J Vet Intern Med 2006;20:1106–1115

Systolic and Diastolic Myocardial Dysfunction in Cats with

Hypertrophic Cardiomyopathy or Systemic Hypertension
Carolina Carlos Sampedrano, Valérie Chetboul, Vassiliki Gouni, Audrey P. Nicolle,
Jean-Louis Pouchelon, and Renaud Tissier

Background: Hypertrophic cardiomyopathy (HCM) and chronic systemic hypertension (SHT) can both lead to left-
ventricular hypertrophy (LVH) in cats. Assessment of LVH-associated myocardial dysfunction could provide new insights in
the understanding of the pathophysiology of these diseases.
Hypothesis: Quantification of left-ventricular free-wall (LVFW) motion using tissue Doppler imaging (TDI) could permit
differentiation of feline HCM from SHT-related LVH (LVH-SHT).
Animals: A total of 108 cats of different breeds were enrolled in this study: 35 cats with HCM, 17 with concentric LVH and
SHT, and 56 healthy cats as a control group.
Methods: All cats were examined by conventional echocardiography and 2-dimensional color TDI.
Results: Radial and longitudinal diastolic LVFW velocities were similarly altered in cats with HCM and LVH-SHT,
compared to controls. Systolic velocities were also lower in the groups with hypertrophy than in the controls, for longitudinal
but not radial motion. To determine whether these diastolic and systolic alterations could also be observed in cats without
LVFW hypertrophy, we performed a subgroup analysis in cats with a normal M-mode examination, that is, with only
a localized subaortic interventricular septum hypertrophy. A significant radial and longitudinal diastolic dysfunction was still
observed in both the HCM and LVH-SHT groups compared to controls, and systolic dysfunction was detected in the
longitudinal motion.
Conclusions: LVFW motion is similarly altered in cats with HCM and LVH-SHT. This dysfunction occurs independently of
the presence of myocardial hypertrophy, demonstrating that TDI is capable of detecting systolic and diastolic segmental
functional changes in nonhypertrophied wall segments in cats with HCM and SHT.
Key words: Diastolic function; Echocardiography; Myocardial velocity; Tissue Doppler.

ypertrophic cardiomyopathy (HCM) is a disease
H that has intrigued veterinary cardiologists for
decades. This primary myocardial disorder is character-
ized by increased cardiac mass and a hypertrophied,
nondilated left ventricle.1–3 HCM is the most common
heart disease in cats; it remains a major cause of
morbidity and mortality and is associated with risk of
sudden death.4,5 Systemic hypertension (SHT) and
hyperthyroidism are the two main causes of feline
secondary left-ventricular hypertrophy (LVH), which
must be excluded before a diagnosis of idiopathic HCM
can be made.1,3 Feline HCM is currently diagnosed
predominantly by 2-dimensional and M-mode echocar-
diography showing diffuse or segmental LVH. However,
this ultrasound technique does not differentiate between
primary HCM and secondary HCM caused by SHT or
hyperthyroidism.1,3,6
Tissue Doppler imaging (TDI) is a more recent
ultrasound technique,7–9 which has already been used
for investigating myocardial function in humans and in
dogs10–12 and cats.13–17 It offers sensitive noninvasive and
From the Unité de Cardiologie d’Alfort (Carlos Sampedrano,
Chetboul, Gouni, Nicolle, Pouchelon, Tissier), Unité de Pharmacie-
Toxicologie (Chetboul, Pouchelon, Tissier), École Nationale Vétér-
inaire d’Alfort, 7 Avenue du Général de Gaulle, 94704 Maisons-
Alfort cedex, France.
Reprint requests: Valérie Chetboul, DVM, MS, PhD, Dipl-
ECVIM-CA (cardiology). Unité de Cardiologie d’Alfort, École
Nationale Vétérinaire d’Alfort, 7 Avenue du Général de Gaulle,
94704 Maisons-Alfort cedex, France; e-mail: vchetboul@vet-alfort.fr.
Submitted September 16, 2005; Revised November 15, 2005, and
January 18, 2006; Accepted February 21, 2006.
Copyright E 2006 by the American College of Veterinary Internal
Medicine
0891-6640/06/2005-0007/$3.00/0
quantitative in vivo analysis of myocardial radial7 and
longitudinal motions.8 We have demonstrated that 2-
dimensional color TDI affords satisfactory repeatability
and reproducibility in healthy cats13 and that TDI is
more sensitive than conventional echocardiography in
detecting myocardial dysfunction in dogs.18,19 In hu-
mans, the TDI technique can differentiate myocardial
alterations resulting from HCM and SHT.20–22 TDI
myocardial dysfunction has already been described in
feline HCM15 using pulsed-wave TDI mode. However,
to our knowledge, the TDI technique has not yet been
used for assessing myocardial dysfunction associated
with LVH-SHT in cats or assessing how this might differ
from dysfunction resulting from HCM. Such a study
could provide new insights in the understanding of the
pathophysiology of these two hypertrophic diseases.
The first goal of this study, therefore, was to compare
the alterations in left-ventricular free-wall (LVFW) TDI
parameters in cats with HCM or LVH-SHT. The second
goal was to determine whether these alterations could
also be observed in nonhypertrophied segments, and in
particular in such segments of the LVFW.
Material and Methods
Animals
Fifty-two cats with myocardial hypertrophy were enrolled in the
present study after examination at the Cardiology Unit of Alfort
(France) between October 2003 and June 2005. Owner’s consent
was obtained before enrollment. Thirty-five cats with HCM (HCM
group) and 17 cats with concentric LVH and chronic SHT (LVH-
SHT group) were included in the study. A complete physical
examination, an ECG, and plasma biochemical tests (glucose and
creatinine concentrations) were performed for all animals. Total
thyroxin plasma levels (T4) were determined for cats older than 4
years. The left-ventricular hypertrophic pattern was determined

Tissue Doppler in Cats
after a conventional echocardiographic examination if the LVFW
or the interventricular septal end-diastolic thicknesses were greater
than 6 mm on the M-mode examination2 or if a subaortic
interventricular septal diastolic hypertrophy (greater than 6 mm)
was detected using the 2-dimensional right-side parasternal long-
axis view of the heart.23 Primary HCM was diagnosed after
excluding SHT (systolic arterial blood pressure .160 mmHg in
unstressed animalsa) and hyperthyroidism (T4 reference interval:
10–50 nmol/L). All cats in the LVH-SHT group presented with
SHT were free of antihypertensive therapy before enrollment in the
study, and presented with at least one sign of SHT, including
anorexia, weight loss, episodes of sudden collapse, lethargy,
gastrointestinal signs, systolic heart murmur, ocular abnormalities
(retinal hemorrhages, detachments, or both). The 35 cats in the
HCM group included 28 asymptomatic cats and 7 with congestive
heart failure. Only the latter were receiving medication: benazepril
(n 5 3) or diltiazem (n 5 4) associated with furosemide for less than
3 months. Animals were excluded if they presented with restrictive
cardiomyopathy, significant valvular disease, or arrhythmias.
During the same period, a population of 56 healthy cats was
also investigated. These cats were free of medication and had no
history of heart or respiratory disease. They were declared healthy
on the basis of a complete physical examination, systemic arterial
blood pressure measurement, full conventional echocardiography
and Doppler, ECG, plasma biochemical tests (glucose and
creatinine concentrations), and total thyroxin plasma levels for
cats older than 4 years.
Blood Pressure Measurements
Systolic arterial blood pressure was measured indirectly in
awake cats by the same trained observers using the standard
Doppler method.b Several measurements were taken over 5 to
10 minutes to obtain the average of five values from a stable set of
readings for the whole feline study population. In addition,
measurements were taken at different moments in the day for
several cats, in order to exclude a ‘‘white coat effect.’’
Conventional Echocardiography and Doppler
Standard transthoracic echocardiography with continuous
ECG monitoring was performed by 2 trained observers (VC,
CCS) in awake standing cats by use of an ultrasonographic unitc
equipped with a 7.5–10 MHz phased-array transducer as pre-
viously described and validated.24 The subaortic interventricular
septal thickness was also measured in end-diastole using 2-
dimensional mode from the right parasternal 5-chamber view at
the level of the attachments of the left chordae to the mitral valve
leaflets.23 Pulsed-wave Doppler parameters included maximal
systolic aortic and diastolic mitral-flow velocities and the
isovolumic relaxation time (time interval between end of aortic
flow velocity and onset of transmitral flow).
Tissue Doppler study
All 2-dimensional color TDI examinations were performed in
awake standing cats with continuous ECG monitoring by one
trained observer (VC) using the same ultrasound unitc as used for
the standard echocardiography, and as previously described and
validated.13,14 Real-time color Doppler was superimposed on the
gray scale with a high frame rate (mostly around 200 frames/s, up
to 280). Doppler receive gain was adjusted to maintain optimal
coloring of the myocardium (ie, without any black spots), and
Doppler velocity range was set as low as possible to avoid aliasing.
All digital images were stored and analyzed using a stand-alone
offline measuring system.d A 2 3 2 mm sample was used and
a tissue-velocity profile displayed in each sample location. The
LVFW velocities resulting from radial left-ventricular motion were
19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
1107
measured using the right parasternal ventricular short-axis view,
and measurements were made between the 2 papillary muscles in
endocardial and epicardial segments of the LVFW. The LVFW
velocities resulting from the longitudinal left-ventricular motion
were measured using the standard left apical 4-chamber view.
Measurements were made in 3 segments: the mitral annulus and 2
myocardial segments in the internal mid portions of the LVFW,
that is, basal and apical segments. Radial myocardial velocity
gradients (MVG, cm/s, defined as the difference between endocar-
dial and epicardial velocities) and longitudinal MVGs (defined as
the difference between basal and apical velocities) were calculated
for each phase of the cardiac cycle.
Statistical Analysis
All data were expressed as mean 6 SD. Age, body weight,
systolic arterial blood pressure, and glucose and creatinine plasma
concentrations, along with conventional echocardiographic and
TDI parameters, were compared among the 3 groups (HCM, LVH-
SHT, and controls) using a one-way analysis of variance (ANOVA)
followed, if necessary, by a Student’s t-test with Bonferroni
correction. An analysis of covariance (ANCOVA) was also used
to compare longitudinal S wave and E/A ratio in basal segments
taking into account age as a cofactor. P values , .05 were
considered statistically significant.
Results
Study Feline Population
The whole population (n 5 108) consisted of 3
different groups of cats (35 cats with HCM, 17 cats with
LVH-SHT, and 56 healthy control cats). Age was
significantly higher in the HCM and LVH-SHT groups
(both P , .05) than in the control group (7.0 6 5.0, 13.8
6 3.8, and 3.4 6 2.6 years, respectively. Body weight,
however, was similar in these 3 groups (4.9 6 1.4, 3.9 6
0.9, and 4.6 6 1.3 kg, respectively). As expected, systolic
blood pressure and creatinine concentration were
significantly (P , .05) higher in the LVH-SHT group
than in the control and HCM groups. A total of 7 cats
with HCM and 10 cats with hypertension had high
serum creatinine concentrations.
Conventional Echocardiographic and
Doppler Parameters
As expected (Table 1), the main significant alterations
associated with HCM and SHT were higher values for
LVFW and interventricular septal thickness, fractional
shortening (%FS), systolic aortic flow velocities, isovolu-
mic relaxation time, and mitral A wave, and lower values
for left ventricular diameters, mitral E wave, and mitral E/
A ratio. These alterations were similar between HCM and
LVH-SHT groups. The left-ventricular geometric patterns
were localized subaortic septal hypertrophy (n 5 17),
symmetric (n 5 16), and asymmetric concentric hypertro-
phic patterns with predominant septal (n 5 11) or LVFW
thickening (n 5 8). Of the 52 diseased cats, 15 had
dynamic outflow-tract obstruction during systole.
TDI Parameters: Whole Feline Population (n = 108)
General Description of LVFW in Healthy Control
Group (n = 56). All velocity profiles included one
 1108

Table 1. Systolic blood pressure, plasma creatinine concentration, conventional echocardiographic and Doppler parameters in different groups of cats.
Control group HCM LVH + SHT

n Mean 6 SD Min–Max n Mean 6 SD Min–Max n Mean 6 SD Min–Max

Systolic blood pressure (mmHg) 56 137 6 12 110–155 35 139 6 16 100–155 17 237 6 38a,b 180–300
Plasma creatinine concentration (mg/dL) 56 1.0 6 0.3 0.5–1.5 35 1.4 6 0.5a 0.7–2.6 17 2.8 6 2.0a,b 0.9–8.1
Conventional echocardiography and Doppler parameters
Left atrium/aorta 56 0.9 6 0.1 0.6–1.2 35 1.1 6 0.2a 0.7–1.6 17 1.0 6 0.1 0.8–1.2
Left ventricular end-diastolic diameter (mm) 56 16 6 2.3 9.7–20.8 35 14.3 6 2.2a 10.7–18.9 17 13.7 6 2.5a 8.7–18.1
Left ventricular end-systolic diameter (mm) 56 8.2 6 1.8 4.2–12.7 35 6.8 6 2.1a 3.8–12.6 17 6.4 6 2.5a 2.0–10.5
Left ventricular end-diastolic free wall (mm) 56 4.5 6 0.7 2.4–5.8 35 6.1 6 1.5a 3.7–9.7 17 5.2 6 1.1a 3.4–7.8
Left ventricular end-systolic free wall (mm) 56 7.5 6 1.1 4.2–10.0 35 9.4 6 1.6a 6.3–12.6 17 8.7 6 1.4a 5.4–11.5
Interventricular end-diastolic septum (mm) 56 4.7 6 0.6 3.1–5.9 35 6.3 6 1.2a 4.0–8.6 17 5.7 6 1.2a 4.1–8.9
Interventricular end-systolic septum (mm) 56 7.7 6 1.2 6.0–12.1 35 9.4 6 1.2a 7.1–11.8 17 8.6 6 1.4a 6.5–12.1
Subaortic interventricular septum in end diastole (mm) 56 4.1 6 0.9 2.6–5.7 35 6.4 6 1.8a 1.6–10.2 17 6.8 6 0.9a 4.7–8.4
Fractional shortening (%) 56 49 6 7 36–75 35 56 6 8a 35–71 17 55 6 13 30–82
Systolic maximum aortic velocity (m/s) 56 1.1 6 0.2 0.8–1.9 35 2.2 6 1.3a 0.8–5.4 17 1.4 6 0.9 0.7–4.5
Carlos Sampedrano et al

Mitral E wave assessed by pulsed wave Doppler (m/s)c 48 0.7 6 0.1 0.5–1.1 27 0.6 6 0.2 0.3–1.2 12 0.7 6 0.1 0.4–0.9
Mitral A wave assessed by pulsed wave Doppler (m/s)c 48 0.5 6 0.1 0.3–0.9 27 0.7 6 0.2a 0.5–1.4 12 0.9 6 0.2a 0.4–1.1
Mitral E/A ratioc 48 1.4 6 0.4 1.1–2.9 27 0.9 6 0.3a 0.5–1.8 12 0.9 6 0.4a 0.6–1.9
Isovolumic relaxation time (ms) 56 54 6 11 34–88 35 65 6 18a 35–100 17 65 6 19a 38–103
Heart rate during exam (beats/min) 56 183 6 36 100–255 35 181 6 33 123–270 17 199 6 15 176–230

HCM, group of cats suffering from hypertrophic cardiomyopathy; LVH + SHT, group of cats suffering from left ventricular hypertrophy associated with systemic arterial hypertension.
a
P , .05 versus corresponding control group.
b
P , .05 versus corresponding HCM group.
c
diastolic Doppler parameters were assessed in cats with distinct mitral E and A waves, that is, in cats without fusion of these waves.

19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

Tissue Doppler in Cats
positive systolic wave (S) and 2 negative diastolic waves
(E and A, in early and late diastole, respectively), with E
consistently greater than A. They also included 2
isovolumic phases: the isovolumic contraction phase
(from the end of the negative diastolic wave A to the
beginning of the positive systolic wave S) and the
isovolumic relaxation phase (from the end of the systolic
wave S to the first negative diastolic wave E). Fusion
of the 2 negative diastolic waves, E and A, into one
negative diastolic wave (EA) was observed in 8 and 9
of the 56 TDI radial and longitudinal examinations,
respectively.
Radial LVFW Motion in Diseased Cats Compared to
the Healthy Control Group. As shown in Table 2,
endocardial and epicardial systolic velocities were
similar across all groups. However, the systolic radial
MVG was significantly lower in cats with HCM than
in the control cats (P , .05). Several diastolic alterations
Fig 1. Radial (A) and longitudinal (B) myocardial velocity
profiles obtained from two cats affected by primary hypertrophic
cardiomyopathy using 2-dimensional color tissue Doppler imaging.
(A) Simultaneous recording of myocardial velocities obtained from
the right parasternal short-axis view in 2 segments of the left-
ventricular free wall (endocardial and epicardial segments, bright
and dark curves respectively) shows that E is much lower than A in
the endocardium. (B) This longitudinal velocity profile, obtained
from a basal segment of the left-ventricular free wall using the left
apical 4-chamber view, shows several abnormalities: small S waves;
presence of large postsystolic contraction waves (arrows); A waves
of high amplitude; and, conversely, absence of early diastolic E
wave. S, E, and A 5 peak mean velocity of left ventricular free wall
during systole, early diastole, and late diastole, respectively.
19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
1109
were observed in the two groups of diseased cats
(Fig 1A): early and late diastolic velocities were re-
spectively significantly decreased and increased com-
pared to the control group in both HCM and LVH-SHT
(P , .05). Moreover, the E/A ratio was lower in the
endocardium for both groups with hypertrophy, com-
pared to the control group (P , .05). In the epicardium,
however, this ratio only proved significantly lower for
the LVH-SHT (P , .05). Early diastolic MVG was also
significantly lower than control in all groups with
hypertrophy (P , .05), and late diastolic MVG was
higher in the LVH-SHT group than in the control group
(P , .05). Last, the isovolumic relaxation time was
significantly higher in all groups with hypertrophy
compared to the control group (P , .05). No significant
differences in any parameters were found between the
HCM and LVH-SHT groups.
Longitudinal Annular and LVFW Motion in Diseased
cats Compared to the Healthy Control Group. As shown
in Table 3, almost all longitudinal TDI parameters were
altered in groups with hypertrophy, with respect to
control. These alterations concerned both systolic and
diastolic parameters, but were similar in the HCM and
LVH-SHT groups. Positive postsystolic shortening
(PSS) waves occurring after the S waves and greater
than these latter were observed in the basal segment in
19 of the 35 cats with HCM (54%) and 15 of the cats
with LVH-SHT (88%). In the apical segment, PSS was
observed in 14 (40%) and 12 (71%) cats in these two
groups, respectively. The PSS wave was markedly
prolonged, leading to absence of a longitudinal E wave
in 8 of 35 (23%) cats in the HCM group and 6 of 17
(35%) cats in the LVH-SHT group (Fig 1B). The
isovolumic contraction time was significantly higher in
the LVH-SHT group than in the control group (P ,
.05). Isovolumic relaxation time was also significantly
higher in the groups with hypertrophy than in the
control group (P , .05).
As the ages of the different groups of cats were not
the same, the correlation between age and the two main
relevant TDI parameters, that is, S wave and E/A ratio
in the basal segments, was analyzed (Fig 2). A signifi-
cant correlation with age was observed for both
parameters in the HCM group but not in the control
or the LVH-SHT groups (P , .05 and P , .01
respectively). Notably, and as illustrated in Figure 2,
the between-group differences in TDI parameters do not
appear to be related to age differences as the regression
lines between the control group and the groups with
hypertrophy are clearly separated. The ANCOVA
analysis also demonstrates significant differences in
HCM and LVH-SHT compared to the controls, taking
into account age as a cofactor (P , .05).
TDI Parameters: Cats with Normal M-mode
Examination (n = 17)
Seven cats in the HCM group (mean age 7.8 6
3 years; mean weight 4.6 6 1.1 kg) and 10 cats in the
LVH-SHT group (mean age 14 6 4.9 years; mean
 1110

Table 2. Radial motion tissue Doppler imaging (TDI) parameters in different groups of cats.
Control group HCM LVH + SHT

n Mean 6 SD Min–Max n Mean 6 SD Min–Max n Mean 6 SD Min–Max

Systolic velocities and gradient
S wave in endocardium (cm/s) 56 5.0 6 1.1 3.2–8.1 35 4.4 6 1.4 1.0–6.5 17 4.5 6 1.5 2.2–7.2
S wave in epicardium (cm/s) 56 2.5 6 0.9 1.1–5.6 35 2.3 6 1.1 0.7–4.8 17 2.3 6 1.1 0.9–4.4
Gradient between endocardium and 56 2.5 6 0.8 1.0–4.3 35 2.1 6 0.7a 0.3–3.2 17 2.2 6 0.7 1.1–4.1
epicardium (cm/s)
Diastolic velocities, ratios and gradients in cats with both E and A wavesb
E wave in endocardium (cm/s) 48 6.1 6 1.7 4.0–10.8 32 2.5 6 1.4a 0.3–6.1 16 2.5 6 1.6a 0.6–7.4
E wave in epicardium (cm/s) 48 2.4 6 1.0 0.5–5.7 32 1.2 6 0.7a 0.1–2.8 16 1.0 6 0.7a 0.3–2.5
A wave in endocardium (cm/s) 48 3.3 6 1.1 0.9–5.0 32 4.3 6 1.7a 1.7–8.6 16 5.1 6 2.0a 2.4–9.7
A wave in epicardium (cm/s) 48 1.3 6 0.7 0.4–3.2 32 1.9 6 1.1a 0.4–5.2 16 2.2 6 1.4a 0.5–6.3
E/A wave in endocardium 47 2.0 6 0.8 1.2–4.1 32 0.7 6 0.5a 0.1–1.9 16 0.6 6 0.5a 0.1–2.4
E/A wave in epicardium 48 1.9 6 0.8 1.0–4.5 32 0.8 6 0.6 0.1–3.5 16 0.7 6 1.2a 0.1–5.0
E wave gradient between endocardium and 48 3.7 6 1.4 1.8–8.4 32 1.4 6 1.0a 0.7–3.7 16 1.6 6 1.2a 0.2–4.9
epicardium (cm/s)
A wave gradient between endocardium and 48 1.9 6 0.8 0.2–3.5 32 2.5 6 1.3 0.7–6.0 16 2.8 6 1.3a 0.2–4.9
epicardium (cm/s)
Carlos Sampedrano et al

TDI time parameters

Isovolumic contraction time (ms)c 56 37 6 8 24–61 35 40 6 9 19–56 17 42 6 12 27–70
Isovolumic relaxation time (ms)c 56 44 6 8 27–63 35 75 6 33a 31–182 17 62 6 15a 35–87
Heart rate during exam (beats/min) 56 182 6 25 123–242 35 183 6 24 131–237 17 187 6 24 148–258

HCM, group of cats suffering from hypertrophic cardiomyopathy; LVH + SHT, group of cats suffering from left ventricular hypertrophy associated with systemic arterial hypertension; S, E, and A,
peak mean velocity of LVFW during systole, early diastole, and late diastole respectively.
a
P , .05 versus corresponding control group.
b
diastolic TDI parameters were assessed in cats without fusion of E and A waves.
c
Time parameters were measured in the endocardium and epicardium and were strictly the same.

19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
 Table 3. Longitudinal motion tissue Doppler imaging (TDI) parameters in different groups of cats.
Control group HCM LVH + SHT

n Mean6 SD Min–Max n Mean6 SD Min–Max n Mean6 SD Min–Max

Systolic velocities and gradients
S wave in annular segment (cm/s) 56 4.7 6 1.4 2.2–8.4 35 3.2 6 1.3a 0.5–6.0 17 2.7 6 0.9a 1.7–4.5
S wave in basal segment (cm/s) 56 4.5 6 1.3 2.4–7.9 35 3.2 6 1.2a 0.9–5.6 17 2.7 6 0.9a 0.7–4.9
S wave in apical segment (cm/s) 56 1.7 6 1.0 0.1–4.5 35 1.3 6 0.7 0.2–3.2 17 0.8 6 0.6a 0.1–2.2
Gradient between basal and 56 2.9 6 0.9 1.2–5.0 35 2.0 6 0.9a 0.3–4.0 17 1.8 6 0.7a 0.5–3.7
apical segments (cm/s)
Diastolic velocities, ratios and gradients in cats with both E and A waveb
E wave in annular segment (cm/s) 47 5.9 6 1.8 3.0–10.2 25c 2.7 6 1.3a 0.6–5.4 9d 2.5 6 1.7a 0.6–5.1
E wave in basal segment (cm/s) 47 5.7 6 1.9 2.8–9.9 25c 3.1 6 1.5a 0.3–5.9 10d 3.1 6 1.2a 1.5–4.6
E wave in apical segment (cm/s) 47 2.3 6 1.1 0.5–4.6 25c 1.2 6 0.9a 0.2–3.5 10d 1.1 6 0.8a 0.2–2.9
A wave in annular segment (cm/s) 47 3.4 6 1.4 0.4–5.8 33 4.5 6 2.9 0.8–12.0 15 4.7 6 2.0a 2.2–8.5
A wave in basal segment (cm/s) 47 3.1 6 1.1 1.1–5.5 33 5.0 6 2.6a 0.6–12.0 16 6.2 6 2.4a 2.2–10.2
A wave in apical segment (cm/s) 47 0.9 6 0.5 0.2–2.1 33 1.8 6 1.7a 0.3–8.7 16 3.0 6 1.9a 0.3–7.0
E/A wave in annular segment 47 2.2 6 1.6 1.0–9.8 25c 0.8 6 0.5a 0.1–2.1 9d 0.5 6 0.2a 0.2–0.9
E/A wave in basal segment 47 2.0 6 0.8 1.1–4.5 25c 0.7 6 0.4a 0.1–1.7 10d 0.5 6 0.1a 0.3–0.6
Tissue Doppler in Cats

E/A wave in apical segment 47 3.3 6 2.0 1.1–9.8 25c 1.0 6 1.1a 0.1–3.9 10d 0.7 6 0.7a 0.1–2.3
E wave gradient between basal 47 3.4 6 1.6 0.3–7.3 25c 1.9 6 1.3a 0.1–4.5 10d 2.0 6 1.1a 0.8–3.7
and apical segments (cm/s)
A wave gradient between basal 47 2.2 6 1.0 0.2–4.4 33 3.2 6 2.0a 0.1–8.2 16 3.2 6 2.2 0.2–7.4
and apical segments (cm/s)
TDI time parameters
Isovolumic contraction time (ms)e 56 35 6 8 21–56 35 42 6 18 21–105 17 45 6 17a 25–87
Isovolumic relaxation time (ms)e 56 53 6 10 28–88 35 106 6 26a 58–161 17 96 6 17a 72–127
Heart rate during exam (beats/min) 56 181 6 29 126–253 35 175 6 28 104–226 17 185 6 29 114–224

HCM, group of cats suffering from hypertrophic cardiomyopathy; LVH + SHT, group of cats suffering from left ventricular hypertrophy associated with systemic arterial hypertension; S, E, and A,
peak mean velocity of the LVFW during systole, early diastole and late diastole respectively.
a
P , .05 vs corresponding control group.
b
Diastolic TDI parameters were assessed in cats without fusion of E and A waves.
c,d
Among these cats and although A wave was clearly determined, E wave could not be observed in 8 and 6 cats, respectively, owing to prolonged postsystolic shortening.
e
Time parameters were measured at the base and at the apex and were strictly the same.
1111

19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

1112 Carlos Sampedrano et al
Fig 2. Relationship between age and peak systolic velocity (upper
panel) and ratio between early and late diastolic peak velocities
(lower panel) in the longitudinal motions of basal segments in the
different groups of cats.
weight 3.9 6 1.0 kg) showed a normal LVFW and
a normal interventricular septal thickness as assessed
by M-mode echocardiography; they presented with only
a segmental myocardial hypertrophy that was localized
in the subaortic interventricular septum. These sub-
groups of cats with hypertrophy experienced significant
alterations in systolic and diastolic TDI parameters
despite the normal LVFW thickness (P , .05). Once
again, these alterations were similar in the HCM and
LVH-SHT groups and included, to varying degrees, an
increase in A wave and a decrease in E wave and E/A
ratio, associated with diminished longitudinal S waves
(Fig 3A,B).
Discussion
This study demonstrates that diastolic and systolic
radial and longitudinal LVFW motions assessed by 2-
dimensional color TDI are impaired in cats with HCM
and cats with hypertension. These myocardial altera-
tions were observed to a similar extent in cats with
HCM and with SHT. More interestingly still, LVFW
dysfunction was even observed in cats without myo-
cardial hypertrophy of the same wall segment as de-
tected by M-mode echocardiography.
Conventional 2-dimensional and M-mode echocardi-
ography is the most common technique for detecting
myocardial hypertrophy in cats1–4 and humans.21,22
However, the precise cause of hypertrophy is usually
19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
difficult or impossible to determine using these tech-
niques.21 Interestingly, TDI is a noninvasive technique
capable of further investigation into left ventricular
function in HCM and hypertensive heart disease, as
demonstrated in humans20–22,25–29 and in experimental
animal models of these diseases.30,31 In a veterinary
clinical setting, several studies have demonstrated the
ability of TDI to analyze left ventricular function in
healthy cats13,14,16,17,32 and in cats with cardiomyopathy.15
However, to our knowledge, this technique has never
been used in cats with hypertension, although the
differential diagnosis between HCM and hypertensive
heart disease has clinical, therapeutic, and prognostic
implications.20 The present study demonstrates that TDI
was able to detect systolic and diastolic LVFW
dysfunction in cats with HCM or LVH-SHT, although
alterations were observed to be of a similar degree in
these 2 groups. This suggests that the etiology of LVFW
hypertrophy in cats is not a major determinant of either
the type or degree of myocardial dysfunction. As several
controversial reports have claimed that TDI can
differentiate between HCM and LVH-SHT in humans,21
we might be tempted to see our findings as a specificity
of feline hypertrophic cardiomyopathies. However, most
studies in humans have focused not only on LVFW but
also on interventricular septal function, the alterations
in which do distinguish HCM from LVH-SHT more
clearly.20,22,26 Our study does not, therefore, fully exclude
the possibility that myocardial dysfunction might differ
in feline HCM and LVH-SHT; further studies will be
needed to clarify this.
Another finding of our study is that cats with
nonhypertrophied wall segments as assessed by M-mode
examination also displayed LVFW dysfunction, thus
proving that functional myocardial alteration is more
widespread than predicted by conventional M-mode
echocardiography. These results also suggest that radial
and longitudinal myocardial dysfunction occurs before
the development of hypertrophy as assessed by 2-
dimensional and M-mode conventional echocardiogra-
phy. The type and the magnitude of this dysfunction
were, again, similar in cats with HCM and cats with
LVH-SHT. Although myocardial dysfunction is well
characterized in feline HCM,15 so far there has been
no description of TDI’s superior sensitivity to M-mode
echocardiography in detecting LVFW dysfunction in
feline LVH-SHT and spontaneous HCM. The accuracy
of TDI in early detection of myocardial alterations has
nevertheless been amply demonstrated in humans with
HCM28,29 or SHT,27 and demonstrated in an experimen-
tal rabbit model of HCM.31 For example, reduced mitral
annulus and LVFW myocardial contraction and re-
laxation TDI velocities have been shown to occur before
LVH in patients with HCM.28,29 TDI has also been
shown to detect left ventricular diastolic alteration in
humans with essential SHT before the onset of LVH,27
thus demonstrating the usefulness of TDI in such
a setting.
Traditionally, diastolic dysfunction has been thought
to be the only abnormality in cats with hypertrophic
heart disease. One important finding of the present

Tissue Doppler in Cats
Fig 3. (A) Systolic and diastolic myocardial velocity gradients
between endocardial and epicardial segments (radial motion, upper
panel) and between basal and apical segments (longitudinal
motion, lower panel) in cats characterized by a normal M-mode
examination. (B) Ratio between early (E) and late (A) diastolic
peak velocities in endocardial and epicardial segments (radial
motion) and in basal and apical segments (longitudinal motion)
in cats characterized by a normal M-mode examination. HCM:
group of cats suffering from hypertrophic cardiomyopathy. LVH-
SHT: group of cats suffering from left-ventricular hypertrophy
associated with systemic arterial hypertension. The corresponding
number of cats is 56, 7, and 10 in the control, HCM, and LVH-
SHT groups, respectively. *P , .05 versus corresponding
control group.
study is that systolic dysfunction appears to be an
additional component of myocardial alteration charac-
terized by a decrease in several systolic velocities and
gradients (despite normal or increased FS%) and the
presence of PSS waves. The decrease in systolic LVFW
velocities and the PSS waves (defined as a delayed
myocardial contraction occurring in late systolic or early
diastolic phase rather than the systole phase33) were
only observed in the longitudinal motion. This suggests
a more pronounced alteration in the longitudinal
myocardial fibers than in the radial ones in cats with
HCM and cats with LVH-SHT. A primary impairment
of longitudinal contraction has been previously demon-
strated in human patients with pathologic LVH
secondary to subendocardial fibrosis34 and in a dog
with SHT and severe arteriosclerosis.35
19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
1113
In studies performed in humans, researchers have
used TDI to analyze the impact of obstruction on
regional myocardial motion36,37: in patients with ob-
structive HCM, the long-axis systolic function is similar
to that of the nonobstructive forms, suggesting a relative
load independence. Conversely, the long- and short-axis
regional diastolic function is, for specific segments and
parameters, different from the nonobstructive forms.
Thus, further studies in a large number of animals are
needed to correctly assess the influence of obstruction on
TDI parameters in cats with left ventricular hypertro-
phy.
The major limitation of our study is that LVFW
function was compared among several feline breeds, and
breed might interact with TDI-assessed cardiac veloci-
ties.32 Moreover, for practical reasons, the present study
could not be blinded: the observer knew the final
diagnosis (ie, HCM or SHT) before performing all the
TDI examinations, as the latter were done on the same
day and in the continuity of standard echo-Doppler
examinations. This point represents another limitation
of our study. In addition, cats in the groups with
hypertrophy were significantly older than those in the
control group (P , .05), and some TDI studies have
demonstrated that LVFW velocity patterns may vary
with age.16 We used a population of 56 healthy cats
under investigation at our unit over the same period as
the cats in the HCM and LVH-SHT groups. It was
difficult to respect the enrollment protocol by including
a sufficient number of old healthy cats without any
organic failure. However, our group has recently
demonstrated in a population of 100 healthy cats that
age is not a major determinant of TDI parameters.32 We
have also demonstrated in the present report that age
cannot explain the observed differences in the two main
TDI parameters. Consequently, even though a slight
effect of age on TDI parameters cannot be totally
excluded, we do not consider it reasonable to speculate
that the differences between the LVH-SHT, HCM, and
control groups in our study are solely attributable to age
differences.
In conclusion, this TDI study demonstrates that
radial and, to a wider extent, longitudinal LVFW
function is similarly altered in cats with HCM and cats
with LVH-SHT. This myocardial dysfunction occurs
independently of the presence of myocardial hypertro-
phy, because it was detected in all cats with a normal M-
mode examination. These data suggest that TDI is more
sensitive than conventional M-mode echocardiography
for detecting regional systolic and diastolic myocardial
alterations in cats. However, further prospective TDI
studies are needed to investigate interventricular septal
motion in large populations of diseased felines.
Footnotes
a
Stepien RL. Blood pressure measurement: Equipment, method-
ology and clinical recommendations. Proceedings of the 22nd
ACVIM forum, Minneapolis, MN, June 2004, 605–607
b
811-BL, Parks Medical Electronics, Inc. Aloha, OR

1114 Carlos Sampedrano et al
c
General Electric medical system, Waukesha, WI
d
Echo Pac 5.4 software for Vivid 5, GE-Vingmed Ultrasound,
Waukesha, WI
References
1. Fox P. Feline cardiomyopathies. In: Fox P, Sisson D, Moise
N, eds. Textbook of Canine and Feline Cardiology, 2nd ed.
Philadelphia, PA: WB Saunders; 1988:621–678.
2. Fox PR, Liu SK, Maron BJ. Echocardiographic assessment
of spontaneously occurring feline hypertrophic cardiomyopathy.
An animal model of human disease. Circulation 1995;92:
2645–2651.
3. Fox PR. Hypertrophic cardiomyopathy. Clinical and path-
ologic correlates. J Vet Cardiol 2003;5:39–45.
4. Kittelson MD, Kienle RD. Hypertrophic cardiomyopathy.
In: Kittelson MD, ed. Small Animal Cardiovascular Medicine, 2nd
ed. St Louis, MO: Mosby; 1998:346–362.
5. Baty CJ. Feline hypertrophic cardiomyopathy: An update.
Vet Clin North Am Small Anim Pract 2004;34:1227–1234.
6. Chetboul V, Lefebvre HP, Pinhas C, et al. Spontaneous feline
hypertension: clinical and echocardiographic abnormalities, and
survival rate. J Vet Intern Med 2003;17:89–95.
7. Rychik J, Tian ZY. Quantitative assessment of myocardial
tissue velocities in normal children with Doppler tissue imaging.
Am J Cardiol 1996;77:1254–1257.
8. Nikitin NP, Witte KKA, Thackray SDR, et al. Longitudinal
ventricular function: Normal values of atrioventricular annular
and myocardial velocities measured with quantitative two-di-
mensional color Doppler tissue imaging. J Am Soc Echocardiogr
2003;16:906–921.
9. Chetboul V. Tissue Doppler imaging: A promising technique
for quantifying regional myocardial function. J Vet Cardiol
2002;4:7–12.
10. Chetboul V, Athanassiadis N, Carlos C, et al. Assessment of
repeatability, reproducibility, and effect of anesthesia on de-
termination of radial and longitudinal left ventricular velocities
via tissue Doppler imaging in dogs. Am J Vet Res 2004;65:909–915.
11. Chetboul V, Carlos Sampedrano C, Concordet D, et al. Use
of quantitative two-dimensional color tissue Doppler imaging for
assessment of left ventricular radial and longitudinal myocardial
velocities in dogs. Am J Vet Res 2005;66:953–961.
12. Chetboul V, Carlos Sampedrano C, Gouni V, et al.
Quantitative assessment of regional right ventricular myocardial
velocities in awake dogs by Doppler tissue imaging: Repeatability,
reproducibility, effect of body weight and breed, and comparison
with left ventricular myocardial velocities. J Vet Intern Med
2005;19:837–844.
13. Chetboul V, Athanassiadis N, Carlos C, et al. Quantifica-
tion, repeatability, and reproducibility of feline radial and
longitudinal left ventricular velocities by tissue Doppler imaging.
Am J Vet Res 2004;65:566–572.
14. Chetboul V, Carlos Sampedrano C, Tissier R, et al.
Reference range values of regional left ventricular myocardial
velocities and time intervals assessed by tissue Doppler imaging in
young nonsedated Maine Coon cats. Am J Vet Res
2005;66:1936–1942.
15. Gavaghan BJ, Kittleson MD, Fisher KJ, et al. Quantifica-
tion of left ventricular diastolic wall motion by Doppler tissue
imaging in healthy cats and cats with cardiomyopathy. Am J Vet
Res 1999;60:1478–1486.
16. Koffas H, Dukes-McEwan J, Corcoran BM, et al. Peak
mean myocardial velocities and velocity gradients measured by
color M-mode tissue Doppler imaging in healthy cats. J Vet Intern
Med 2003;17:510–524.
19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
17. Schober KE, Fuentes VL, Bonagura JD. Comparison
between invasive hemodynamic measurements and noninvasive
assessment of left ventricular diastolic function by use of Doppler
echocardiography in healthy anesthetized cats. Am J Vet Res
2003;64:93–103.
18. Chetboul V, Carlos C, Blot S, et al. Tissue Doppler
assessment of diastolic and systolic alterations of radial and
longitudinal left ventricular motions in Golden Retrievers during
the preclinical phase of cardiomyopathy associated with muscular
dystrophy. Am J Vet Res 2004;65:1335–1341.
19. Chetboul V, Escriou C, Tessier D, et al. Tissue Doppler
imaging detects early asymptomatic myocardial abnormalities in
a dog model of Duchenne’s cardiomyopathy. Eur Heart J
2004;25:1934–1939.
20. Cardim N, Longo S, Ferreira T, et al. Tissue Doppler
imaging assessment of long axis left ventricular function in
hypertensive patients with concentric left ventricular hypertrophy:
differential diagnosis with hypertrophic cardiomyopathy. Rev Port
Cardiol 2002;21:709–740.
21. Palka P, Lange A, Fleming AD, et al. Differences in
myocardial velocity gradient measured throughout the cardiac
cycle in patients with hypertrophic cardiomyopathy, athletes and
patients with left ventricular hypertrophy due to hypertension.
J Am Coll Cardiol 1997;30:760–768.
22. Nuñez J, Zamorano JL, Perez de la Isla L, et al. Differences
in regional systolic and diastolic function by Doppler tissue
imaging in patients with hypertrophic cardiomyopathy and
hypertrophy caused by hypertension. J Am Soc Echocardiogr
2004;17:717–722.
23. Peterson EN, Moise NS, Brown CA, et al. Heterogeneity of
hypertrophy in feline hypertrophic heart disease. J Vet Intern Med
1993;7:183–189.
24. Chetboul V, Concordet D, Pouchelon JL, et al. Effects of
inter- and intra-observer variability on echocardiographic measure-
ments in awake cats. J Vet Med A Physiol Pathol Clin Med
2003;50:326–331.
25. Vinereanu D, Florescu N, Sculthorpe N, et al. Differenti-
ation between pathologic and physiologic left ventricular hyper-
trophy by tissue Doppler assessment of long-axis function in
patients with hypertrophic cardiomyopathy or systemic hyperten-
sion and in athletes. Am J Cardiol 2001;88:53–58.
26. Pela G, Bruschi G, Cavatorta A, et al. Doppler tissue
echocardiography: Myocardial wall motion velocities in essential
hypertension. Eur J Echocardiogr 2001;2:108–17.
27. Di Bello V, Giorgi D, Pedrinelli R, et al. Left ventricular
hypertrophy and its regression in essential hypertension. A tissue
Doppler imaging study. Am J Hypertension 2004;17:882–890.
28. Nagueh SF, Bachinski LL, Meyer D, et al. Tissue Doppler
imaging consistently detects myocardial abnormalities in patients
with hypertrophic cardiomyopathy and provides a novel means for
an early diagnosis before and independently of hypertrophy.
Circulation 2001;104:128–130.
29. Nagueh SF, McFalls J, Meyer D, et al. Tissue Doppler
imaging predicts the development of hypertrophic cardiomyo-
pathy in subjects with subclinical disease. Circulation 2003;108:
395–398.
30. Derumeaux G, Mulder P, Richard V, et al. Tissue Dop-
pler imaging differentiates physiological from pathological pres-
sure-overload left ventricular hypertrophy in rats. Circulation
2002;105:1602–1608.
31. Nagueh SF, Kopelen HA, Lim DS, et al. Tissue Doppler
imaging consistently detects myocardial contraction and relaxation
abnormalities, irrespective of cardiac hypertrophy, in a transgenic
rabbit model of human hypertrophic cardiomyopathy. Circulation
2000;102:1346–1350.
32. Chetboul V, Sampedrano CC, Tissier R, et al. Quantitative
assessment of velocities of the annulus of the left atrioventricular

Tissue Doppler in Cats
valve and left ventricular free wall in healthy cats by use of two-
dimensional color tissue Doppler imaging. Am J Vet Res 2006;
67:250–258.
33. Yu CM, Fung JWH, Zhang O, et al. Tissue Doppler
imaging is superior to strain rate imaging and postsystolic
shortening on the prediction of reverse remodeling in both ischemic
and nonischemic heart failure after cardiac resynchronization
therapy. Circulation 2004;110:66–73.
34. Tabata T, Oki T, Yamada H, et al. Subendocardial motion
in hypertrophic cardiomyopathy: assessment from long- and short-
axis views by pulsed tissue Doppler imaging. J Am Soc
Echocardiogr 2000;13:108–115.
19391676, 2006, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2006.tb00708.x by Readcube (Labtiva Inc.), Wiley Online Library on [22/07/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
1115
35. Nicolle AP, Carlos Sampedrano C, Fontaine JJ, et al.
Longitudinal left ventricular myocardial dysfunction assessed by
2D colour tissue Doppler imaging in a dog with systemic
hypertension and severe arteriosclerosis. J Vet Med A Physiol
Pathol Clin Med 2005;52:83–87.
36. Cardim N, Oliveira AG, Castela S, et al. Regional myocardial
function by tissue Doppler in hypertrophic cardiomyopathy: the
impact of obstruction. Rev Port Cardiol 2002;21:1413–1435.
37. Cardim N, Torres D, Morais H, et al. Tissue Doppler
imaging in hypertrophic cardiomyopathy: Impact of intraventric-
ular obstruction on longitudinal left ventricular function. Rev Port
Cardiol 2002;21:271–297.