HCM in Maine Coon cats

The prevalence of HCM in Maine Coon cats that were asymptomatic (got the disease but no symptoms) and in Sweden is set out below:

Background

Maine coon cats have a familial disposition for developing hypertrophic cardiomyopathy (HCM) with evidence of an autosomal dominant mode of inheritance [1]. The current method to diagnose HCM is by the use of echocardiography. However, definite reference criteria have not been established. The objective of the study was to determine the prevalence of echocardiographic changes consistent with hypertrophic cardiomyopathy in Swedish Maine coon cats, and to compare echocardiographic measurements with previously published reference values.

Echocardiography is cardiac ultrasound.

Methods

All cats over the age of 8 months owned by breeders living in Stockholm, listed on the website of the Maine Coon breeders in Sweden by February 2001, were invited to participate in the study. Physical examination and M-mode and 2D echocardiographic examinations were performed in all cats.

Results

Examinations of 42 asymptomatic Maine coon cats (10 males and 32 females) were performed. The age of the cats ranged from 0,7 to 9,3 years with a mean of 4,8 ± 2,3 years. Four cats (9,5%) had a diastolic interventricular septal (IVSd) or left ventricular free wall (LVPWd) thickness exceeding 6,0 mm. In 3 of these cats the hypertrophy was segmental. Two cats (4,8%) had systolic anterior motion (SAM) of the mitral valve without concomitant hypertrophy. Five cats (11,9%) had IVSd or LVPWd exceeding 5,0 mm but less than 6,0 mm.

Conclusion

Depending on the reference values used, the prevalence of HCM in this study varied from 9,5% to 26,2%. Our study suggests that the left ventricular wall thickness of a normal cat is 5,0 mm or less, rather than 6,0 mm, previously used by most cardiologists. Appropriate echocardiographic reference values for Maine coon cats, and diagnostic criteria for HCM need to be further investigated.



HCM in Maine Coon cats (the original title is "Prevalence of myocardial hypertrophy in a population of asymptomatic Swedish Maine coon cats" - This article is reproduced under a Attribution 2.0 Generic license. These are the details appertaining to this article:

(HCM in Maine Coon cats) - Copyright © 2008 Gundler et al; licensee BioMed Central Ltd.

Prevalence of myocardial hypertrophy in a population of asymptomatic Swedish Maine coon cats

Suzanne Gundler,corresponding author1 Anna Tidholm,2 and Jens Häggström3

1Bagarmossen Animal Hospital, Ljusnevägen 17, S-128 48 Bagarmossen, Sweden

2Albano Animal Hospital, Rinkebyvägen 23, S-182 36 Danderyd, Sweden

3Department of Physiology, Faculty of Veterinary Medicine, Swedish University of Agricultural Science, PO box 7018, Uppsala, Sweden



Update

9th July 2011: VG, a work colleague and a professor has added some useful scientific thought to the matter of the limitations of the echocardiography. You can see her comments on the document referred to above annotated to the document.

 These are VG's comments:
  • How the cardiogram is done is important. (not for amateurs), say at cat shows (my comment: the person who I saw at a cat show in Oklahoma doing ultrasound was a professional and he used a mobile ultrasound device (see video above).
  • Cats’ hearts are affected in different ways and there is no typical pattern of morphological measures/ abnormalities from echocardiograms for cats with HCM. So, it’s not a simple thing, like “look here” “see that” It’s not like getting your car’s muffler checked.
  • Seems like the breeders in Stockholm were interested in participating in this study.
  • There may be other heart abnormalities that eventuate in HCM, or possibly sudden cardiac death.
  • Whatever heart anatomy abnormalities [were] observed via echocardiogram [they] were not due to random other diseases.
  • The diagnostic criteria differ according to cardiologists, and how different researchers define “abnormality”. This is important! So, It is not an exact science.
  • They are being cautious as to how the percentage range of HCM they report for the cats in their study would extrapolate to the global MC population. This is a responsible statement. It does not, however, take away from the more general thrust of the problems with using echocardiograms to assess HCM.
  • [a] more recent article I am analyzing certainly suggests that the one identified genetic mutation for MCs is not the only mutation responsible for HCM. From the Meurs study (or studies), - different mutations in Maine coons and Ragdolls.

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