterinary Therapy VIII Small Animal Practice. Philadelphia Pa, WB Saunders: pp 329-337.


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