Page 143 - Feline Cardiology

142 Section D: Cardiomyopathies

relaxation in the beginning of diastole. Postsystolic A genetic screening test for cardiac myosin binding
thickening occurred in 6 of 23 cats with HCM in one protein C is commercially available through the North
study, providing additional evidence of systolic dys- Carolina State University College of Veterinary
function in cats with HCM (Kaffas et al. 2006). Medicine’s Veterinary Cardiac Genetics Laboratory and
Traditional estimates of systolic function such as ejec- may be used to screen Maine coon cats and Ragdoll cats
tion fraction or fractional shortening reflect global LV in breeding programs. Cats may develop HCM despite
chamber function, which is altered by heart rate, hydra- negative tests, and cats with positive tests should be
tion, and other preload-associated factors, rather than evaluated by echocardiography to assess whether there
intrinsic myocardial contractility. Possible factors is phenotypic evidence of disease.
Neurohormones such as natriuretic peptides serve as
involved in reduced systolic myocardial velocity in useful circulating biomarkers for diagnosis of heart
Cardiomyopathies ray, heterogeneity of regional wall stress, and myocar- failure and may help justify whether further workup is
HCM include subendocardial ischemia, myocyte disar-
needed, including echocardiography in asymptomatic
dial fibrosis (Tabata et al. 2000). It has been hypothesized
cats to evaluate for cardiac disease. There are disparate
that reduced myocardial systolic function may be an
findings regarding the utility of NT-proBNP as a screen-
early abnormality in HCM, but the compensatory con-
centric LV hypertrophy overcomes the reduced contrac-
2009; Fox et al. 2008). Hormonal assays including insu-
tile ability of the mutated cardiomyocytes (Marian et al. ing test for asymptomatic cats with HCM (Hsu et al
1995). However, other studies have shown a hypercon- linlike growth factor-1 and growth hormone may be
tractile state or normal contractility in certain sarco- done in cats with left ventricular hypertrophy and clini-
meric mutations of familial HCM (Witt et al. 2001; cal abnormalities consistent with acromegaly, but they
Palmiter et al. 2000; Saito et al. 1987). Strain and strain are not recommended for routine use in cats with echo-
rate imaging are new echocardiographic imaging cardiographic evidence of concentric hypertrophy of the
methods based on color TDI ultrasound, devised to left ventricle.
overcome pitfalls of overall heart motion, cardiac rota- Markers of hemostasis, including thrombin-antithrombin
tion, and contraction in adjacent segments encountered complex, D-dimer, and FDP are invariably abnormal in
when using TDI measurement of tissue velocity. The cats with HCM and are not routinely necessary for clini-
rate of systolic ventricular wall deformation (strain) is cal patients.
another way to assess systolic myocardial function and
can be done using color TDI and offline postprocessing Cardiac magnetic resonance imaging (cMRI)
programs. Systolic strain rate is decreased, indicating
systolic myocardial failure, in people with HCM
(Runqing et al. 2006; Ganame et al. 2007, 2008). Systolic
function is impaired in hypertrophied and nonhyper- Key Points
trophied segments, as well as in regions of myocardial
fibrosis evidenced as delayed enhancement on cardiac • Cardiac MRI is the most accurate test to measure
MRI, and it is correlated with reduced exercise capacity left ventricular mass in cats with HCM, making it the
in people with HCM (Runqing et al. 2006; Ganame et gold standard for quantification of severity of left
al. 2007). Strain rate has been evaluated in normal cats ventricular hypertrophy, but it is limited to a research basis
at this time.
(Wess et al. 2006). In summary, the findings of systolic • Limitations of cardiac MRI include an expensive
dysfunction on TDI of cats with HCM, while provoca- imaging system with a 1.5 Tesla (or greater) magnet,
tive, remain preliminary, and are not sufficiently tested a highly skilled operator with the ability to appropriately
or validated in cats to justifiably influence treatment interpret images, expensive postprocessing software
decisions or prognostication, nor imply or justify the for quantification of left ventricular mass and function,
use of positive inotropic agents for standard therapy of and a requirement of a light plane of general
HCM in cats. anesthesia.
• Delayed enhancement may be identified in regions of
myocardial fibrosis. Although 80% of people with HCM
Advanced Cardiovascular Diagnostic Testing have evidence of delayed enhancement secondary to
Overview myocardial fibrosis, cats with HCM rarely have evidence
of delayed enhancement on cardiac MRI and do not
Although not necessary to achieve a diagnosis, advanced have different myocardial contrast enhancement than
imaging with cardiac magnetic resonance imaging has normal cats. Cardiac MRI does not appear to be useful
been done to quantify the severity of left ventricular to quantify myocardial fibrosis in asymptomatic cats
hypertrophy and assess response to therapy for clinical with HCM.
trials.