Page 141 - Feline Cardiology

140 Section D: Cardiomyopathies

function in cats, with low error (within-day coefficient al. 1996; Rodriguez et al.1996). E’ accurately discrimi-
of variation 6.5%, between-day 13.6%) (Chetboul et al. nates between people with HCM and from athletes
2004; Schuster et al. 2004). with physiologic hypertrophy or from patients with
In PW Doppler TDI, the wave that occurs during hypertensive heart disease with a high sensitivity of
ventricular systole is called Sm or S’ (see Figure 11.19). 87% and specificity of 97% (Vinereanu et al. 2001).
E’ (or Em) is the wave that occurs during LV relaxation Reduced E’ velocity occurs in cardiac diseases with
and elastic recoil in early diastole, and A’ (or Am) is the myocardial fibrosis, and is negatively correlated
wave that occurs during atrial contraction at end- (R = −0.7) with percent interstitial fibrosis in people
diastole atrial systole (see Figure 11.19). Mitral annular with coronary artery disease and LV dysfunction (Shan
motion is determined by the summation of the et al. 2000).
Cardiomyopathies assessment of global diastolic and systolic function with HCM (see Figure 11.20) (Chetboul et al. 2004;
TDI is useful to detect diastolic dysfunction in cats
longitudinal motion of myocardial fibers and allows
(Nikitin and Witte 2004; De Boeck et al. 2003).
Gavaghan et al. 1999; Koffas et al. 2003). E’ is often
Impairment in diastolic function results in reduced
reduced in cats with HCM when compared to normal
cats (Carlos et al. 2009; Gavaghan et al. 1999; Koffas
amplitude of E’, and systolic dysfunction results in
reduced S’ velocity (see Figure 11.19). In the normal
heart, there is a progressive increase in E’ from apex to et al. 2006). There are only a few studies that have evalu-
ated PW TDI in normal cats and cats with HCM. Normal
mitral annulus, and the lateral LV free wall has a higher E’ in cats was 12.1 ± 2.3 cm/sec in one study, and
E’ than the septum (Nikitin and Witte 2002, 2004). E’ 8.39 ± 2.58 in another study (Gavaghan et al. 1999;
measured by PW TDI, color M-mode, and peak negative Koffas et al. 2006). E’ of cats with HCM generally is
MVG correlates closely with invasive indices of diastolic lower than E’ of normal cats, and was 7.9 ± 1.7 cm/sec
function including tau, dP/dT, and LV end-diastolic in one study and 5.24 ± 1.22 cm/sec in another study
pressure in normal people and people with HCM (Oki (Gavaghan et al. 1999; Koffas et al. 2006). A cutoff of
et al. 2000; Ohte et al. 1998; Bruch et al. 1999; Kato et >7.2 cm/sec is highly sensitive (92%) and specific (87%)
al. 2003; Border et al. 2003). E’ is also positively corre- for discriminating normal cats from cats with HCM
lated with heart rate in cats, such that tachycardia- (Koffas et al. 2006). Other TDI measurements of dia-
associated elevations in E’ velocities may potentially stolic function have been shown to be abnormal in cats
falsely normalize the E’ of cats with HCM with mild with HCM including prolonged acceleration and decel-
diastolic dysfunction (Chetboul et al. 2004; Gavaghan eration times of E’ and prolonged isovolumic relaxation
et al. 1999). Although E’ and A’ waves may become sum- time (Koffas et al. 2006).
mated (EA’) with heart rates >160–180 BPM, there are TDI has been useful to detect diastolic dysfunction
discordant results in several studies regarding whether in people and in animal models of HCM prior to devel-
the velocity of summated EA’ is higher compared to opment of concentric hypertrophy. E’ is reduced in
nonsummated E’ (Chetboul et al. 2004; Gavaghan et al. humans with familial HCM and in transgenic β-MHC
1999; MacDonald et al. 2008). mutation-bearing rabbits with HCM before myocardial
One advantage of PW TDI over color TDI is that hypertrophy develops (Nagueh et al. 2000, 2003; Ho
specialized postprocessing software is not necessary for et al. 2002; Oki et al. 2000; Li et al. 2004; Severino et al.
measurement of diastolic and systolic velocities, and 1998). This early diastolic dysfunction likely reflects
peak velocities can be immediately measured at the mechanical impairment in familial HCM prior to
time of examination. Limitations include the inability development of the final phenotype of LV hypertrophy
to simultaneously assess velocities at more than one (Marian and Roberts 1995). E’ is further reduced as
region of the myocardium and inability to obtain diastolic dysfunction progresses, and is strongly nega-
endocardial to epicardial velocity gradients. Given the tively correlated with amount of increase in LV mass
translational movement of the heart within the chest (Nagueh et al. 2003). In people with HCM, the greatest
due to breathing and intrinsic cardiac forces, stable impairment of diastolic function (lowest E’) occurs
consecutive PW Doppler tracings are often difficult to in the regions with the greatest amount of hypertrophy,
obtain. but other nonhypertrophied regions also have impaired
TDI has been used to diagnose diastolic dysfunction diastolic function (Oki et al. 2000). PW TDI identifies
in humans and in animals with various types of cardiac diastolic dysfunction in 50% of adult Maine coon cats
diseases including HCM, endomyocardial fibrosis, that are genotypically affected with the MYBPC3 muta-
hypertensive heart disease, restrictive cardiomyopathy, tion, despite no echocardiographic phenotypic evidence
and Duchenne’s muscular dystrophy (Chetboul et al. of left ventricular concentric hypertrophy or SAM of
2004; Gavaghan et al. 1999; Oki et al. 2000; Garcia et the mitral valve (MacDonald et al. 2007). E’ is decreased