Page 118 - Feline Cardiology

Chapter 11: Hypertrophic Cardiomyopathy 117

physical obstruction of blood flow in the artery, the SIGNALMENT
thrombus releases vasoactive amines including throm-
boxane and serotonin that cause massive vasoconstric-
tion of the collateral arteries, leading to lack of perfusion Key Points
to the limb (Schaub et al. 1977, 1982). Approximately
50% of cats regain partial or complete motor control • The average age of diagnosis of HCM is ∼6 years but
without the aid of thrombolytic therapy in 1–6 weeks may vary from 6 months to geriatric.
(Fox 1987). Other studies estimate survival with our • Predisposed breeds include Maine coon cats, Ragdoll
cats, American shorthair, British shorthair, Siberian,
without thrombolytic therapy to be 30–40% (Laste and Turkish Van, Scottish fold, Sphynx, Persian, Himalayan,
Harpster 1995; Smith et al. 2003). and Birman. However, the domestic shorthair cat is the
most common breed diagnosed.
End-stage Hypertrophic Cardiomyopathy • Purebred cats, especially the Ragdoll, may develop
rapidly progressive, severe HCM at a young age.
Although rare, some cats develop end-stage HCM (i.e., Cardiomyopathies
“burnt-out” HCM) characterized by systolic myocardial
failure, dilation of the left ventricle, and thinning of the
septum and left ventricular wall (Cesta et al. 2005).
Congestive heart failure is a consistent feature of end- There is a wide range of patient characteristics in feline
stage HCM, and may include pulmonary edema and/or HCM, with any age being possible for HCM to develop.
pleural effusion. Intracardiac thrombi or arterial throm- Historically, cats were typically first diagnosed at early
to middle age, with mean ages ranging from 5.5–6.5
boembolism appears to be very common in this subset
of cats. It is likely that cats with end-stage remodeling years in several large-scale studies; but at present, both
asymptomatic and decompensated HCM is routinely
suffer from decreased myocardial perfusion, possibly
due to coronary arterial thromboembolism and small recognized in cats ranging from young juvenile to geri-
atric (Ferasin et al. 2003; Rush et al. 2002; Atkins et al.
vessel coronary artery disease, with histopathologic evi-
dence of myocardial infarctions and fibrosis. 1992). Although unusual, cats may even be diagnosed
with HCM as young as 3 months of age, especially in
genetically predisposed purebred cats (Meurs et al.
Resolution of Left Ventricular Hypertrophy 2007). In a family of Maine coon cats with familial
in Some Cats HCM, cats homozygous for the MYBPC3 mutation
Although unusual, some cats diagnosed with HCM causing HCM developed phenotypic echocardiographic
experience regression, rather than progression or evidence of LV hypertrophy between 4–6 months of age,
plateau, of left ventricular hypertrophy over time when and severe LV hypertrophy by 7–12 months of age
evaluated by echocardiography. This may be seen as a (Kittelson et al. 1999). Heart failure usually developed
spontaneous change, or secondary to antihypertrophic by 20 months of age, and most of these cats died by 4
therapy (i.e., atenolol, diltiazem, etc.). Regression of years of age (Kittelson et al. 1999). Male Maine coon cats
hypertrophy in absence of pharmacologic intervention that were homozygous for the MYBPC3 mutation typi-
is poorly understood, and mechanisms have not been cally develop more severe disease at an earlier age.
defined. Possible explanations may be the disappearance Heterozygous affected Maine coon cats may live many
of a modulating factor (ill-defined) responsible for stim- years with moderate left ventricular hypertrophy and
ulating or maintaining hypertrophy, correction of dehy- atrial dilation without development of CHF or sudden
dration and normalization of pseudohypertrophy (i.e., death. Ragdoll cats can develop a severe, early-onset
wall thickness measured too thick but was due to form of familial HCM, with a mean age of diagnosis of
decreased chamber volume), or potentially a transition 15 months in one study (ages range from 6 months to 2
to end-stage cardiomyopathy with diffuse small vessel years) (Lefbom et al. 2001). In a genetic study, Ragdoll
myocardial infarctions and ischemia causing atrophy cats that were homozygously affected with the MYBPC3
and fibrosis. However, the end-stage remodeled ventricle mutation developed HCM 18 months earlier than het-
typically does not contract normally and may have erozygously affected cats (Meurs et al. 2007). These find-
hyperechoic myocardium due to myocardial fibrosis, ings support the hypothesis that gene dosage may affect
rather than reversion to normal ventricular wall thick- the penetrance and phenotype of HCM in genetically
ness, echotexture, and function. The more common affected cats.
cause of regression of ventricular hypertrophy is suc- Although there is no sex-linked heritability pattern,
cessful treatment of secondary causes of hypertrophy approximately three-fourths of cats diagnosed with
such as hyperthyroidism or systemic hypertension. HCM are male neutered, which has been described in