Spontaneous Cardiovascular Disease in Animals

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Cardiovascular disease occurs commonly in companion animals, particularly in domestic cats and dogs [1]. Myocardial disease represents a substantial portion of these disorders, many of which closely resemble cardiomyopathies in human patients [2]. Such disorders in cat, include hypertrophic [3,4], dilated [5], restrictive [6, 7], and arrhythmogenic right ventricular cardiomyopathies (ARVC/D) [8]. A heritable form of hy-pertrophic cardiomyopathy associated with a cardiac myosin binding protein C mutation has been recently reported in the Maine Coon cat breed [4]. In dogs, chronic myxomatous valve disease is the most prevalent cardiac disorder [9,10], but cardiomyopathies occur frequently, particularly within certain medium and large-sized breeds [10]. Familial forms of dilated car-diomyopathy have been described in the Doberman Pinscher [11], Irish wolfhound [12], and Great Dane [13], and a familial form of ARVC/D has been reported in the boxer breed [14,15]. Dysplastic conditions of the right ventricle (RV) have been described in other mammals including minks [16] and rodents. In mice, ARVC/D has been associated with mutation of the gene laminin receptor [17]. One of the authors (PF) has observed a case of ARVC/D in a primate.

Recently, the canine genome has been mapped using a boxer dog [18], and the US National Human Genome Research Institute has recognized the canine to be an unrivaled model for the study of human disease. Detailed investigations of the genetic basis of ARVC/D in the boxer dog should now be possible. Spontaneous ARVC/D in cats [8] - and particularly dogs [15], have strikingly similar clinical and pathologic features to this condition in humans [19]. Because the pathology of ARVC/D in both the canine and feline models is characterized by myocyte injury and repair, these models provide the opportunity to investigate the ultrastructural features as well as the underlying molecular basis of these changes. Moreover, the high familial incidence of ventricular arrhythmias and sudden death in boxer dogs with ARVC/D makes this model particularly suited for studying the electrophysiologic mechanisms of arrhythmias, the efficacy of antiarrhythmic drugs and therapies, and strategies directed to modify the progression of disease or clinical outcome. Thus, the study of cardiomyopathies in these animals should serve to increase the understanding of the genetic basis of human disease, including development of improved diagnostic assays and assessment of clinical therapies.

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