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body size is not accounted for in cats. After all, some males may have a lean weight twice the weight of a small female, and pure breed cats have a body weight ranging between 2.5 kg to >10kg. A recent report including almost 20 000 cats shows that the body weight does have a clinically relevant effect on the echocardiographic measurements in cats too, and should be taken into account when evaluating the wall thickness and other echocardiographic dimensions. It should be noted that a measure outside this range does not necessarily indicate that the cat has HCM. Measurements that fall outside this range may be caused by unusual phenotypes (such as false tendons and ectopic papillary muscles etc.), and/or by suboptimal quality of the examination and/or acquisition. Other evidence of HCM is the presence of systolic anterior motion of the mitral valve (SAM). Not all cats which manifest HCM have SAM, but this abnormal motion of the mitral valve may be present in some cats before they have overt evidence of wall thickening.
Breed screening
Because of the great interest from breeders and veterinarians in Europe to reduce the incidence of
HCM in purebred cats, extensive screening is currently undertaken using echocardiography. Breeds currently being screened include most of the popular breeds. Completely asymptomatic HCM cats have been diagnosed in cat families of these breeds in frequencies slightly less than previously reported in Maine coon cats. However, the experience from this screening is that, although, the diagnosis of moderate to severe HCM is often not controversial as long as the most common differential diagnoses, such as systemic hypertension and hyperthyroidism, have been ruled out, the diagnosis of HCM is much more dif cult and controversial. Indeed, some of these cats were diagnosed with HCM, but many cats are classi ed as equivocal, which means that re-examinations are recommended to verify or refute HCM, and that breeding restrictions are recommended. The main problem for the examiner has been how to classify cats with lesser wall thickening, or only regional thickening, or slightly to moderately hypertrophied papillary muscles on the echocardiogram. Thus,
there has been a problem distinguishing mild disease from unusual, but, presumably, normal phenotypes (regarding HCM). Indeed, the examination itself and the interpretation of some of the echocardiograms may very well be one of the most dif cult examinations currently undertaken in veterinary cardiology. Because of the dif culty of the examination and multiple examiners, there have been cases where different examiners have classi ed a speci c cat differently, although these cases have, so far, been very few. However, to distinguish
mild to moderate disease from hypertrophy secondary to other abnormalities (such as hyperthyroidism, renal failure, dehydration etc.) appears to have been less problematic.
An Urban Experience
For the individual cat that is neutered or not intended
to be used for breeding, it may not be so important. These cats have a good-short term and possibly long- term prognosis, because the chance that heart failure will develop in the near future is little, owing to minor in uence of the hypertrophy on cardiac performance, and the chance for other complications such as
arterial thromboebolism is small. However, for breeding purposes it is important that borderline cats (classi ed as equivocal or mild HCM) are eventually correctly diagnosed to reduce the overall incidence of overt disease. The breeders are, therefore, instructed to re-examine these cats and to submit their cat to post- mortem and histopathologic examinations once it dies. The reasons are twofold. The importance of speci c echocardiographic  ndings, such as slight to moderate papillary muscle hypertrophy, need to be evaluated longitudinally, and the breeder needs the information for planning future breeding. The additional information from the post-mortem and histopathological examination is important to verify or refute the diagnosis of HCM.
Selected References
Fox PR, Liu SK, Maron BJ. Echocardiographic assessment of spontaneously occurring feline hypertrophic cardiomyopathy. An animal model of human disease. Circulation 1995;92:2645-2651.
Fox PR, Basso C, Thiene G, et al. Spontaneously occurring restrictive nonhypertrophied cardiomyopathy in domestic cats: a new animal model of human disease. Cardiovasc Pathol 2014;23:28-34.
Kittleson MD, Meurs KM, Munro MJ, et al. Familial hypertrophic cardiomyopathy in maine coon cats: an animal model of human disease. Circulation 1999;99:3172-3180.
Meurs KM, Norgard MM, Ederer MM, et al. A substitution mutation in the myosin binding protein C gene in ragdoll hypertrophic cardiomyopathy. Genomics 2007;90:261-264.
Wess G, Schinner C, Weber K, et al. Association of A31P and A74T polymorphisms in the myosin binding protein C3 gene and hypertrophic cardiomyopathy in Maine Coon and other breed cats. J Vet Intern Med 2010;24:527-532.
Haggstrom J, Andersson AO, Falk T, et al. Effect of Body Weight on Echocardiographic Measurements in 19,866 Pure-Bred Cats with or without Heart Disease. J Vet Intern Med 2016;30:1601-1611.
Haggstrom J, Luis Fuentes V, Wess G. Screening for hypertrophic cardiomyopathy in cats. J Vet Cardiol 2015;17 Suppl 1:S134-149

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