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Cardiomyopathy in Boxer Dogs: a Retrospective Study of the Clinical Presentation, Diagnostic findings and Survival

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Cardiomyopathy in Boxer Dogs: a Retrospective Study of the Clinical Presentation, Diagnostic findings and Survival Journal of Veterinary Cardiology (2011) 13,45e55 www.elsevier.com/locate/jvc Cardiomyopathy in Boxer dogs: A retrospective study of the clinical presentation, diagnostic findings and survival Valentina Palermo, DVM, PhD, MRCVS a,d,*, Michael J. Stafford Johnson, MVB, CertSAM, DVC, MRCVS b, Elisabetta Sala, PhD c, Paola G. Brambilla, DVM, PhD a, Mike W.S. Martin, MVB, DVC, MRCVS b a Dipartimento di Scienze Cliniche Veterinarie, Sezione di Clinica Medica Veterinaria, Facolta` di Medicina Veterinaria, via Celoria 10, 20131 Milano, Italy b Veterinary Cardiorespiratory Center, Thera House, Waverley Road, Kenilworth CV8 1JL, UK c Busto Arsizio Hospital, Varese, Italy Received 5 October 2009; received in revised form 21 June 2010; accepted 22 June 2010 KEYWORDS Abstract Objectives: To retrospectively compare and contrast the clinical Boxer; presentation, diagnostic findings and survival in Boxer dogs with cardiomyopathy, Ventricular with or without left ventricular (LV) systolic failure. arrhythmia; Animals, materials and methods: Medical records of Boxers referred between 1993 Cardiomyopathy; and 2008 in which a diagnosis of ventricular arrhythmias and/or cardiomyopathy was Survival made, were reviewed. Dogs were divided into two groups according to their left ventricular (LV)systolic diameter, groupA normal (20 dogs) or group B dilated(59 dogs). Results: Dogs in group A had a better outcome than dogs in group B (median survival time of 124 and 17 weeks respectively, p < 0.001). In group B, dogs with a history of collapse had a worse outcome (median survival time of 10 weeks) compared with dogs not showing collapse (median survival time 24 weeks) (p ¼ 0.031). Conclusions: The majority of dogs, in this UK study, presented with the myocardial dysfunction form of the disease, with LV dilation and congestive heart failure signs. The prognosis was worse in dogs with LV dilation compared to dogs with a normal LV and ventricular arrhythmias. In the Boxers with LV dilation, dogs with collapse had a worse prognosis than those without. ª 2011 Elsevier B.V. All rights reserved. * Corresponding author. E-mail address: [email protected] (V. Palermo). d Present address: Hospital for Small Animals, Royal (Dick) School of Veterinary Studies, Roslin, Midlothian EH25 9RG, Scotland, UK. 1760-2734/$ - see front matter ª 2011 Elsevier B.V. All rights reserved. doi:10.1016/j.jvc.2010.06.005 46 V. Palermo et al. Introduction Much research has been carried out to try to identify a mutation or genetic abnormality linked to ARVC. In cardiomyopathic Boxer dogs myocar- Harpster first described “Boxer cardiomyopathy” dial calstabin2 mRNA and protein were signifi- (BCM) in 1983 proposing three clinical categories of cantly decreased as compared to healthy control the disease: concealed, overt and a myocardial dogs8 and recently a 7 base pair deletion in dysfunction form.1 The concealed form is charac- a regulatory region of a calcium modulating gene terized by the absence of clinical signs but pres- was identified and observed to be highly associ- ence of ventricular premature complexes (VPCs). ated with the disease status.9 In the overt form, syncope or episodic weakness There are few publications describing pop- and tachyarrhythmias are present, while the third ulations of Boxers affected by cardiomyopathy and group is characterized by myocardial systolic the majority were reported by Harpster in 1983 dysfunction (affecting mainly the left ventricle) and 1991.1,2 Moreover, most of the more recent sometimes with congestive heart failure (CHF) and e work on ARVC comes from the USA9 17 and no arrhythmias.1e3 survival studies are available. Boxer cardiomyopathy has been characterized The aim of this study was to retrospectively as a degenerative myocardial disease with exten- evaluate signalment, clinical and diagnostic find- sive and unique right ventricular histologic findings ings, survival and prognostic factors in a pop- that include myocyte atrophy and fatty infiltra- ulation of Boxer dogs with cardiomyopathy from tion.1 Similarities in clinical presentation, patho- the UK, in order to improve our knowledge of this logical findings and presumed aetiology with disease. Given the difficulties in differentiating a human myocardial disease called arrhythmo- ARVC from idiopathic DCM affected Boxers were genic right ventricular cardiomyopathy, have sug- divided into two groups according to their left gested reclassification of the disease as Boxer ventricular systolic diameter, either normal or arrhythmogenic right ventricular cardiomyopathy increased. The two groups were then compared in (ARVC).3,4 terms of presentation, outcome and possible In Boxers, ARVC is an adult-onset familial relationship between the two populations. disease apparently inherited as an autosomal dominant trait.5 ARVC is primarily an electrical disease sometimes associated with myocardial dysfunction. Diagnosis is best based on a combina- Materials and methods tion of findings that may include a family history of disease, a history of syncope, presence of Medical records of client-owned Boxer dogs ventricular tachyarrhythmias with a left bundle referred to the Veterinary Cardiorespiratory branch block (LBBB) morphology or post mortem Centre, Kenilworth, UK, between January 1993 findings. Most affected dogs have a normal echo- and July 2008, in which a diagnosis of cardiomy- cardiographic examination, particularly with opathy or ventricular arrhythmia had been made, regard to evaluation of the size and function of the were reviewed. Only dogs that were referred with left ventricle.3 a clinical history or presence of a clinical or ECG Idiopathic dilated cardiomyopathy (DCM) is abnormality were included in the study. Dogs a primary myocardial disorder characterized by examined for routine breed screening were reduced contractility and ventricular dilation excluded. Information obtained included: age, involving the left ventricle or both ventricles, of sex, clinical presentation; results of standard unknown or uncertain aetiology.6,7 Some Boxer 6-lead electrocardiography (HR, rhythm, presence dogs have a clinical and echocardiographic and morphology of VPCs), 24-h Holter monitoring, presentation consistent with idiopathic dilated thoracic radiography, Doppler echocardiography cardiomyopathy, of which the etiology is unknown. and survival time. Harpster refers to these cases as the myocardial Diagnosis of cardiomyopathy was based on dysfunction form (category 3) which is considered a combination of factors including a history of to be less common.3 syncope or exercise intolerance, presence of ECG Whether the three forms proposed by Harpster and/or Holter abnormalities (number and complexity of VPCs) and echocardiographic represent a continuum of the disease has not been 3 well documented and it is also not clear how many, examination. Dogs in which an ECG was not per- if any, cases of cardiomyopathy in Boxers are due formed, but that underwent a Holter study, as well to “conventional” idiopathic DCM or other forms of as dogs in which ECG was performed by the myocardial disease. primary veterinarian and returned (thus not Cardiomyopathy in Boxer dogs 47 available for our retrospective analysis, but the Right ventricular dilation was defined as follows: findings were present in the medical record) were mild dilation if it was between 30 and 50% of left included. We used a modification of the Holter ventricular size, moderate dilation if it was from ventricular arrhythmia classification grading 50 to 100% of left ventricular size, and severe defined by Meurs3 including arrhythmias present on dilation when right ventricular size exceeded that both ECG and Holter as detailed in Table 1. Dogs of the left ventricle. Assessment of cardiomegaly were excluded if there was gross left atrial dilation on thoracic radiography was based on the verte- (i.e. significantly larger than the diameter of the bral heart scale system (VHS)23 and clinical expe- left ventricle in diastole) that could suggest rience, and the presence of signs of congestive primary mitral valve disease.6 Dogs with aortic heart failure (pulmonary venous congestion or velocity > 2.4 m/s, with congenital or other pulmonary oedema) was recorded. acquired heart diseases, myocardial failure Date and cause of death (either spontaneous secondary to rapid supraventricular tachycardia death or euthanasia) were recorded and survival (where myocardial function returned to normal time was measured from the date of referral. Dogs after the arrhythmia was controlled), or systemic euthanized for severe chronic heart failure were diseases that might affect the cardiovascular considered as cardiac-related deaths. Sudden system (e.g. hypothyroidism) were excluded. deaths were counted as cardiac-related if no other Doppler echocardiographic examinations were cause of death was obvious. Dogs still alive, dogs performed according to standard criteria for that died or were euthanized for reasons unrelated dogs18 (with continuous ECG monitoring). Left to cardiac disease were censored in the statistical ventricular measurements were compared to analysis; subjects lost to follow-up were included normal values for the Boxer dog19 and for the in the survival analysis up until the last time point purposes of this study, dogs were divided into two at which they were known to be alive and then groups based on echocardiographic measurement were thereafter censored in the analysis. (M-mode and 2-D) of the systolic left ventricular diameter. When M-mode and 2-D measurements
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