|Year : 2014 | Volume
| Issue : 1 | Page : 130-135
Effects of isolated obesity on left ventricular function: a longitudinal strain imaging study
Walaa F. Abdelazez, Rehab I. Yaseen, Ahmed M. Alkersh, Mohammad A.H. Ebada
Department of Cardiology, Faculty of Medicine, Menoufia University, Menufia, Egypt
|Date of Submission||17-Apr-2013|
|Date of Acceptance||30-Jul-2013|
|Date of Web Publication||20-May-2014|
Mohammad A.H. Ebada
MBBCH, Al-Mansoura, Al-Dakahlia, 35516
Source of Support: None, Conflict of Interest: None
Obesity is associated with heart failure, cardiovascular morbidity, and mortality. A direct effect of weight on left ventricular (LV) structure and myocardial function is not well established.
The aim of this study was to determine the effect of isolated obesity on LV morphology and systolic function using LV standard ECG indices and strain imaging indices.
Patients and methods
Sixty-five individuals were enrolled into this study: 45 with isolated obesity, defined as a BMI of 30 kg/m 2 or higher with no other cardiovascular comorbidities, and 20 nonobese age-adjusted and sex-adjusted controls. All participants underwent standard two-dimensional ECG and myocardial strain imaging.
There was no significant difference between patients and controls as regards height (P > 0.05). In contrast, weight, BMI, and waist circumference were significantly higher in the patient group compared with the control group (P < 0.001). Obese participants had significantly increased left atrial diameter, aortic diameter, septal wall thickness, LV posterior wall thickness, and LV mass (P < 0.001). There was no significant difference between patients and controls as regards LV diastolic diameter, LV systolic diameter, ejection fraction, fractional shortening, LV mass index, E velocity, A velocity, and the E/A ratio (P > 0.05). Comparative analysis of LV two-dimensional longitudinal strain parameters between patients and controls shows a significant decrease in longitudinal strain in obese patients in the apical long-axis, apical four-chamber, and apical two-chamber views (P < 0.001).
Obesity is associated with morphologic alterations in the LV, in the form of increased LV mass, interventricular septum thickness, and LV posterior wall thickness, as well as subclinical changes in LV systolic function, which can be detected by strain imaging even without overt heart disease.
Keywords: Diastolic function, obesity, strain rate imaging, systolic function
|How to cite this article:|
Abdelazez WF, Yaseen RI, Alkersh AM, Ebada MA. Effects of isolated obesity on left ventricular function: a longitudinal strain imaging study. Menoufia Med J 2014;27:130-5
|How to cite this URL:|
Abdelazez WF, Yaseen RI, Alkersh AM, Ebada MA. Effects of isolated obesity on left ventricular function: a longitudinal strain imaging study. Menoufia Med J [serial online] 2014 [cited 2021 Mar 3];27:130-5. Available from: http://www.mmj.eg.net/text.asp?2014/27/1/130/132785
| Introduction|| |
The data from the National Health Examination Survey from 1999 to 2000 reported the prevalence of overweight (defined as BMI ≥ 25 kg/m 2 ) as 64.5% and obesity (defined as BMI ≥ 30 kg/m 2 ) as 30.5% among US adults .
The prevalence of obesity has increased significantly in the recent years. Worldwide, an estimated 135 million people were obese in 1995, which is presumed to increase to 300 million by 2025 .
Obesity is an independent risk factor for cardiovascular diseases, such as arterial hypertension, congestive heart failure, and ischemic heart disease, and has been proposed as a risk factor for ventricular arrhythmias and sudden death .
Although the mechanisms leading to heart failure in obese patients have not been fully 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 .
Impairment of cardiac function has been reported to be correlated with BMI and duration of obesity, with most studies reporting abnormal diastolic function without consistent association with systolic dysfunction .
However, conventional noninvasive imaging modalities are often suboptimal for detailed evaluation of cardiac structures and for detection of subtle functional changes associated with obesity.
Newer ECG techniques such as tissue Doppler imaging and tissue Doppler imaging-derived techniques, strain imaging/strain rate imaging, could better characterize these possible cardiac abnormalities associated with obesity.
The aim of the present study is to examine LV regional and global performance using these new strain imaging techniques and to define the subclinical changes in LV structure and function associated with obesity, in the absence of other confounding comorbidities.
| Patients and methods|| |
The study included 45 consecutive patients with isolated obesity, defined as a BMI of more than 30 kg/m 2 , who presented to Menoufia University Hospital, and 20 age-matched and sex-matched healthy controls.
Patients with congestive heart failure, a history of coronary artery disease, cardiomyopathies (hypertrophic, dilated, and restrictive), pericardial diseases, hypertension, diabetes mellitus, chest disease (chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis), thyroid disease, renal diseases, hepatic diseases, significant valvular lesions, and poor image quality on ECG, as well as pregnant women, were excluded from the study.
Four groups were identified: group 1 included patients with class I obesity (BMI, 30-34.9 kg/m 2 ; n = 15), group 2 included patients with class II obesity (BMI, 35-49.9 kg/m 2 ; n = 15), group 3 included patients with class III obesity (BMI40 kg/m 2 ; n = 15), and group 4 included healthy referent patients (BMI < 30 kg/m 2 ; n = 20).
Written informed consent for participation was obtained from all participants, and the hospital ethics committee approved the protocol.
The participants were subjected to full history taking, thorough physical examination, and 12-lead ECG.
Each participant's height was determined while he/she was standing without shoes, and his/her weight (kg) was determined using a mechanical scale.
The BMI was calculated as weight in kilograms divided by the square of height in meters, and obesity was defined as a BMI of 30 kg/m 2 or higher .
The waist circumference was measured at the part of the trunk located midway between the lower costal margin and the iliac crest at the end of expiration with the participant in the standing position with his/her feet about 25-30 cm apart. An increased waist circumference was defined as that greater than 88 cm in women and 102 cm in men .
Standard transthoracic ECG and LV longitudinal strain imaging were performed for each participant.
ECG was performed on a standard ultrasound machine (Vivid 9; General Electric Medical Systems, Horten, Norway) equipped with 5 MHz variable-frequency harmonic-phased array transducers with simultaneous ECG signaling.
All participants were studied in the left lateral recumbent position .
Images were recorded in the standard parasternal long-axis and short-axis views and the apical four-chamber, two-chamber, and five-chamber views.
Routine M-mode, two-dimensional, pulsed, and continuous wave Doppler recordings were obtained for each participant.
The left atrial diameter, LV internal cavity dimensions, interventricular septal thickness, posterior wall thickness, LV ejection fraction, and LV fractional shortening were measured from the two-dimensional targeted M-mode ECG tracings in the parasternal long-axis view.
All measurements were made on the basis of the standards of the American Society of ECG .
For measurement of the LV longitudinal strain, two-dimensional images in the apical four-chamber, two-chamber, and three-chamber views were obtained.
All recordings including at least three cardiac cycles were digitally stored for offline analysis.
Stored images were opened using the machine software, which automatically opens the end-systolic frame of the cardiac cycle.
At the end-systolic frame, endocardial border was traced manually, beginning at one end of the mitral annulus and ending at the other end [Figure 1].
The software then generated a region of interest (ROI) including the entire myocardial thickness. The ROI was manually adjusted to achieve a satisfactory image.
The software then tracked the myocardial speckles frame by frame and generated moving images showing the tracking.
Careful visual inspection of the moving images was performed to determine the adequacy of the tracking. If the tracking was not accurate, readjustment of the ROI or selection of a new ROI was performed.
The software divided the LV myocardium into six segments and generated segmental and global longitudinal strain, strain rate, velocity, and displacement curves. As the myocardium usually shortens in longitudinal direction during systole, the longitudinal strain and strain rate curves are shown below the baseline [Figure 1].
The apical long-axis image (i.e. three-chamber view) was the first image to be analyzed. In this view, the movement of the aortic valve leaflets helps in timing the aortic valve closure, which is essential for the software to be able to perform the deformation analysis .
The same process was then repeated with the apical four-chamber and two-chamber images. The strain values for all the segments were recorded and averaged to obtain the global longitudinal strain. The ultrasound system also provided a bull's eye view of the regional and global longitudinal strain [Figure 2].
Using SPSS version 16 (SPSS Inc., Chicago, Illinois, USA), data from the patients and controls were collected and subjected to statistical analysis.
The level of significance was 95%. Hence, a P-value greater than 0.05 was considered a nonsignificant result, that less than 0.05 was considered a significant result, and that less than 0.001 was considered a highly significant result .
| Results|| |
This study included 45 obese patients with a mean age 33.80 8.34 years, including 11 men and 34 women, and 15 control participants with mean age 30.90 4.99 years, including eight men and 12 women.
[Table 1] shows that there was no significant difference between patients and controls as regards age and sex (P > 0.05).
As regards anthropometric measurements, there was no significant difference between patients and controls as regards height (P > 0.05); however, weight, BMI, and waist circumference were significantly higher in the patient group compared with the control group (P < 0.001).
[Table 2] shows that the class of obesity increased with increasing body weight.
[Table 3] shows that the aortic diameter and left atrial diameter were significantly higher in patients compared with controls (P < 0.05).
|Table 3: Conventional echocardiographic parameters of patients and controls|
Click here to view
In addition, interventricular septal thickness and LV posterior wall thickness were significantly higher in patients compared with controls (P < 0.001).
Similarly, LV mass was significantly higher in patients compared with controls (P < 0.001).
In contrast, there was no significant difference between patients and controls as regards LV diastolic diameter, LV systolic diameter, ejection fraction, fractional shortening, LV mass index, E velocity, A velocity, and the E/A ratio (P > 0.05).
Comparative analysis of the LV two-dimensional longitudinal strain parameters between patients and controls shows a significant decrease in longitudinal strain in obese patients in the apical long-axis view, the apical four-chamber view, and the apical two-chamber view (P < 0.001; [Table 4]).
|Table 4: Left ventricular two-dimensional longitudinal strain parameters of patients and controls|
Click here to view
In addition, there was significant decrease in the average longitudinal strain in obese patients compared with normal controls (P < 0.001; [Table 4]).
As shown in [Table 5], there is a significant decrease in LV two-dimensional longitudinal strain, which is observed in all classes of obesity.
|Table 5: Left ventricular two-dimensional longitudinal strain parameters of patient groups and controls|
Click here to view
| Discussion|| |
Epidemiological studies have clearly shown a strong relationship between obesity and increased risk for cardiovascular disease and mortality in the general population .
The higher prevalence of cardiovascular disease in obese individuals is indirectly mediated, to a large extent, by the increased frequency of various well-known risk factors such as hypertension, diabetes, and dyslipidemia, either individually or as a part of the metabolic syndrome. However, there are several ways in which obesity directly affects the cardiovascular system .
Obesity has been shown to be an important risk factor for the development of heart failure irrespective of the presence of other cardiovascular risk factors .
It is well established that obesity leads to LV diastolic dysfunction, which is present in all grades of isolated obesity and is correlated with BMI .
However, limited data are available on the effect of isolated obesity on LV systolic function.
Early detection of subclinical pathological cardiac changes associated with obesity is important in potentially influencing the initiation of treatment and in preventing the progression to heart failure .
In our study, we assessed LV systolic function in 45 obese asymptomatic patients without additional risk factors for heart failure by conventional ECG and LV two-dimensional longitudinal strain imaging.
As patients with hypertension and diabetes may have early subclinical myocardial abnormalities , patients with such comorbidities were excluded.
We found that strain imaging was able to detect significant impairment in LV systolic function in obese patients, although conventional ECG systolic parameters showed no statistically significant differences between obese and control groups. This may be explained by the relative insensitivity of conventional ECG methods.
We found that LV ejection fraction and fractional shortening were similar between obese and control groups.
In contrast, Pascual et al.  reported that early stages of obesity were associated with increased systolic function.
On conventional ECG, we found that obesity is associated with increased aortic diameter, left atrial enlargement, and increased LV mass, with increased septal wall and posterior wall thickness.
BMI was found to be an independent predictor of these functional alterations even after adjusting for other clinical variables.
LV mass was suggested to be an early marker of LV dysfunction in morbidly obese individuals preceding the development of an increased LV wall thickness .
The likely causes for the increased LV mass in obese individuals include an increase in the total blood volume, as a result of an increase in the size of the vascular bed in the excess adipose tissue; an increase in the cardiac output; a resultant increase in the afterload; hyperinsulinemia and insulin resistance; possible disruption of leptin signaling; changes in respiratory workload; and other metabolic mechanisms, such as renal sodium retention, oxidative stress, and inflammation due to cytokines .
As each of these changes may occur in obese individuals, they induce cardiac hypertrophy and play a part in LV morphologic alterations. Each of these changes may have different degrees of action in the process in each participant, and this may explain the variance in the resultant structural alterations .
Our results related to aortic diameter are comparable with the findings of the study by Nemes et al. , who reported that obesity is associated with aortic enlargement and increased stiffness.
The E, A, and E/A values did not differ between obese patients and controls.
The associations of these indices with obesity, reported in previous studies, have been variable. Zarich et al.  observed a significant decrease in the maximum velocity of passive mitral filling (E) among obese patients, whereas the values for active mitral filling (A) were not significantly affected, resulting in a decrease in the E/A ratio.
Conversely, Chakko et al.  did not find significant differences in the values of E, but values of A were increased, resulting in a decreased E/A ratio.
Stoddard et al.  found a significant increase in both E and A values, which were positively correlated with the percentage of body weight in excess of the ideal, so that the E/A ratio was not altered.
Our strain imaging data suggest that obesity is an independent predictor of subclinical abnormalities of regional myocardial function in adult obese individuals without overt heart failure.
Di Salvo et al.  used strain rate imaging to evaluate LV systolic function in obese children and found that obesity is associated with significant reductions in systolic myocardial deformation properties.
Previous studies on uncomplicated obese individuals indicated only impaired diastolic function but normal or hyperdynamic systolic function .
However, we could also detect impairment in systolic function using strain imaging.
Results on effects of BMI on systolic and diastolic function were in concordance with previous reports .
Potential mechanisms that might contribute to the pathogenesis of cardiac dysfunction in obesity include accumulation of lipids in or around myocytes producing lipotoxicity, insulin resistance, and neuroendocrine activation .
In addition, obesity may result in ventricular dysfunction by promoting other risk factors such as hypertension, dyslipidemia, and diabetes mellitus .
However, the precise pathophysiological mechanism for the observed myocardial dysfunction in our patient group with isolated obesity is unknown.
Despite the fact that various mechanisms may play a role in the pathogenesis of cardiac dysfunction in obesity, early detection of these myocardial abnormalities may be important in the management of the disease.
The promotion of optimal body weight through lifestyle modification is undoubtedly the centerpiece to improving the public health burden created by obesity.
Additional, larger scale studies are needed to determine whether ECG strain imaging will have a role in disease prevention and management.
| Conclusion|| |
The presence of isolated obesity was found to be associated with subclinical abnormalities in cardiac function. A better understanding of the pathophysiology of obesity-related myocardial alterations will enable us to modify the disease process, resulting in regression of subclinical cardiac changes.
The use of newer sensitive ECG methods, such as strain imaging, could lead to early detection of subclinical cardiac functional changes. Hence, this may help prevent the progression of obesity and related cardiac dysfunction.
| Acknowledgements|| |
Conflicts of interest
| References|| |
|1.||Aronne LJ. Obesity as a disease: etiology, treatment, and management considerations for the obese patient. Obes Res 2002; 10 :95S-96S. |
|2.|| Bassuk SS, Manson JE. In: Robinson MK, Thomas A. Overview of the obesity epidemic and its relationship to cardiovascular disease Obesity and cardiovascular disease 2006; Milton Park, Abingdon, Oxfordshire, UK, Taylor & Francis Group. p. 1-32. |
|3.|| Pontiroli AE, Pizzocri P, Saibene A, et al. Left ventricular hypertrophy and QT interval in obesity and in hypertension: effects of weight loss and of normalisation of blood pressure. Int J Obes 2004; 28 :1118-1123. |
|4.|| Alpert MA. Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. Am J Med Sci 2001; 321 :225-236. |
|5.|| Wong CY, O′Moore-Sullivan T, Leano R, et al. Alterations of left ventricular myocardial characteristics associated with obesity. Circulation, 2004; 110 :3081-3087. |
|6.|| World Health Organization. Obesity: preventing and managing the global epidemic of obesity. Report of the WHO Consultation of Obesity. Geneva: World Health Organization; 1997. |
|7.|| World Health Organization. Waist circumference and waist-hip ratio. Report of a WHO Expert Consultation. Geneva: World Health Organization; 2008. |
|8.|| Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography′s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiography 2005; 18 :1440-1463. |
|9.|| Bansal M, Kasliwal RR. How do I do it? Speckle-tracking echocardiography. Indian Heart J 2013; 65 :117-123. |
|10.||1Morton RF, J. Richard Hebel, McCarter R. Medical statistics. In: A study guide to epidemiology and biostatistics, 5 th ed. Maryland: Aspen publication Gaithersburg; 2001. p. 71-74. |
|11.||1Lavie CJ, Mehra MR, Milani RV. Obesity and heart failure prognosis: paradox or reverse epidemiology?. Eur Heart J 2005; 26 :5-7. |
|12.||1Mathew B, Francis L, Kayalar A, et al. Obesity: effects on cardiovascular disease and its diagnosis. J Am Board Fam Med 2008; 21 :562-568. |
|13.||1Kenchaiah S, Evans JC, Levy D, et al. Obesity and the risk of heart failure. N Engl J Med 2002; 347 :305-313. |
|14.||1Pascual M, Pascual DA, Soria F, et al. Effects of isolated obesity on systolic and diastolic left ventricular function. Heart 2003; 89 :1152-1156. |
|15.||1Orhan AL, Uslu N, Dayi SU, et al. Effects of isolated obesity on left and right ventricular function: a tissue Doppler and strain rate imaging study. Echocardiography 2010; 27 :236-243. |
|16.||1Russo C, Jin Z, Homma S, et al. Effect of diabetes and hypertension on left ventricular diastolic function in a high-risk population without evidence of heart disease. Eur J Heart Failure 2010; 12 :454-461. |
|17.||1Messerli FH, Christie B, DeCarvalho JGR, et al. Obesity and essential hypertension: hemodynamics, intravascular volume, sodium excretion, and plasma renin activity. Arch Intern Med 1981; 141 :81-85. |
|18.||1Tumuklu MM, Etikan I, Kisacik B, et al. Effect of obesity on left ventricular structure and myocardial systolic function: assessment by tissue Doppler imaging and strain/strain rate imaging. Echocardiography 2007; 24 :802-809. |
|19.||1Nemes A, Gavallér H, Csajbók É, et al. Obesity is associated with aortic enlargement and increased stiffness: an echocardiographic study. Int J Cardiovasc Imaging 2008; 24 :165-171. |
|20.||2Zarich SW, Kowalchuk GJ, McGuire MP, et al. Left ventricular filling abnormalities in asymptomatic morbid obesity. Am J Cardiol 1991; 68 :377-381. |
|21.||2Chakko S, Mayor M, Allison MD, et al. Abnormal left ventricular diastolic filling in eccentric left ventricular hypertrophy of obesity. Am J Cardiol 1991; 68 :95-98. |
|22.||2Stoddard MF, Tseuda K, Thomasb M, et al. The influence of obesity on left ventricular filling and systolic function. Am J Cardiol 1992; 124 :694-699. |
|23.||2Di Salvo G, Pacileo G, Del Giudice EM, et al. Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study. Eur Heart J 2006; 27 :2689-2695. |
|24.||2Iacobellis G. True uncomplicated obesity is not related to increased left ventricular mass and systolic dysfunction. J Am Coll Cardiol 2004; 44 :2257-2257. |
|25.||2Scaglione R, Dichiara MA, Indovina A, et al. Left ventricular diastolic and systolic function in normotensive obese subjects: influence of degree and duration of obesity. Eur Heart J 1992; 13 :738-742. |
|26.||2Iacobellis G, Ribaudo MC, Leto G, et al. Influence of excess fat on cardiac morphology and function: Study in uncomplicated obesity. Obes Res 2002; 10 :767-773. |
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]