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International Journal of Cardiovascular ResearchISSN: 2324-8602

Research Article, Int J Cardiovas Res Vol: 6 Issue: 1

Role of Tissue Doppler and Strain/Strain Rate Imaging in the Assessment of the Effects of Obesity on Left Ventricular Structure and Myocardial Systolic Function

Reda Biomy*, Heba Mansour, Mohamad Hassan, Neama Elmeligy and Hany Ebaid
Cardiology Department, Faculty of Medicine, Benha Univeristy, Egypt
Corresponding Author : Reda Biomy
Assistant professor of cardiology, Cardiology Department, Faculty of Medicine, Benha Univeristy, Egypt
Tel: 00201114383333
E-mail: [email protected]
Received: November 22, 2016 Accepted: December 13, 2016 Published: January 03, 2017
Citation: Biomy R, Mansour H, Hassan M, Elmeligy N, Ebaid H (2017) Role of Tissue Doppler and Strain/Strain Rate Imaging in the Assessment of the Effects of Obesity on Left Ventricular Structure and Myocardial Systolic Function. Int J Cardiovasc Res 6:1. doi: 10.4172/2324-8602.1000300

Abstract

Aim: Obesity is a major contributor to the global burden of disease and disability. Objectives: Assessment of subclinical effects of obesity on left ventricular structure and systolic function by strain and strain rate tissue Doppler imaging. Patients and methods: Fifty obese patients with body mass index >30 kg/m² and without cardiovascular disease were included. Twenty five patients of this group were severely obese (BMI>35 kg/ m²) and another 25 were mildly obese (BMI 30-35 kg/m²). Another 50 age-and sex-matched healthy volunteers (BMI <25 kg/m²) were included as a control group. Conventional echodopplercardiography and tissue Doppler strain/strain rate imaging were done. Results: Obese persons have a larger LV mass and LV mass index and a significant direct correlation was found between body mass index and left ventricular mass index there was significant reduction in the mean systolic myocardial velocity in the obese group versus non obese groups. Mean systolic strain was significantly lower in the obese group versus non obese. Mean systolic strain rate was significantly lower in obese group versus non obese groups. Global longitudinal strain & average peak systolic strain rate was lower in obese versus non obese groups and a significant inverse relation was found between body mass index and the peak systolic velocity of strain and strain rate. Conclusions: strain and strain/rate tissue Doppler imaging can predict sub-clinical cardiac functional and structural changes in obesity.

Keywords: BM; LV; SRI; Tissue doppler imaging

Keywords

BM; LV; SRI; Tissue doppler imaging

Introduction

The prevalence of obesity is increasing in both the developed and developing worlds, with about 20% of the US adult population being reported as obese [1]. Obesity is a risk factor for numerous medical conditions such as heart disease, diabetes, hypertension, and stroke [2]. Obesity is associated with a substantial reduction in life expectancy and a severe level of obesity (BMI>45) during early adulthood may reduce a man’s life expectancy by up to 13 years and a woman’s by up to 8 years [3]. Obesity is associated with increased cardiac output to meet the metabolic demand of the adipose tissue and is achieved mainly through an increase in stroke volume. The left ventricular chamber dilates to accommodate the increased venous return and, in turn, develops an eccentric type of hypertrophy to keep the wall stress normal [4]. Impairment of cardiac function has been reported to correlate with the degree of obesity, body mass index and duration of obesity [5]. Abnormal diastolic function is the most important component of the impaired cardiac function, while systolic dysfunction is not so common [6]. Although the mechanisms leading to heart failure in obese patients have not been clarified, severe obesity has long been recognized to cause a form of cardiomyopathy characterized by chronic volume overload, left ventricular (LV) hypertrophy, and LV dilatation. Echocardiography has consistently been the most accurate non-invasive method of assessing LVF [7]. However, conventional echocardiographic modalities are often suboptimal for detailed evaluation of cardiac structures and for detection of subtle functional changes associated with obesity. Newer echocardiographic techniques such as tissue Doppler imaging (TDI) [8] and TDI-derived techniques—strain imaging/strain rate imaging (SRI) [9], could better characterize these possible cardiac abnormalities associated with obesity.

Patients and Methods

Patients
This study included 100 persons and was classified into two groups: Group 1 included 50 obese patients with BMI>30 Kg/m² aged 35 years or older, referred for cardiovascular assessment in the out-patient clinic with no obvious cardiovascular disease. Group 1 was subdivide into two groups: Group A included 25 morbidly obese patients (BMI>35 Kg/m²) and Group B included 25 mildly obese patients (BMI 30-35 Kg/m²). Group 2 included 50 age and sex matched healthy normal volunteers (BMI<25 Kg\m²) and considered as normal group. Exclusion criteria included: patients with any history or findings of cardiovascular disease (as previous myocardial infarction, heart failure, valvular heart disease, overt cardiomyopathy, etc.), patients with diabetes mellitus or hypertension, patients with renal or liver disease and patients with malignancy, thyroid disease or anemia
Methods
The following data were collected in all patients in the studied groups after obtaining informed consent from all participants. Clinical examination and laboratory investigations including biometric measurements (height, weight) and blood pressure readings. BMI was calculated by dividing an individual’s weight in kilograms (kg) by the square of height in meters (m²) [10]. Laboratory investigations included: fasting blood glucose, serum creatinine level, and complete blood count. Echocardiography: Echocardiography was done using VIVID 7 GE cardiac ultrasound scanners, with 2.5-MHz transducer. All measurements were analyzed by the same experienced echocardiographer on an average of three cardiac cycles. Data were obtained with the patients at rest, lying in lateral decubitus position at end-expiration. Conventional echocardiography was used to assess LV dimensions, LV functions, LV mass (LVM) and LV mass index (LVMI). M-mode measurements were obtained from the left parasternal and apical views. Measurements were taken at the end diastole and at the end systole and the diastolic measurements obtained were the interventricular septal wall thickness (IVSD), the LV internal diameter at end diastole (LVDD) and posterior wall thickness (PWT). In systole, the LV systolic diameter was measured (LVSD). LV ejection fraction (LVEF) was estimated according to biplane Simpson’s method (55-75%). Fractional shortening (FS) was calculated as percent change in LV internal dimension between systole and diastole. LV internal volumes were derived from LV internal dimension by Teicholz’sformula [11,12]. Stroke volume was obtained as the difference between end-diastolic and end-systolic volumes. Left ventricular mass (LV mass) was calculated by Devereaux’ equation: LVM=1.04{(LVEDD+PWD +IVSD)³- LVEDD³} x 0,8+0.6 Where LVEDD is the left ventricular end diastolic dimension, PWD is the posterior wall thickness, IVSD is the interventricular septal thickness in diastole, 1.04 is the specific gravity of the myocardium, and 0.8 is the correction factor [13]. LVMI can be calculated by dividing LVM on body surface area: LVMI=LVM\BSA where the BSA are calculated by a variation of DuBois and DuBois (13) that gives virtually identical results using the formula: BSA (m²)=0.007184 × Height (cm) 0.725 × Weight (Kg) 0.425. Diastolic function assessment was done using Pulsed Doppler LV inflow recordings performed in the apical four-chamber view, within the sample volume at the tips of the mitral valve. Peak E, peak A; E/A ratio, and mitral deceleration time were measured. Tissue Doppler Imaging and Strain/Strain Rate Imaging are obtained by analysis of Color-Coded Doppler myocardial velocity data from parasternal short axis view at papillary muscle level, apical fourfour chamber and apical two- chamber views. Regional velocity were performed for six LV myocardial segments: basal lateral, mid lateral, and mid posterior segments from apical four chamber view and mid anterior segment and mid inferior segment from apical two chamber view and posterior wall at papillary muscle level from parasternal short axis view. From the strain rate curve, peak systolic strain rate (PSSR) was measured. From the strain curve, peak systolic strain (PSS) was measured. In all study subjects, global systolic contraction amplitude (glsca) and averaged peak systolic strain (apss) were computed, as global longitudinal LV indices by dividing sum of each longitudinal peak strain and peak strain rate values to the number of the used segments. glasca= The ratio of the sum of measured peak strain values from LV basal lateral, mid-lateral, mid posterior septum, mid-anterior, and mid-inferior regions to number of measured segments. Averaged peak systolic strain rate (apss)=The ratio of the sum of measured peak systolic strain rate values from LV basal lateral, mid-lateral, mid posterior septum, mid anterior, and mid inferior regions to number of measured segments.

Results

There was significant increase in EF (72.9 ± 3.6) in group 1A&1B versus (69.5 ± 4.1) in group 2 p<0.05 and there was significant increase in SV in group 1A & 1B (75.17 ± 6.7 ml) versus (60.3 ± 8.2) in group 2 (p<0.001). IVSD & PWT was larger in group 1A &1B in comparison with group 2 p<0.001 and the values are (0.99. ± 0.09 mm versus 0.85 ± 0.10 mm) and (0.99 ± 0.8 mm versus 0.85 ± 0.10 mm). LVEDD, LVES were significantly higher in group 1A &1B in comparison with group 2(4.71 ± 17 and 4.37 ± 17) respectively and LA diameter was significantly higher (3.50 ± 0.30 versus 3.15 ± 0.15) within p<0.001, Table 1. There was increase in the LV mass and LVMI in obese versus non obese group (164.09 ± 20.07 vs 118.28 ± 19.39) and (80.41 ± 9.6 vs 68.821 ± 2.2) respectively, p<0.001, Table 2. There is significant higher values of E, A, and deceleration time in obese patients versus non obese patients and the different values were (0.81 ± 0.7 versus 0.71 ± 0.05) for E velocity, p<0.05, (0.69 ± 0.10 versus0.51. ± 0.06) for A wave velocity, p<0.001 and (224.94 ± 8.71 versus 214.1 ± 6.18) for deceleration time, p<0.05. E/A ratio were significantly lower in obese group versus non obese groups (1.19 ± 0.10 versus 1.39 ± 0.09) p<0.001 (Table 3) Comparing obese versus non-obese groups, there was significant reduction in the mean systolic velocity of the six selected segments and the values were(6.55 ± 0.5 vs7.87 ± 0.3), ( 5.10 ± 0.9 vs 6.53 ± 0.2),( 4.6 ± 0.4 vs.6.1 ± 0.2),( 4.5 ± 0.4 vs 6.1 ± 0.2),( 4.6 ± 0.38 vs. 5.7 ± 0.22) and (4.1 ± 0.2 vs 5.2 ± 0.3) respectively.Mean systolic strain was significantly lower in the obese group versus non obese groups in mid lateral, mid posterior septum, mid anterior & mid inferior segments and the values were (-13.72± 1.4 vs. -20.48± 2.4),(- 16.78± 1.9 vs. -21.64± 2),(-14.42 ± 1.5 vs. -20.34 ± 2.7) and (-15.5± 1.3 vs. -21± 1.7) respectively Mean systolic strain rate was significantly lower in obese group versus non obese groups in mid lateral, mid posterior septum, mid anterior & mid inferior segments and the values were (-1.17± 0.13 vs.1.46± 0.13), (-1.33± 0.12 vs.-1.68± 0.13) , (-1.26± 0.16 vs. 1.77± 0.13) and (-1.2 ±0.14 vs. -2± 0.18) respectively . Global longitudinal strain & average peak systolic strain rate was significantly lower in obese versus non obese groups 17.99 ± 0.7 vs. 22.56 ±1.1) and ( 1.37±0. 3 vs. 1.77± 0.3) respectively.(Table 4 and Table 5).
Table 1: Echocardiographic data in the obese versus non obese groups.
Table 2: Left ventricular mass & left ventricular mass index in obese versus non obese groups.
Table 3: Global diastolic diameters of the obese versus non obese groups.
Table 4: Systolic velocity & mean systolic strain/strain rate in the obese versus non obese groups in basal lateral, mid lateral and mid posterior myocardial segment.
Table 5: Mean systolic velocity & mean systolic strain/strain rate in the mid anterior, mid inferior and posterior wall segments and global longitudinal starin (glsca) and average peak systolic strain (apss) in obese versus non obese groups.

Discussion

Overweight and obesity are the most common nutritional disorders and this has heightened the concern regarding the association between obesity and cardiovascular morbidity. This has been attributed to chronic volume overload characterized by left ventricular dilatation, increased left ventricular wall stress and compensatory eccentric left ventricular hypertrophy. In this study it was found that, obesity was associated with elevated LV endsystolic dimension, elevated LV end-diastolic dimension, left atrial enlargement, increased septal wall thickness, posterior wall thickness in diastole, with increased LV mass, and LV mass index. In this study, regional mean systolic velocities were found to be reduced in the obese group in all six selected segments, this was obvious when comparing either morbid obese or mild obese versus control group. Tissue velocities do not discriminate between actively contracting muscle and passive motion due to heart translation and tethering effects [14]. To separate this two-typed motion, strain and strain rate have been proposed as measures of regional contractility [15].
Strain and strain rate assess function in heart segments. Strain is directly related to fiber shortening and strain rate is the speed of fiber shortening, which is a measure of contractility [16]. Strain rate imaging, which reflects the rate of myocardial deformation, has been developed by estimating the spatial gradients in myocardial velocities. It is independent of overall heart motion, cardiac rotation, or motion induced by contraction in adjacent myocardial segments. Therefore, it is accepted as a true measure of local deformation [17]. The concept of strain is complex. It is a dimensionless index, and reflects the total deformation of the myocardium during cardiac cycle relative to (or as per cent of) its initial length. Whereas Strain rate is the rate by which the deformation occurs (deformation or strain per unit time). Mean systolic strain in the present study was found to be reduced in mid lateral, mid posterior septum, mid anterior & mid inferior segments,. The mean systolic strain rate was reduced in the six selected segments except the basal lateral segment & posterior segment, where there was significant reduction in the strain rate in the six selected segments in morbidly obese group versus non obese group. Mildly obese group showed reduction in systolic strain rate in mid posterior septum, mid anterior & mid inferior segments versus control group These results are supported by a prospective study involving healthy and obese individuals aged between 10 to 18 years, Lorch and Sharkey found a decrease in systolic strain in the obese group in comparison to the lean group [18]. The measurement of regional strain rate and strain can be performed in either the longitudinal or radial direction for a myocardial segment, and each direction reflects different aspects of regional myocardial function. One of the aims of this study was to define the effect of obesity on these different aspects of LV myocardial function. The present study showed that obesity affected LV systolic function in global, regional longitudinal and also in radial aspects. The present study compared two mean indices as global longitudinal LV systolic indices: global systolic contraction amplitude and averaged peak systolic strain rate. Averaged peak strain and strain rate value was significantly lower in obese subjects. In addition, BMI was found to be strongly correlated with global systolic contraction amplitude and averaged peak strain rate values of different regions of left ventricle showing inverse relation.

Conflict of Interest

No Relationships

Conclusion

Strain and strain/rate tissue Doppler imaging can predict subclinical cardiac functional and structural changes in obesity.

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