Page 186 - Small Animal Internal Medicine, 6th Edition

158 PART I Cardiovascular System Disorders

CHAPTER 8
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Myocardial Diseases of

the Cat

Myocardial disease in cats encompasses a diverse collec- approximately 70%-80%), whereas heterozygotes are much
tion of idiopathic and secondary processes affecting the less commonly affected. The prevalence of the Ragdoll
myocardium. The spectrum of anatomic and pathophysi- mutation is estimated at approximately 20% to 30%, and
ologic features is wide. Disease characterized by myocardial Ragdoll cats homozygous for the mutation frequently are
hypertrophy is most common, although features of multiple severely affected with HCM at an early age (often less than 2
pathophysiologic categories coexist in some cats. Restrictive years). The discrepancy in phenotype between homozygous
pathophysiology often develops. Classic dilated cardiomy- and heterozygous cats suggests a “partial” or “incomplete”
opathy (DCM) is now uncommon in cats; its features are dominance pattern. Besides the two identified mutations,
similar to those of DCM in dogs (see Chapter 7). Myocardial other mutations are likely involved because not all cats with
disease in some cats does not fit neatly into the categories of evidence for HCM have the identified breed-specific muta-
hypertrophic, dilated, or restrictive cardiomyopathy (RCM), tion. Testing for these mutations is available and can be
and therefore it is considered “unclassified” cardiomyopathy. particularly helpful in directing breeding programs (contact
Rarely, arrhythmogenic right ventricular cardiomyopathy https://cvm.ncsu.edu/genetics/).
(ARVC) is identified in cats. In contrast to dogs, arterial In addition to mutations of genes that encode for myo-
thromboembolism is a major complication in cats with myo- cardial contractile or regulatory proteins, possible causes of
cardial disease (see Chapter 12). the disease include an increased myocardial sensitivity to or
excessive production of catecholamines; an abnormal hyper-
trophic response to myocardial ischemia, fibrosis, or trophic
HYPERTROPHIC CARDIOMYOPATHY factors; a primary collagen abnormality; and abnormalities
of the myocardial calcium-handling process. Cats with HCM
Etiology are skeletally larger and may be more likely to be obese
The cause of primary or idiopathic hypertrophic cardiomy- compared with cats without HCM, possibly suggesting a role
opathy (HCM) in cats is unknown, but a heritable abnormal- of early growth and nutrition in development of cardiomy-
ity is likely in many cases. Autosomal dominant inheritance opathy. Some cats with HCM have high serum growth
has been identified in the Maine Coon, Ragdoll, Sphynx, and hormone and insulin-like growth factor-1 (IGF-1) concen-
American Shorthair breeds. Disease prevalence is high in trations. Myocardial hypertrophy with foci of mineralization
other breeds as well, including British Shorthairs, Norwegian occurs in cats with hypertrophic feline muscular dystrophy,
Forest Cats, Scottish Folds, Bengals, Siberians, and Rex. an X-linked recessive dystrophin deficiency similar to Duch-
There also are reports of HCM in littermates and other enne muscular dystrophy in people; however, congestive
closely related domestic shorthair cats. In human familial heart failure (CHF) is uncommon in these cats. It is not clear
HCM, many different genetic mutations involving sarco- whether viral myocarditis has a role in the pathogenesis of
meric proteins have been identified. feline cardiomyopathy.
Two separate mutations in the cardiac myosin binding
protein C gene have been associated with HCM in cats, Pathophysiology
one in Maine Coon cats and one in Ragdolls. However, Abnormal sarcomere function is thought to underlie acti-
these mutations exhibit incomplete penetrance and variable vation of abnormal cell signaling processes that eventu-
expressivity. Prevalence of the mutation in Maine Coons ally produce myocyte hypertrophy and disarray, as well as
has been estimated at approximately 30% to 40%, with increased collagen synthesis. The characteristic result is
some geographic variation. Maine Coon cats homozygous thickening of the left ventricular (LV) wall and/or inter-
for the mutation are likely to develop HCM (penetrance ventricular septum, but the extent and distribution of

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