Page 152 - Feline Cardiology

Chapter 11: Hypertrophic Cardiomyopathy 151

sured in 31 cats with HCM, 38 normal cats, and 35 cats Cats diagnosed with HCM may be at increased risk of
with other cardiac disease. Sixty percent of cats with developing arterial thromboembolism (ATE), especially
HCM and 18% of normal cats had increased serum if there is significant left atrial dilation (see Chapter 20).
growth hormone concentrations (Kittleson et al. 1992). Twelve to seventeen percent of cats diagnosed with HCM
Serum growth hormone levels were higher in cats with have a chief complaint of ATE, but no studies have evalu-
HCM compared to normal cats or cats with other cardiac ated the incidence of ATE in HCM cats over their lifetimes
diseases. The increase in growth hormone in cats with (Rush et al. 2002; Atkins et al. 1992). In one study of ATE
HCM was considered mild compared to markedly ele- in cats, the left atrium was severely enlarged in 57%,
vated growth hormone levels in cats with acromegaly. No moderately enlarged in 14%, and mildly enlarged in 22%,
cats with HCM had evidence of pituitary tumors on with only 5% having a normal left atrial size (Laste and
necropsy, and none had clinical evidence of acromegaly. Harpster 1995). Thrombus formation may develop when
Other factors are likely present in cats with HCM that there is an abnormality in one or more of the components
stimulate release of growth hormone. In contrast to the of Virchow’s triad, which consists of hypercoagulability, Cardiomyopathies
previous study, another study found that although cats endothelial disruption, and blood stasis. Hyperc-
with HCM often have larger body size (i.e., larger somato- oagulability may occur when there is an imbalance or
type) than normal cats, IGF-1 levels in these cats were excess of coagulation factors (Factor VII and fibrinogen)
not increased compared to normal cats (Yang et al. 2008). and/or a deficiency of coagulation inhibitors, and is char-
Insulinlike growth factor-1 and growth hormone acterized by increased products formed during thrombin
should be measured in any cat with concentric left ven- generation (prothrombin fragment 1 and 2), increased
tricular hypertrophy and clinical suspicion of acromeg- products generated by increased thrombin activity (fibri-
aly. Typical clinical signs of acromegaly include nopeptide A, thrombin-antithrombin complex (TAT)),
insulin-resistant diabetes mellitus; increased soft tissue or products generated by fibrinolysis (D-dimer and fibrin
growth of the viscera, tongue, cartilage and nasal tissue; degradation products [FDP]). Abnormalities of two or
and increased bony formation often of the calvarium, more coagulation parameters are typically necessary to
mandible, and vertebrae (Peterson et al. 1990). Cats with classify a hypercoagulable state, and elevation in only one
elevated IGF-1 and GH should be further evaluated with parameter is suggestive. Forty-five percent of asymptom-
by cranial imaging by computed tomography or mag- atic cats with HCM had suspected evidence (but not
netic resonance imaging to assess presence of a pituitary strong evidence) of hypercoagulability based on elevated
mass. Echocardiography reveals concentric hypertrophy TAT or D-dimer (Bedard et al. 2007). In contrast, another
of the left ventricle in a majority of cats diagnosed with study reported no evidence of hypercoagulability in 11
acromegaly. Concentric hypertrophy of the left ventricle asymptomatic cats with cardiomyopathy and left atrial
may regress in acromegalic cats treated with pituitary dilation (Stokol et al. 2008). The same study reported that
irradiation or medical therapy to suppress growth half of cats with spontaneous contrast or a thrombus
hormone secretion. Overall, the significance of elevated within the left atrium or with overt arterial thromboem-
serum growth hormone levels in feline HCM remains a bolism were hypercoagulable. However, only 50% of cats
matter of speculation, and elevated levels do not neces- with overt ATE had increased D-dimer, making it an
sarily imply that they are causative of HCM, but may insensitive test to detect presence of thromboembolism
represent a secondary change. in these cats. Coagulation parameters (TAT, D-dimer,
FDP) were evaluated and no correlation was observed
Hemostatic markers with left atrial size in either study.

Conclusive Diagnosis of HCM
Echocardiography is necessary to establish the diagnosis
Key Points of HCM in cats. Presence of clinical signs, a murmur or
gallop, radiographic evidence of cardiomegaly, or elec-
• A thrombus may form secondary to vascular stasis, trocardiographic abnormalities are variable and often
endothelial disruption, or hypercoagulability (i.e., absent. Left ventricular concentric hypertrophy is the
Virchow’s triad). main abnormality identified by echocardiography in
• Asymptomatic cats with HCM do not have strong cats with HCM, but it may also be seen in cats with
evidence of a hypercoagulable state. hyperthyroidism, systemic hypertension, or aortic ste-
• Half of cats with spontaneous contrast, left atrial
thrombus, or arterial thromboembolism are nosis. Left ventricular concentric hypertrophy is defined
hypercoagulable. as a left ventricular free wall or interventricular septal
end-diastolic thickness of 6 mm or greater. Identification