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An Urban Experience
J. Haggstrom1
1Swedish University of Agriculural Sciences, Department of Clinical Sciences, Uppsala, Sweden
J. Häggström
Professor, DVM, PhD, DECVIM-CA (Cardiology)
Department of Clinical Sciences, Faculty of Veterinary Medicine and Animal Science
Swedish University of Agricultural Sciences, Uppsala, Sweden
Depending on the morphological appearance and pathophysiology, cardiomyopathy in cats is frequently classified as hypertrophic (HCM), dilated (DCM), and restrictive (RCM). Unfortunately, many cases have overlapping features or do not fit into a particular category. This has given rise to the increasingly used classification “unclassified cardiomyopathy”. With
the exception for taurine dependent feline DCM, it is currently not known if and how these different types of cardiomyopathy are related. HCM is currently the most commonly diagnosed form of feline cardiomyopathy. Primary HCM is identified as a hypertrophied non- dilated left ventricle where the extent of hypertrophy
is not attributable to other causes including systemic, congenital cardiac or infiltrative diseases. Interest in
this disease has been twofold. Owners are particularly disturbed by incidence of sudden death and thromboembolic episodes that appear in apparently healthy cats. In turn, this has led to an interest of breeders to establish breeding programs aimed at reducing the incidence of HCM. Secondly, since HCM is an important disease in people, especially as a cause of sudden death in adolescents and young adults, there is an interest in feline HCM as a model for the human disease. This presentation is limited to genetic, diagnostic and breeding aspects of HCM in purebred cats in light of experiences of screening cats in Europe.
Genetic testing and classification of disease
Familial hypertrophic cardiomyopathy (HCM) has been shown an inherited trait in some cat breeds, such as American Shorthair, Maine Coon, and Persian. The disease is suspected to be inherited also in other breeds, such as Sphynx. In American Shorthair and Maine Coon cats it has been shown that familial HCM
is inherited as an autosomal dominant trait. Because
of two studies, one in Maine Coon Cats and one in Ragdoll cats, genetic tests for the disease in both breeds are available to the public. The proportion of gene test positive cats appears to be very high in the Maine Coon population both in the USA and in Europe. The value
of the genetic test in European Maine Coon cats has recently been questioned. Therefore, the presence of HCM has relied, still relies today, and will in the near future rely largely on characterization of the phenotype by use of echocardiography. Even in the future when effective genetic tests may be available, there may still be a need for screening cats using echocardiography, because other mutations may spread in cat families, either through propagation of an existing mutation,
or through a spontaneous de novo gene mutation
(i.e. the sire and dam are unaffected but the offspring have the mutation). Fortunately, the vast technical improvement over the years has led to better image quality and image acquisition, which facilitate detection of HCM in feline patients. Feline HCM used to be characterized as global thickening of all portions of the left ventricle often together with left atrial enlargement. With increasing knowledge of feline HCM and improved diagnostic methods, the disease is now considered to be characterized by a broad range of phenotypic patterns
of left ventricular hypertrophy ranging from localized
and relatively mild wall segment to the overall thickened classical type, and no single pattern can be considered characteristic for the disease. In localized forms, the entire interventricular septum or free wall or a region
of them may be affected, the apex may be primarily affected, or the papillary muscles. Because of the heterogeneity, HCM is a diagnosis that should be made by examining several two-dimensional echocardiographic views and measuring wall thicknesses in diastole
from the region of thickening on the two-dimensional images. A standard M-mode echocardiogram of the
left ventricle (taken from immediately below the mitral valve) may miss regional wall thickening. The upper limit for left ventricular thickness has traditionally been set
at a maximum of 5.5 mm and anything above 6 mm is thought to be evidence of concentric hypertrophy. This limit is conservative because a recent report indicates a more narrow body-weight dependent reference interval. Because echocardiographic measurements are usually corrected for body size in dogs, it may be confusing that

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