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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 15  |  Issue : 2  |  Page : 164-167

Echocardiographic study of left ventricular mass in normotensive young obese


1 Department of Physiology, J. J. M. Medical College, Davangere, Karnataka, India
2 Department of Cardiology, J. J. M. Medical College, Davangere, Karnataka, India
3 Department of Cardiology, City Central Hospital, Davangere, Karnataka, India
4 Department of Cardiology, SSNH, Davangere, Karnataka, India

Date of Submission18-Jan-2022
Date of Acceptance05-Apr-2022
Date of Web Publication24-May-2022

Correspondence Address:
Dr S B Lohitashwa
Department of Cardiology, J. J. M. Medical College, Davangere - 577 004, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/kleuhsj.kleuhsj_85_22

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  Abstract 


BACKGROUND: Obesity is increasing worldwide due to decreased physical activity and easy availability of high-energy foods. Increased adiposity is a risk factor for the development of cardiovascular disease. One of the characteristic cardiac adaptations to obesity is the left ventricular hypertrophy. We evaluate the echocardiography changes in the left ventricular structure and function in uncomplicated young obese.
MATERIALS AND METHODS: The study was conducted in age-matched 24 young male obese and 26 male controls. Anthropometric parameters such as height (cm) and weight (kg) were measured. Body mass index (BMI) was calculated. A group of obese subjects with BMI ≥30 of kg/m2 compared with a group of controls with BMI of 18.50–24.99 kg/m2. Echocardiograms were performed using GE Vivid T8 by standard techniques. Left ventricular (LV) mass, LV mass/body surface area index, LV mass/height, Posterior wall thickness, and relative wall thickness (RWT) were found out. Statistical analysis was done using “t”-test.
RESULTS: The mean values of LV mass, LV mass/body surface area index, LV mass/height, posterior wall thickness, and RWT were greater in the group of obese when compared with the controls. The linear regression analysis showed a strong association between the degree of obesity and LV mass.
CONCLUSION: The present study suggests that the LV mass parameters are increased in obese when compared with the controls. Echocardiographic study should be included in the evaluation of obese for the early detection of subclinical structural and morphological changes in the left ventricle because obesity itself is an independent predictor for left ventricular hypertrophy. Preventive measures should be taken in the control of obesity, thus, contributing to decrease the morbidity and mortality and reducing the cardiovascular disease burden on our society.

Keywords: Body mass index, echocardiography, obesity


How to cite this article:
Ashwini S, Johncy S S, Lohitashwa S B, Venkatesh B P, Mallesh P. Echocardiographic study of left ventricular mass in normotensive young obese. Indian J Health Sci Biomed Res 2022;15:164-7

How to cite this URL:
Ashwini S, Johncy S S, Lohitashwa S B, Venkatesh B P, Mallesh P. Echocardiographic study of left ventricular mass in normotensive young obese. Indian J Health Sci Biomed Res [serial online] 2022 [cited 2022 Jul 2];15:164-7. Available from: https://www.ijournalhs.org/text.asp?2022/15/2/164/345838




  Introduction Top


Obesity is a multifaceted disorder of appetite regulation and energy metabolism. Few decades back, obesity was considered an indicator of wealth and well-being.[1] However, nowadays, it has become epidemic globally and threatens global well-being even in children and adolescents. The prevalence of obesity is steadily increasing worldwide due to the combination of genetic predisposition, easy availability of high-energy foods, and decreased requirement for physical activity in modern society.[2] In India, there is an alarming increase in the prevalence of obesity. At present, obesity constitutes a major health issue because of its association with morbidity, mortality, and cardiovascular diseases. One of the characteristic cardiac adaptations to obesity is left ventricular hypertrophy and also linked to increased left ventricular mass, an independent predictor of mortality.[3] In the general population, obesity is an independent risk factor for the incidence of heart failure.[4] The probable pathophysiology for the occurrence of heart failure in increased body weight might therefore be the LV diastolic dysfunction that starts early in the obese individual. Long-standing obesity affects the left ventricle (LV) structure and function.[5],[6] It may present as eccentric LV hypertrophy and diastolic dysfunction and rarely systolic dysfunction. Along with cardiovascular risk factors and structural changes in the heart that are associated with obesity/overweight also plays a role and determinants of LV diastolic dysfunction.[7],[8] Various studies were done on the effect of obesity, but till now, whether an obesity is associated with an impairment of LV diastolic mechanics, independent of associated risk factors, has not been fully established.[9]

In this study, we sought to evaluate the relationship between obesity and diastolic dysfunction by evaluating the echocardiography changes in the left ventricular structure and function in uncomplicated young obese, with absent other known risk factors such as diabetes, hypertension, and ischemic heart disease.


  Materials and Methods Top


After obtaining the institutional ethical clearance, this study was done. All the participants were informed about the procedure and informed consent was obtained. A brief history was taken followed by cardiovascular and respiratory system examinations. A structured pro forma is used to collect the relevant data. Our study group consists of 24 young male obese and 26 male controls. All subjects were matched for age. Anthropometric parameters such as height (cm) and weight (kg) were measured. Body mass index (BMI) was calculated using Quetelet's index, i.e., body weight (kilograms) divided by the square of the height (meters). A group of obese subjects with BMI ≥30 of kg/m2 compared with a group of controls with BMI of 18.50–24.99 kg/m2. Heart rate and blood pressure measurements were done.

Inclusion criteria

Healthy males in the age group of 25–40 years, nonsmokers, nonalcoholic.

Exclusion criteria

Adults above the age of 40 years and below 25, systemic illness including hypertension, diabetic mellitus, renal or endocrinal diseases, subjects on any medications, and subjects of acute or chronic illness.

Ethical clearance

Ethical Clearance was obtained from Institutional Ethical committee, JJM Medical College, Davanagere to conduct the study with Ref no – JJMMC/IEC – 07 – 2019 dated 26/03/2019.

Echocardiographic studies

All the subjects underwent a transthoracic two-dimensional (2D)-guided M-mode Doppler echocardiogram. Echocardiograms were performed using GE Vivid T8 by standard techniques with subjects in the left lateral decubitus position. Echocardiograms were recorded on videotape. 2D-echo measurements comprised LV end diastolic, the LV percent fractional shortening (%FS) obtained from the parasternal short axis and calculated as %FS = ([Ded-Des]/Ded) ×100, where Ded and Des are the LV mid-cavity dimensions at end diastole and end systole, respectively. The left ventricular mass (LVM) was estimated using the area length method; the LVM index and LVM/height were calculated by dividing body surface area and by the height, respectively. The relative wall thickness (RWT) was calculated as RWT = (2 × Posterior wall thickness [PWth])/Ded, where PWth is posterior wall thickness at end diastole. Entire measurements were performed according to the guidelines of the American Society of Echocardiography.

Statistical analysis

Data are presented as mean ± standard deviation. The comparison between obese and controls was done using the Student's t-test. A P = 0.05 or less was considered for statistical significance. Linear regression analysis was applied to test the association between LV mass and the degree of obesity was performed. The SPSS version 16 (Chicago, Illinois, USA) software was used for all the analysis.


  Results Top


[Table 1] summarizes the demographic and clinical characteristics of the subjects. Twenty-six controls and 24 obese were taken for the study. No significant difference was found out regarding age and height between the controls and the obese. However, a statistically significant increase in the weight and BMI were found out between them. Even though the heart rate, systolic blood pressure, and diastolic blood pressure were more in obese when compared to the controls, but the increase was not statistically significant.
Table 1: Clinical and demographic characteristics of the subjects

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[Table 2] summarizes the echocardiographic morphological parameters in controls and obese. The LV mass was statistically increased in obese groups compared to controls. P < 0.001. LV mass/body surface area index was increased in obese when compared to the controls this difference was highly significant statistically. P < 0.001. LV mass/h was increased in obese when compared to the controls and was statistically significant. P = 0.01. Even though the RWT was increased in obese groups compared with controls but was not statistically significant. The posterior wall thickness was also increased in obese groups compared with controls. The linear regression analysis showed a strong association between the degree of obesity and LV mass [Figure 1].
Table 2: Echocardiographic morphological parameters in controls and obese

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Figure 1: Correlation between left ventricular mass and body mass index

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  Discussion Top


In our study, the mean values of LV mass, LV mass/body surface area index, LV mass/height, posterior wall thickness, and RWT were greater in the group of obese when compared with the controls. This shows an association between obesity and cardiac structural changes. One of the probable reasons behind the structural and morphological changes, especially in the left ventricle may be due to increased metabolic demand associated with excess fat deposition in obesity. This elevates the cardiac output and total blood volume. These compensatory circulatory changes cause left ventricular structural change mainly a geometric remodeling in the form of cavity dilatation. This increases the ventricular wall stress leading to a compensatory left ventricular hypertrophic response.[10],[11]

Another reason behind the structural and morphological changes in the ventricle may be the hormonal changes in obesity with several alternative mechanisms. The levels of serum leptin are closely linked with increased visceral and subcutaneous adiposity. Higher levels of serum leptin are the hallmark of human obesity.[12]

Studies showed that in humans and in animal model hyperinsulinemia, have been linked to ventricular hypertrophy. Previous study was done by Chiew and his co-workers showed that LV wall thickness, diameters, volumes, and LV mass indexed to height increased with increasing BMI. They also showed significantly different in mild and severely obese groups as compared with the controls are seen in the morphological measures, except for left ventricular end diastolic diameter. Both the indexed LV mass and wall thickness were correlated with insulin levels.[7]

A study was done by Crisostomo et al. showed that cardiac manifestations can occur in young, normotensive obese women due to the association of obesity with LV mass. The study also demonstrated a higher chance of LV hypertrophy in obese as compared to lean women. They explained that expansion of blood volume and increased cardiac output increase the left ventricular filling in obesity and leads to an increase in LV cavity dimension and enlargement of ventricular mass which can be measured by echocardiography. This will identify patients at high risk of future morbid events if the LV hypertrophy is detected early irrespective of age, blood pressure, and ventricular function in relaxation.[10]

In our study, we found a positive correlation between BMI and left ventricular mass. Lauer et al. demonstrated that BMI was strongly correlated with left ventricular mass. They showed that BMI remained a strong independent predictor of left ventricular mass, left ventricular wall thickness, RWT, and left ventricular internal dimension after adjusting for age and blood pressure. This is particularly true for subjects with a BMI exceeding 30 kg/m2.[13]


  Conclusion Top


Based on the data obtained by the present study, we suggest that the LV mass is increased in obese when compared with the controls and that echocardiographic study should be included in the evaluation of obese for early detection of subclinical structural and morphological changes in the left ventricle because obesity itself is an independent predictor for left ventricular hypertrophy. Preventive measures should be taken in the control of obesity, thus, contributing to decrease the morbidity and mortality and reducing the cardiovascular disease burden on our society.

Acknowledgment

Authors are grateful to the Head of the department, Physiology J. J. M. Medical College for his support and encouragement. Authors are deeply indebted to all volunteers who participated in this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Praveen KH, Monika M, Badjatiya HC. A study on prevalence of diastolic dysfunction in normotensive obese young adults. Indian J Clin Pract 2013;23:698-700.  Back to cited text no. 1
    
2.
Iacobellis G, Ribaudo MC, Leto G, Zappaterreno A, Vecci E, Di Mario U, et al. Influence of excess fat on cardiac morphology and function: Study in uncomplicated obesity. Obes Res 2002;10:767-73.  Back to cited text no. 2
    
3.
Iacobellis G, Ribaudo MC, Zappaterreno A, Iannucci CV, Di Mario U, Leonetti F. Adapted changes in left ventricular structure and function in severe uncomplicated obesity. Obes Res 2004;12:1616-21.  Back to cited text no. 3
    
4.
Russo C, Jin Z, Homma S, Rundek T, Elkind MS, Sacco RL, et al. Effect of obesity and overweight on left ventricular diastolic function: A community-based study in an elderly cohort. J Am Coll Cardiol 2011;57:1368-74.  Back to cited text no. 4
    
5.
Punekar J, Jain N, Nargawe H, Punekar P. To study effect of isolated obesity on diastolic dysfunction in echocardiography. Int J Contemp Med Res 2017;4:695-8.  Back to cited text no. 5
    
6.
Kossaify A, Nicolas N. Impact of overweight and obesity on left ventricular diastolic function and value of tissue Doppler echocardiography. Clin Med Insights Cardiol 2013;7:43-50.  Back to cited text no. 6
    
7.
Wong CY, O'Moore-Sullivan T, Leano R, Byrne N, Beller E, Marwick TH. Alterations of left ventricular myocardial characteristics associated with obesity. Circulation 2004;110:3081-7.  Back to cited text no. 7
    
8.
Peterson LR, Waggoner AD, Schechtman KB, Meyer T, Gropler RJ, Barzilai B, et al. Alterations in left ventricular structure and function in young healthy obese women: Assessment by echocardiography and tissue Doppler imaging. J Am Coll Cardiol 2004;43:1399-404.  Back to cited text no. 8
    
9.
Crisostomo LL, Araújo LM, Câmara E, Carvalho C, Silva FA, Vieira M, et al. Comparison of left ventricular mass and function in obese versus nonobese women &lt; 40 years of age. Am J Cardiol 1999;84:1127-9, A11.  Back to cited text no. 9
    
10.
Crisostomo LL, Araújo LM, Câmara E, Carvalho C, Silva FA, Vieira M, et al. Left ventricular mass and function in young obese women. Int J Obes Relat Metab Disord 2001;25:233-8.  Back to cited text no. 10
    
11.
Bella JN, Devereux RB, Roman MJ, O'Grady MJ, Welty TK, Lee ET, et al. Relations of left ventricular mass to fat-free and adipose body mass: The strong heart study. The Strong Heart Study Investigators. Circulation 1998;98:2538-44.  Back to cited text no. 11
    
12.
Rider OJ, Francis JM, Ali MK, Byrne J, Clarke K, Neubauer S, et al. Determinants of left ventricular mass in obesity; a cardiovascular magnetic resonance study. J Cardiovasc Magn Reson 2009;11:9.  Back to cited text no. 12
    
13.
Lauer MS, Anderson KM, Kannel WB, Levy D. The impact of obesity on left ventricular mass and geometry. The Framingham Heart Study. JAMA 1991;266:231-6.  Back to cited text no. 13
    


    Figures

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    Tables

  [Table 1], [Table 2]



 

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