Sage Journals: Discover world-class research

Abstract

Objectives

The aim of this study was to investigate left ventricular (LV) longitudinal systolic function in cats with hypertrophic cardiomyopathy (HCM) and healthy control cats using tissue motion annular displacement (TMAD).

Methods

The study included 26 control cats and 21 HCM cats. All cats underwent assessment using two-dimensional echocardiography, M-mode echocardiography, pulsed-wave Doppler, tissue Doppler imaging techniques, longitudinal strain and TMAD.

Results

Global TMAD and percentage (%) global TMAD were not influenced by breed, sex, age or heart rate. Mean global TMAD and % global TMAD significantly decreased in the HCM group (2.86 ± 0.86 mm and 11.46% ± 3.37%, respectively) compared with the control group (3.95 ± 0.89 mm and 16.12% ± 2.94%, respectively) (P <0.001 for both), suggesting LV longitudinal systolic dysfunction in HCM cats. LV fractional shortening showed no difference between the control (52.76% ± 11.63%) and the HCM groups (59.80% ± 13.51%) (P = 0.061). Global TMAD and % global TMAD were significantly correlated with global longitudinal strain (P <0.001). The intraclass correlation coefficient of global TMAD and % global TMAD was considered moderate.

Conclusions and relevance

Global TMAD and % global TMAD were significantly decreased in cats with HCM compared with the control group, and were sensitive and repeatable techniques for evaluating LV longitudinal systolic dysfunction in cats with HCM.

Plain language summary

Evaluating heart function in cats with hypertrophic cardiomyopathy using tissue motion annular displacement

This study aimed to evaluate left ventricular (LV) longitudinal systolic function in cats with hypertrophic cardiomyopathy (HCM) and healthy control cats using tissue motion annular displacement (TMAD). The study involved 26 control cats and 21 HCM cats, all of which were assessed using echocardiographic techniques. The results showed that global TMAD and % global TMAD were significantly lower in HCM cats compared with controls. These techniques proved to be sensitive and repeatable for assessing LV dysfunction in HCM cats.

Keywords

Echocardiography hypertrophic cardiomyopathy longitudinal systolic function speckle tracking

Introduction

In cats, cardiomyopathy is the most common cardiovascular disorder and is considered one of the top 10 leading causes of death.¹ The most common form of feline cardiomyopathy is hypertrophic cardiomyopathy (HCM).^2,3 Currently, echocardiography is recommended as the definitive diagnostic test for feline cardiomyopathies.³

Cardiac systolic function results from longitudinal, radial and circumferential myocardial deformation, which leads to the twisting and retwisting deformation of the left ventricular (LV) wall, a process crucial for both systolic and diastolic function.⁴ Longitudinal contraction is responsible for approximately 60% of the total cardiac stroke volume.⁵ A study of HCM cats demonstrated that even when conventional echocardiographic parameters were within normal limits, longitudinal systolic myocardial deformation was significantly decreased compared with the control group and further decreased with LV hypertrophy.⁶

Speckle tracking echocardiography (STE) identifies speckles within the myocardium on grayscale echocardiographic imaging and presents the results as strain and strain rate (SR).^4,7 Many studies have shown that STE is a useful tool for evaluating LV longitudinal myocardial deformation, helping clinicians diagnose and assess cats with HCM in both preclinical and clinical stages.^7
–9 Tissue motion annular displacement (TMAD), an STE technique, provides information on LV systolic function by assessing the degree of mitral annulus deformation towards the cardiac apex in the longitudinal axis. In human medicine, TMAD is considered a rapid, sensitive, highly reproducible, user-friendly and accurate estimation of LV ejection fraction.^10,11 Studies in dogs and cats suggest that TMAD is a reliable tool and should be considered an option for evaluating longitudinal systolic function.^12
–14 The objective of this study was to investigate LV longitudinal systolic function in HCM cats and healthy cats using TMAD.

Material and methods

Animals

All procedures used in this study were approved by the Chulalongkorn University Animal Care and Use Committee (Animal Use Protocol number 2331025). The study population consisted of adult cats aged 1 year or older, of any sex and breed. Cats presented to the cardiology clinic at the Small Animal Teaching Hospital, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand, between June 2023 and May 2024 for the diagnosis of heart disease were recruited for the study. Healthy cats, with no history of systemic illnesses, from households willing to participate in the project were enrolled in the study. All cats underwent a standard physical examination, non-invasive blood pressure measurement, thoracic radiography, electrocardiography (ECG) and echocardiography. In addition, plasma and serum samples were collected for complete blood cell count, renal profile, liver profile and thyroid hormone (total T4) analysis.

Cats with an LV wall thickness <6 mm at the end-diastolic phase and no other cardiac diseases were included in the control group. Cats with LV wall thickness >6 mm at the end-diastolic phase, with or without heart failure, were enrolled in the HCM group.³ Cats with HCM were subdivided into three stages. Stage B1 refers to subclinical HCM cats with a left atrium:aorta (LA:Ao) ratio ⩽1.5. Stage B2 refers to subclinical HCM cats with an LA:Ao ratio >1.5.¹⁵ Stage C refers to HCM cats that have developed clinical signs of congestive heart failure. Cats with renal disease (creatinine >2.0 mg/dl), systemic hypertension (systolic blood pressure >160 mmHg), hyperthyroidism (serum total T4 concentration >4 μg/dl),¹⁶ any clinical illness or any cardiac rhythm other than sinus rhythm were excluded from the study.

Conventional echocardiography

Two-dimensional and M-mode echocardiography were performed by a single investigator (SS), certified as a Diplomate of the Asian College of Veterinary Internal Medicine (Cardiology). The same ultrasound machine (Eko7; Samsung Medison) with a 4–12 MHz phased array transducer was used throughout the study.

All cats underwent echocardiographic examination without sedation. The right parasternal long-axis four-chamber view was used to perform M-mode measurements of the internal dimension of the left ventricle at end-diastole and end-systole (LVIDd and LVIDs, respectively), interventricular septum thickness at end-diastole and end-systole (IVSd and IVSs, respectively) and LV posterior wall thickness at end-diastole and end-systole (LVFWd and LVFWs, respectively). Fractional shortening of the left ventricle (LVFS) was calculated using the following formula: (LVIDd – LVIDs)/LVIDd × 100. The cursor was placed at the level of the chordae tendineae and vertically to both ventricular walls. In addition, the interventricular septum and LV free wall were aligned as parallel as possible. Maximum left atrial dimension (LADmax) was measured at end-systole, one frame before the opening of the mitral valve, and minimum left atrial dimension (LADmin) was measured at peak atrial contraction, one frame before closure of the mitral valve. The fractional shortening of the left atrium (LAFS) was then calculated using the following formula: (LADmax – LADmin)/LADmax × 100.^15,16 Two-dimensional echocardiography was used to measure the left atrial diameter (LA) and the LA:Ao ratio on the right parasternal short-axis view during the diastolic phase.¹⁵

Transmitral flow velocities were measured from the left apical four-chamber view, with the gate placed at the tips of the mitral valve leaflets when they were wide open.¹⁷ The peak velocity of early diastolic transmitral flow (E), the peak velocity of late diastolic transmitral flow (A) and the ratio of peak velocity of early diastolic to late diastolic transmitral flow (E:A ratio) were recorded. The isovolumic relaxation time (IVRT) was measured from the left apical five-chamber view by placing the gate in the LV outflow tract near the anterior mitral valve leaflet to capture both aortic ejection flow and LV inflow.^18,19 Pulmonary vein flow velocities were measured from the right parasternal short-axis view, including peak velocity of systolic pulmonary vein flow (S), diastolic pulmonary vein flow (D) and flow reversal at atrial contraction (AR).¹⁸ Myocardial motion in the longitudinal axis of the heart was investigated by placing the gate on the subendocardial portions of the lateral corner of the mitral annulus.²⁰ Peak velocity of systolic (S’), early (E’) and late (A’) diastolic mitral annular motion and the ratio of peak velocity of early to late diastolic mitral annular motion determined by pulsed-wave Doppler echocardiography were recorded. The ratio of peak velocity of early diastolic transmitral flow to peak velocity of late diastolic mitral annular motion (E’:A’ ratio) was also calculated.²¹

Longitudinal strain

Longitudinal strain (LT) was acquired from the left apical four-chamber (AP4) and apical two-chamber (AP2) views. The LV myocardium was detected automatically using the machine software with manual corrections made when the automatic tracking was obviously incorrect. The global longitudinal strain (GLS) and global strain rate (GSR) were calculated using the following formula:¹³

GLS = ({LT}_{AP4} + {LT}_{AP2}) / 2

GSR = ({SR}_{AP4} + {SR}_{AP2}) / 2

Tissue motion annular displacement

TMAD was measured using auto motion tracking, a feature within the QLab advanced quantification software (Eko7; Samsung Medison).

TMAD was measured from the AP4 and AP2 chamber views. Three regions of interest (ROIs) were set: the first and second ROIs at both mitral annuli, and the third ROI at the epicardium of the LV apex¹¹ (Figure 1). The program creates a midpoint between the two mitral annuli and calculates the degree of displacement of the midpoint towards the cardiac apex in millimetres (mm) and as a percentage (%). Global TMAD values were calculated as the average of each result measured from both views.¹³

Figure 1

TMAD is acquired in left (a) AP4 and (b) AP2. Three regions of interest need to be identified: medial and lateral mitral annulus and LV epicardial apex. TMAD 1 represents the displacement of the septal (AP4) or anterior (AP2) annulus and TMAD 2 represents the lateral (AP4) or inferior (AP2) annulus. AP2 = apical two-chamber; AP4 = apical four-chamber; LV = left ventricular; ROI = region of interest; TMAD = tissue motion annular displacement

Statistical analysis

The sample size was calculated using G*Power 3.1. The effect size was set at 1.151, the power at 0.95 and α (confidence level or type I error rate) at 0.05. The sample size calculation was 42 cats (21 cats with HCM and 21 healthy cats). Parametric data were presented as mean ± SD. Normality was assessed using the Shapiro–Wilk test and the constant variance was evaluated using Levene’s test. The difference in TMAD between the control and HCM groups was evaluated using an unpaired t-test. The difference in TMAD between the control group and HCM subgroups was assessed using one-way ANOVA followed by Tukey’s post-hoc test. The influence of sex was evaluated by an unpaired t-test. The relationship between TMAD, age, heart rate, systolic blood pressure and other echocardiography parameters was evaluated using Pearson’s correlation coefficient. Intra- and inter-observer reliability tests were assessed using the SPSS statistical package (SPSS). The classification of Pearson’s correlation coefficient and intraclass correlation coefficient (ICC) is described in Table 1.^22,23 Two investigators (ND and SS) with different levels of echocardiographic experience, a Diplomate of the Asian College of Veterinary Internal Medicine (Cardiology) and a master’s student, evaluated and acquired the ICC. A P value ⩽0.05 was considered significant.

Table 1

Classification of Pearson’s correlation coefficient and intraclass correlation coefficient (ICC)

Variable	Classification
Pearson’s correlation coefficient
0.1–0.39	Weak
0.40–0.69	Moderate
0.7–0.89	Strong
>0.9	Very strong
ICC
0.1–0.5	Poor
>0.5–0.75	Moderate
>0.75–0.9	Good
>0.9	Excellent

Results

A total of 47 cats participated in the study: 26 control cats and 21 HCM cats. The characteristics of the cats in each group are summarised in Table 2. Age, body weight, heart rate, systolic blood pressure and vertebral heart score did not differ significantly between the control and HCM groups. Males and purebred cats were overrepresented in the HCM group.

Table 2

General characteristics of cats in the control and hypertrophic cardiomyopathy (HCM) groups

Variable	Control	HCM	P value
Number of cats	26	21	–
Age (years)	4.27 ± 2.16	5.33 ± 3.6	0.242
Body weight (kg)	4.67 ± 1.25	4.18 ± 1.36	0.095
Sex
Male	12	14	–
Female	14	7	–
Heart rate (beats per minute)	211.64 ± 31.91	192.29 ± 50.66	0.122
Systolic blood pressure (mmHg)	135.27 ± 16.78	131.81 ± 16.43	0.482
Breed
Crossbred	16	3	–
Purebred	10	18	–
American Shorthair	–	2	–
Persian	–	5	–
Scottish Fold	8	8	–
British Shorthair	–	1	–
Sphynx	–	2	–
Bengal	2	–	–
Vertebral heart score	7.27 ± 0.37	7.7 ± 2.0	0.358

Data are n or mean ± SD. Significant differences were assessed using an unpaired t-test

The IVSd, left ventricular posterior wall thickness at end-diastole (LVPWd), LA and LA:Ao ratio were significantly higher in the HCM group compared with the control group. The HCM group had a significantly higher E value than the control group. LAFS significantly decreased in the HCM group, while LVFS did not reach statistical significance (P = 0.061) (Table 3).

Table 3

Comparison of conventional echocardiographic values in the control and hypertrophic cardiomyopathy (HCM) groups

Variable	Control	HCM	P value
Number of cats	26	21	–
Size and structure
IVSd (cm)	0.44 ± 0.82	0.75 ± 0.16	<0.001*
IVSs (cm)	0.68 ± 0.12	0.95 ± 0.14	<0.001*
LVIDd (cm)	1.46 ± 0.2	1.26 ± 0.26	0.005*
LVPWd (cm)	0.36 ± 0.06	0.73 ± 0.21	<0.001*
LVIDs (cm)	0.69 ± 0.19	0.49 ± 0.17	<0.001*
LVPWs (cm)	0.68 ± 0.15	1.02 ± 0.2	<0.001*
LA (cm)	1.09 ± 0.16	1.44 ± 0.37	<0.001*
Ao (cm)	0.81 ± 0.19	0.84 ± 0.19	0.562
LA:Ao	1.41 ± 0.29	1.81 ± 0.61	0.011*
LV function
FS (%)	52.76 ± 11.63	59.80 ± 13.51	0.061
E (m/s)	0.81 ± 0.19	1.09 ± 0.51	0.02*
A (m/s)	0.66 ± 0.17	0.56 ± 0.44	0.345
E:A	1.26 ± 0.27	0.91 ± 0.91	0.108
IVRT (m/s)	50.23 ± 19.2	45.19 ± 21.24	0.398
S (cm/s)	0.43 ± 0.1	0.45 ± 0.16	0.695
D (cm/s)	0.37 ± 0.11	0.36 ± 0.14	0.707
AR (cm/s)	0.16 ± 0.14	0.17 ± 0.06	0.699
AR dur (ms)	49.46 ± 16.13	58.57 ± 14.73	0.049*
S:D	1.2 ± 0.27	1.3 ± 0.39	0.294
E’ (m/s)	0.11 ± 0.03	0.09 ± 0.03	0.09
A’ (m/s)	0.09 ± 0.02	0.1 ± 0.05	0.214
S’ (m/s)	0.07 ± 0.04	0.07 ± 0.03	0.817
E’:A’	1.35 ± 0.4	0.98± 0.40	0.003*
E:E’	7.25 ± 1.64	15.74 ± 12.82	0.007*
LA function
LAFS (%)	28.83 ± 6.58	20.28 ± 8.60	<0.001*

Data are mean ± SD unless otherwise indicated. Significant differences were assessed using an unpaired t-test

A = peak velocity of late diastolic transmitral flow; A’ = peak velocity of late diastolic mitral annular motion as determine by pulsed-wave Doppler; Ao = aorta; AR = peak velocity of pulmonary vein flow reversal at atrial contraction; AR dur = duration of pulmonary vein flow reversal at atrial contraction; D = peak velocity of diastolic pulmonary vein flow; E = peak velocity of early diastolic transmitral flow; E’ = peak velocity of early diastolic mitral annular motion as determined by pulsed-wave Doppler; E:A = ratio of E to A; E’:A’ = ratio of E’ to A’; E:E’ = ratio of E to E’; FS = left ventricular fractional shortening; IVRT = isovolumic (isovolumetric) relaxation time; IVSd = interventricular septum thickness at end-diastole; IVSs = interventricular septum thickness at end-systole; LA = left atrium; LA:Ao = ratio of LA to Ao; LAFS = left atrium fractional shortening; LV = left ventricle; LVIDd = left ventricular internal dimension at end-diastole; LVIDs = left ventricular internal dimension at end-systole; LVPWd = left ventricular posterior wall thickness at end-diastole; LVPWs = left ventricular posterior wall thickness at end-systole; S = peak velocity of systolic pulmonary vein flow; S’ = peak velocity of systolic mitral annular motion as determined by pulsed-wave Doppler; S:D = ratio of S to D

Global TMAD, % global TMAD and GSR were significantly lower in the HCM group compared with the control group. GLS was significantly less negative in the HCM group compared with the control group (Table 4). Global TMAD and % global TMAD showed no significant differences between sexes or between the purebred and domestic shorthair cats (Table 5).

Table 4

Comparison of two-dimensional speckle tracking echocardiographic values in the control and hypertrophic cardiomyopathy (HCM) groups

Variable	Control	HCM	P value
Number of cats	26	21	–
Global TMAD (mm)	3.95 ± 0.89	2.86 ± 0.86	<0.001*
% global TMAD	16.12 ± 2.94	11.46 ± 3.37	<0.001*
GLS (%)	−19.43 ± 3.92	−14.84 ± 6.15	0.003*
GSR (m/s)	4.52 ± 1.4	3.51 ± 1.16	0.011*

Data are mean ± SD. Significant differences were assessed using an unpaired t-test

Indicates statistical difference at P <0.05 between the control and HCM groups

GLS = global longitudinal strain; GSR = global strain rate; TMAD = tissue motion annular displacement

Table 5

Comparison of tissue motion annular displacement (TMAD) values between sex and breed

Variable	Male	Female	P value	Purebred	Crossbred	P value
Number of cats	26	21	–	28	19	–
Global TMAD (mm)	3.42 ± 0.9	3.52 ± 1.18	0.742	3.46 ± 1.05	3.48 ± 1.01	0.958
% global TMAD	13.05 ± 3.17	15.27 ± 4.41	0.051	13.53 ± 3.87	14.79 ± 3.91	0.28

Data are mean ± SD. Significant differences were assessed using an unpaired t-test

Cats with HCM were subdivided into three subgroups: five cats with stage B1; five cats with stage B2; and 11 cats with stage C. Global TMAD was significantly lower in the HCM stage C subgroup compared with both the control group and the HCM stage B1 subgroup. The % global TMAD and GLS were significantly lower and less negative, respectively, in the HCM stage C subgroup compared with the control group. The GSR showed no significant difference among groups (Table 6).

Table 6

Comparison of conventional echocardiography and two-dimensional speckle tracking echocardiographic values in the control group and hypertrophic cardiomyopathy (HCM) subgroups categorised by American College of Veterinary Internal Medicine consensus statement guidelines

Variable	Control	HCM stage B1	HCM stage B2	HCM stage C	P value
Number of cats	26	5	5	11	–
Global TMAD	3.95 ± 0.89*	3.74 ± 0.37^†	2.97 ± 0.75	2.42 ± 0.77	<0.001^‡
% global TMAD	16.12 ± 2.94*	12.73 ± 2.44	12.33 ± 3.85	10.49 ± 3.5	<0.001^‡
GLS	−19.43 ± 3.92*	−17.47 ± 4.18	−12.98 ± 7.6	−14.49 ± 6.35	0.015^‡
GSR	4.52 ± 1.4	9.94 ± 1.06	3.3 ± 0.95	3.42 ± 1.33	0.073

Data are mean ± SD. Significant differences were assessed using ANOVA

P <0.05 between the control and HCM stage C subgroup

†

P <0.05 between the HCM stage B1 and HCM stage C subgroup

‡

Indicates statistical difference at P <0.05

GLS = global longitudinal strain; GSR = global strain rate; TMAD = tissue motion annular displacement

There was no significant correlation between global TMAD or % global TMAD and age and heart rate. However, the % global TMAD had a significant negative correlation with body weight (Table 7). The correlations between global TMAD and % global TMAD and GLS and GSR are shown in Table 7 and Figure 2.

Table 7

Correlations between global TMAD and % global TMAD and age, body weight, heart rate and conventional echocardiographic parameters in the entire study population

Variable	Global TMAD			% global TMAD
	r	P value	95% CI	r	P value	95% CI
Age (years)	0.168	0.259	−0.434 to 0.125	−0.104	0.487	−0.380 to 0.189
BW (kg)	−0.185	0.214	−0.448 to 0.108	−0.292	0.046*	−0.535 to –0.006
HR (bpm)	0.086	0.571	−0.367 to 0.210	0.017	0.911	−0.275 to 0.306
Two-dimensional speckle tracking echocardiography
GLS	−0.573	<0.001*	−0.739 to –0.342	−0.75	<0.001*	−0.853 to –0.590
GSR	0.373	0.01*	0.097 to 0.597	0.633	<0.001*	0.422 to 0.778

Significant correlations were assessed using Pearson’s correlation coefficient

Indicates statistical difference at P <0.05

BW = body weight; CI = confidence interval; GLS = global longitudinal strain; GSR = global strain rate; HCM = hypertrophic cardiomyopathy; HR = heart rate; TMAD = tissue motion annular displacement

Figure 2

Scatter plots of correlations between (a) global TMAD and (b) % global TMAD and GLS. GLS = global longitudinal strain; TMAD = tissue motion annular displacement

Inter-observer reliability of global TMAD, % global TMAD, GLS and GSR was considered moderate. Intra-observer reliability of global TMAD, % global TMAD and GSR was also considered moderate, while GLS showed good intra-observer reliability (Table 8).

Table 8

Intra- and inter-observer variations for two-dimensional speckle tracking echocardiography

Variable	ICC	95% CI
Inter-observer variations
Global TMAD	0.568	−0.052 to 0.872
% global TMAD	0.737	0.243 to 0.928
GLS	0.570	−0.049 to 0.873
GSR	0.577	−0.038 to 0.875
Intra-observer variations
Global TMAD	0.665	0.105 to 0.905
% global TMAD	0.745	0.258 to 0.930
GLS	0.872	0.570 to 0.967
GSR	0.563	−0.059 to 0.870

CI = confidence interval; GLS = global longitudinal strain; GSR = global strain rate; ICC = intraclass correlation coefficient; TMAD = tissue motion annular displacement

Discussion

This study revealed several significant findings. First, global TMAD, % global TMAD and GLS were lower in the HCM group compared with the control group. In addition, variations in TMAD measurements were observed across different subgroups of HCM, indicating changes in LV deformation in different stages of HCM. Furthermore, the study demonstrated that the reliability of TMAD measurements was moderate.

In the HCM group, male cats were overrepresented, with a mean age of 5 years. This is probably because HCM is more common in male and middle-aged cats.^2,3,24–27 The number of purebred cats was also high, possibly due to the unintentional inclusion of a greater proportion of purebred cats in the study.

According to conventional echocardiographic parameters, the HCM group showed cardiac structural changes, LV diastolic dysfunction and LA systolic dysfunction in contrast to the control group.

The HCM group had significantly lower global TMAD, % global TMAD and less negative GLS values compared with the control group. This finding reflected LV longitudinal systolic dysfunction in HCM cats and is consistent with other studies showing decreased LV longitudinal strain, which has been detected in both preclinical and clinical HCM cats.^7,28 However, LVFS remained within normal limits in the control and HCM groups. This finding is consistent with a study of myxomatous mitral valve disease (MMVD) in dogs in which LVFS remained within normal limits in all groups, while both global TMAD and % global TMAD decreased in the clinical MMVD group compared with the stage B2 group, indicating that TMAD is a sensitive technique for identifying LV longitudinal systolic dysfunction.¹³ In another study, involving healthy cats, global TMAD was recorded as 4.6 ± 0.8 mm and % global TMAD was 18% ± 2.7%.¹² In addition, GLS was recorded as –29.4% ± 4.6%. These findings align with those in the present study. However, the STE values between studies cannot be directly compared, which may be attributed to differences in investigators, cat populations, software or ultrasound machines. Notably, TMAD demonstrated less variation across studies.^12,29,30

In this study, global TMAD, % global TMAD and GLS significantly decreased in the HCM stage C subgroup compared with the control group, suggesting LV longitudinal systolic dysfunction in clinical HCM cats. However, LVFS remained within the normal limits. In human patients with HCM, TMAD was reduced while LVFS was preserved owing to compensatory effects from circumferential systolic functions, indicating a greater susceptibility of longitudinal myocardial fibres to LV systolic dysfunction.^11,31
–33 In preclinical HCM cats, longitudinal systolic dysfunction was detected early while circumferential systolic function remained preserved.^7,28 Moreover, in the HCM stage C subgroup, global TMAD was significantly decreased compared with the HCM stage B1 subgroup, while % global TMAD and GLS showed no significant differences. This indicates that global TMAD is a more sensitive technique compared with % global TMAD or GLS.

The % global TMAD has a weak negative correlation with body weight. This finding suggests that global TMAD might be superior to % global TMAD, which may alter with body weight. Global TMAD and % global TMAD had a moderate and strong negative correlation with GLS, respectively, demonstrating that TMAD can be used to evaluate longitudinal systolic function in HCM cats. This finding is consistent with those of other studies.^10,33,34

Similar to a previous study that reported moderate ICCs in healthy cats, we found moderate ICCs of global TMAD and % global TMAD.¹² The only moderate agreement observed in this study may result from differences in operator experience, which could be mitigated by standardising the measurement method or increasing the number of cardiac cycles analysed. Another possible explanation is that the faster heart rate of cats, compared with humans, poses challenges for accurately tracking myocardial movement using software designed for human heart rates. TMAD can be achieved with lower image quality because the mitral annulus is usually visible and easily tracked, which likely explains why TMAD is considered a repeatable technique.³⁵ When compared with global TMAD, % global TMAD had higher inter- and intra-observer reliability, possibly because the proportional nature of % global TMAD reduces individual variation.

This study has some limitations. Firstly, although the sample size between the HCM group and the control group was clarified by statistical calculations, the sample size of the HCM subgroups was not, which might limit the generalisability of the findings. A larger sample size could provide more robust data. Secondly, the absence of an influence of heart rate on global TMAD and % global TMAD might be due to a uniform heart rate across the population. Therefore, the influence of heart rate should be further studied. Lastly, the effect of cardiogenic medications on echocardiographic parameters was not assessed. These medications might affect myocardial performance and cardiovascular loading conditions, potentially interfering with some echocardiographic parameters.

Conclusions

This study shows that global TMAD, % global TMAD and GLS were lower in the HCM group compared with the control group, whereas LVFS did not reach statistical significance. This indicates that TMAD is a sensitive technique for the early detection of LV longitudinal systolic dysfunction in HCM cats. In addition, variations in TMAD measurements were observed across different subgroups of HCM, indicating changes in LV deformation in different stages of HCM. Furthermore, the study demonstrated that the reliability of TMAD measurements was moderate, highlighting the potential usefulness of these parameters in assessing myocardial function in cats with HCM.

Footnotes

Acknowledgements

The authors wish to thank all staff at the Small Animal Hospital and Faculty of Veterinary Science, Chulalongkorn University, Thailand.

Accepted: 6 January 2025

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received financial support from the 90th Anniversary of Chulalongkorn University Scholarship.

Ethical approval

The work described in this manuscript involved the use of non-experimental (owned or unowned) animals and procedures that differed from established internationally recognised high standards (‘best practice’) of veterinary clinical care for the individual patient. The study therefore had prior ethical approval from an established (or ad hoc) committee as stated in the manuscript.

Informed consent

Informed consent (verbal or written) was obtained from the owner or legal custodian of all animal(s) described in this work (either experimental or non-experimental animals, including cadavers, tissues and samples) for all procedure(s) undertaken (prospective or retrospective studies). For any animals or people individually identifiable within this publication, informed consent (verbal or written) for their use in the publication was obtained from the people involved.

ORCID iD

Sirilak Disatian Surachetpong

References

Egenvall

Nødtvedt

Häggström

, et al. Mortality of life-insured Swedish cats during 1999–2006: age, breed, sex, and diagnosis. J Vet Intern Med 2009; 23: 1175–1183.

Ferasin

Sturgess

Cannon

, et al. Feline idiopathic cardiomyopathy: a retrospective study of 106 cats (1994–2001). J Feline Med Surg 2003; 5: 151–159.

Luis Fuentes

Abbott

Chetboul

, et al. ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats. J Vet Intern Med 2020; 34: 1062–1077.

Bansal

Kasliwal

RR.

How do I do it? Speckle-tracking echocardiography.

Indian Heart J 2013; 65: 117–123.

MacIver

DH.

The relative impact of circumferential and longitudinal shortening on left ventricular ejection fraction and stroke volume.

Exp Clin Cardiol 2012; 17: 5–11.

Wess

Sarkar

Hartmann

Assessment of left ventricular systolic function by strain imaging echocardiography in various stages of feline hypertrophic cardiomyopathy.

J Vet Intern Med 2010; 24: 1375–1382.

Spalla

Boswood

Connolly

, et al. Speckle tracking echocardiography in cats with preclinical hypertrophic cardiomyopathy. J Vet Intern Med 2019; 33: 1232–1241.

Sugimoto

Fujii

Sunahara

, et al. Assessment of left ventricular longitudinal function in cats with subclinical hypertrophic cardiomyopathy using tissue Doppler imaging and speckle tracking echocardiography. J Vet Med Sci 2015; 77: 1101–1108.

Suzuki

Mochizuki

Yoshimatsu

, et al. Myocardial torsional deformations in cats with hypertrophic cardiomyopathy using two-dimensional speckle-tracking echocardiography. J Vet Cardiol 2016; 18: 350–357.

10.

Buss

Mereles

Emami

, et al. Rapid assessment of longitudinal systolic left ventricular function using speckle tracking of the mitral annulus. Clin Res Cardiol 2012; 101: 273–280.

11.

Suzuki

Akashi

Mizukoshi

, et al. Relationship between left ventricular ejection fraction and mitral annular displacement derived by speckle tracking echocardiography in patients with different heart diseases. J Cardiol 2012; 60: 55–60.

12.

Tuleski

GLR

Wolf

Pscheidt

MJGR

, et al. Tissue motion annular displacement to assess the left ventricular systolic function in healthy cats. Vet Res Commun 2022; 46: 823–836.

13.

Wolf

Lucina

Silva

, et al. Assessment of longitudinal systolic function using tissue motion annular displacement in dogs with degenerative mitral valve disease. J Vet Cardiol 2021; 38: 44–58.

14.

Wolf

Lucina

Brüler

, et al. Assessment of longitudinal systolic function using tissue motion annular displacement in healthy dogs. J Vet Cardiol 2018; 20: 175–185.

15.

Abbott

Maclean

HN.

Two-dimensional echocardiographic assessment of the feline left atrium.

J Vet Intern Med 2006; 20: 111–119.

16.

Linney

Dukes-McEwan

Stephenson

, et al. Left atrial size, atrial function and left ventricular diastolic function in cats with hypertrophic cardiomyopathy. J Small Anim Pract 2014; 55: 198–206.

17.

Disatian

Bright

Boon

Association of age and heart rate with pulsed-wave Doppler measurements in healthy, nonsedated cats.

J Vet Intern Med 2008; 22: 351–356.

18.

Boon

JA.

Veterinary echocardiography. 2nd ed. Oxford: Wiley-Blackwell, 2011.

19.

Schober

Maerz

Assessment of left atrial appendage flow velocity and its relation to spontaneous echocardiographic contrast in 89 cats with myocardial disease.

J Vet Intern Med 2006; 20: 120–130.

20.

Koffas

Dukes-McEwan

Corcoran

, et al. Colour M-mode tissue Doppler imaging in healthy cats and cats with hypertrophic cardiomyopathy. J Small Anim Pract 2008; 49: 330–338.

21.

Koffas

Dukes-McEwan

Corcoran

, et al. Pulsed tissue Doppler imaging in normal cats and cats with hypertrophic cardiomyopathy. J Vet Intern Med 2006; 20: 65–77.

22.

Schober

Boer

Schwarte

LA.

Correlation coefficients: appropriate use and interpretation.

Anesth Analg 2018; 126: 1763–1768.

23.

Koo

MY.

A guideline of selecting and reporting intraclass correlation coefficients for reliability research.

J Chiropr Med 2016; 15: 155–163.

24.

Paige

Abbott

Elvinger

, et al. Prevalence of cardiomyopathy in apparently healthy cats. J Am Vet Med Assoc 2009; 234: 1398–1403.

25.

Kittleson

Côté

The feline cardiomyopathies: 2. Hypertrophic cardiomyopathy.

J Feline Med Surg 2021; 23: 1028–1051.

26.

Payne

Borgeat

Connolly

, et al. Prognostic indicators in cats with hypertrophic cardiomyopathy. J Vet Intern Med 2013; 27: 1427–1436.

27.

Peterson

Moise

Brown

, et al. Heterogeneity of hypertrophy in feline hypertrophic heart disease. J Vet Intern Med 1993; 7: 183–189.

28.

Suzuki

Mochizuki

Yoshimatsu

, et al. Determination of multidirectional myocardial deformations in cats with hypertrophic cardiomyopathy by using two-dimensional speckle-tracking echocardiography. J Feline Med Surg 2017; 19: 1283–1289.

29.

Mor-Avi

Lang

Badano

, et al. Current and evolving echocardiographic techniques for the quantitative evaluation of cardiac mechanics: ASE/EAE consensus statement on methodology and indications endorsed by the Japanese Society of Echocardiography. Eur J Echocardiogr 2011; 12: 167–205.

30.

Santarelli

Toaldo

Bouvard

, et al. Variability among strain variables derived from two-dimensional speckle tracking echocardiography in dogs by use of various software. Am J Vet Res 2019; 80: 347–357.

31.

Mizuguchi

Oishi

Miyoshi

, et al. The functional role of longitudinal, circumferential, and radial myocardial deformation for regulating the early impairment of left ventricular contraction and relaxation in patients with cardiovascular risk factors: a study with two-dimensional strain imaging. J Am Soc Echocardiogr 2008; 21: 1138–1144.

32.

Carasso

Yang

Woo

, et al. Systolic myocardial mechanics in hypertrophic cardiomyopathy: novel concepts and implications for clinical status. J Am Soc Echocardiogr 2008; 21: 675–683.

33.

Liu

Tuo

Zhang

, et al. Reduction of left ventricular longitudinal global and segmental systolic functions in patients with hypertrophic cardiomyopathy: study of two-dimensional tissue motion annular displacement. Exp Ther Med 2014; 7: 1457–1464.

34.

Ficial

Benfari

Bonafiglia

, et al. Tissue-tracking mitral annular displacement in neonates: a novel index of left ventricular systolic function. J Ultrasound Med 2024; 43: 729–739.

35.

Tsang

Ahmad

Patel

, et al. Rapid estimation of left ventricular function using echocardiographic speckle-tracking of mitral annular displacement. J Am Soc Echocardiogr 2010; 23: 511–515.

Assessment of longitudinal systolic function using tissue motion annular displacement in cats with hypertrophic cardiomyopathy: a prospective case-control study

Abstract

Objectives

Methods

Results

Conclusions and relevance

Plain language summary

Keywords

Introduction

Material and methods

Animals

Conventional echocardiography

Longitudinal strain

Tissue motion annular displacement

Statistical analysis

Results

Discussion

Conclusions

Footnotes

Acknowledgements

Conflict of interest

Funding

Ethical approval

Informed consent

ORCID iD

References