Difference between revisions of "Hypertrophic Cardiomyopathy - Feline Cardiomyopathies"
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In humans, more than half of HCM cases are due to heritable genetic defects, the remaining cases are a result of spontaneous mutations that arise de-novo. Several hundred genetic mutations have been associated with HCM. These mutations usually affect genes that encode proteins that are encorporated into contractile elements or sarcomeres of the cardiomyocyte. There is familial heritability in some pedigree cats, including the Ragdoll and Maine Coon. Other breeds that may be predisposed include the British Shorthair, Norwegian Forest Cat, Turkish Van, Scottish Fold, Bengal and Rex. | In humans, more than half of HCM cases are due to heritable genetic defects, the remaining cases are a result of spontaneous mutations that arise de-novo. Several hundred genetic mutations have been associated with HCM. These mutations usually affect genes that encode proteins that are encorporated into contractile elements or sarcomeres of the cardiomyocyte. There is familial heritability in some pedigree cats, including the Ragdoll and Maine Coon. Other breeds that may be predisposed include the British Shorthair, Norwegian Forest Cat, Turkish Van, Scottish Fold, Bengal and Rex. | ||
==Pathophysiology== | ==Pathophysiology== | ||
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==Clinical Signs== | ==Clinical Signs== | ||
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==Diagnosis== | ==Diagnosis== | ||
===Genetic Testing=== | ===Genetic Testing=== | ||
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* Systemic hypertension | * Systemic hypertension | ||
* Hyperthyroidism | * Hyperthyroidism | ||
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* Hypovolaemia (pseudohypertrophy) | * Hypovolaemia (pseudohypertrophy) | ||
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* Methylprednisolone acetate administration | * Methylprednisolone acetate administration | ||
* Infiltrative myocardial neoplasia e.g. Lymphoma | * Infiltrative myocardial neoplasia e.g. Lymphoma | ||
* Feline muscular dystrophy | * Feline muscular dystrophy | ||
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==Treatment== | ==Treatment== | ||
==Prognosis== | ==Prognosis== | ||
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Revision as of 11:49, 3 December 2012
This article is still under construction. |
Overview
Hypertrophic cardiomyopathy (HCM) is the most common myocardial disease in cats (75% of cardiomyopathies). It is characterised by a hypertrophied left ventricle, however there is phenotypical variability since hypertrophy can affect different portions of the interventricular septum (IVS), left ventricular free wall (LVFW) or both.
Aetiology
In humans, more than half of HCM cases are due to heritable genetic defects, the remaining cases are a result of spontaneous mutations that arise de-novo. Several hundred genetic mutations have been associated with HCM. These mutations usually affect genes that encode proteins that are encorporated into contractile elements or sarcomeres of the cardiomyocyte. There is familial heritability in some pedigree cats, including the Ragdoll and Maine Coon. Other breeds that may be predisposed include the British Shorthair, Norwegian Forest Cat, Turkish Van, Scottish Fold, Bengal and Rex.
Pathophysiology
Clinical Signs
Diagnosis
Genetic Testing
A causative mutation for HCM has been identified in Maine Coon and Ragdoll cats. This mutation involves the sarcomeric gene for cardiac myosin binding protein C (MYBPC3) in both breeds. However, the mutation in the two breeds appears in different regions of this gene. In Maine Coons it is between domains C0 and C1, in Ragdolls it is in domain 6. There are likely additional mutations that are yet to be identified in Maine Coon cats, as some cats with phenotypic evidence of HCM do not have an identifyable mutation in the MYBPC gene. Conversely, cats may carry the mutation without having phenotypic evidence of HCM.
Differential Diagnoses
Before a diagnosis of HCM can be made, causes of secondary myocardial hypertrophy need to be excluded. These include:
- Systemic hypertension
- Hyperthyroidism
- Hypovolaemia (pseudohypertrophy)
- Methylprednisolone acetate administration
- Infiltrative myocardial neoplasia e.g. Lymphoma
- Feline muscular dystrophy