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Hypertrophic Cardiomyopathy - Feline Cardiomyopathies (view source)
Revision as of 11:55, 3 December 2012
, 11:55, 3 December 2012→Pathophysiology
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==
An abnormality in the sarcomere, a contractile unit of the cardiac myocyte, is hypothesised to be the initial abnormaility in HCM. Altered sarcomeric function leads to increased signal transduction of kinases, calcium sensitive signalling molecules and trophic factors. This results in activation of transcriptional machinery of the myocyte, leading to myocyte hypertrophy, collagen synthesis and myofibre disarray. The phenotype of LV hypertrophy is a compensatory change which occurs later in disease.
===Dynamic Left Ventricular Outflow Obstruction (LVOTO)===
==Clinical Signs==
==Clinical Signs==
==Diagnosis==
==Diagnosis==