Literature DB >> 7586368

Echocardiographic assessment of spontaneously occurring feline hypertrophic cardiomyopathy. An animal model of human disease.

P R Fox1, S K Liu, B J Maron.   

Abstract

BACKGROUND: Necropsy studies in domestic cats have suggested the occurrence of a primary cardiac disease resembling hypertrophic cardiomyopathy (HCM) in humans. We used two-dimensional echocardiography to define morphological and functional features of HCM during life in 46 domestic cats evaluated in a subspecialty veterinary clinic. Cats were 8 months to 14 years old (mean, 6 years). METHODS AND
RESULTS: During the follow-up period of as long as 49 months, 18 cats died (or were euthanatized) due to congestive heart failure, peripheral embolization, or both, and 3 other cats experienced out-of-hospital sudden, unexpected death. Echocardiography showed a small left ventricular cavity, associated with a variety of patterns of hypertrophy. Wall thickening was most often diffuse (involving ventricular septum and free wall) in 31 cats (67%) and segmental in 15 (33%), including 12 with thickening confined to anterior septum; wall thickening was judged to be asymmetrical in 42 and symmetrical (concentric) in 4. In 30 cats (65%), marked mitral valve systolic anterior motion produced dynamic obstruction to left ventricular outflow (Doppler estimated gradients, 25 to 110 mm Hg). Compared with survivors, cats with HCM that died with heart failure had greater left ventricular thickness (8.1 +/- 1.5 versus 7.3 +/- 0.9 mm; P < .05) and larger left atria (20.1 +/- 4.6 versus 16.8 +/- 3.4 mm; P = .01) and more often had the nonobstructive form (89% versus 48%; P < .01).
CONCLUSIONS: A spontaneously occurring disease of domestic cats was identified by echocardiography and was similar in its phenotypic expression to HCM in humans; it was characterized by unexplained left ventricular hypertrophy in a variety of patterns with or without evidence of outflow obstruction. Unfavorable prognosis was associated with greater magnitude of hypertrophy and absence of outflow obstruction. Feline HCM may prove to be a valuable animal model of the human disease.

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Year:  1995        PMID: 7586368     DOI: 10.1161/01.cir.92.9.2645

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  57 in total

1.  Benazepril and subclinical feline hypertrophic cardiomyopathy: a prospective, blinded, controlled study.

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2.  Serum microRNA profiles in cats with hypertrophic cardiomyopathy.

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Review 4.  Inherited cardiomyopathies in veterinary medicine.

Authors:  Joshua A Stern; Yu Ueda
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5.  The A31P missense mutation in cardiac myosin binding protein C alters protein structure but does not cause haploinsufficiency.

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7.  Hypertrophic cardiomyopathy in young Maine Coon cats caused by the p.A31P cMyBP-C mutation--the clinical significance of having the mutation.

Authors:  Mia T N Godiksen; Sara Granstrøm; Jørgen Koch; Michael Christiansen
Journal:  Acta Vet Scand       Date:  2011-02-09       Impact factor: 1.695

8.  Assessment of left ventricular longitudinal function in cats with subclinical hypertrophic cardiomyopathy using tissue Doppler imaging and speckle tracking echocardiography.

Authors:  Keisuke Sugimoto; Yoko Fujii; Hiroshi Sunahara; Takuma Aoki
Journal:  J Vet Med Sci       Date:  2015-04-16       Impact factor: 1.267

9.  A genetic polymorphism in P2RY1 impacts response to clopidogrel in cats with hypertrophic cardiomyopathy.

Authors:  Yu Ueda; Ronald H L Li; Nghi Nguyen; Eric S Ontiveros; Samantha L Kovacs; Maureen S Oldach; Karen M Vernau; Michael H Court; Joshua A Stern
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10.  Prevalence of myocardial hypertrophy in a population of asymptomatic Swedish Maine coon cats.

Authors:  Suzanne Gundler; Anna Tidholm; Jens Häggström
Journal:  Acta Vet Scand       Date:  2008-06-18       Impact factor: 1.695

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