Obesity is a global pandemic and is a recognised risk factor for cardiovascular diseases. However, its impact on cardiac structure and function using echocardiography, as well as its association with anthropometric parameters in otherwise healthy individuals, requires further investigation. Therefore, we conducted an observational study with a cohort of 196 participants, comparing various echocardiographic parameters in normal weight individuals and those who were overweight or obese but had no other risk factors. Our findings revealed that obese participants had significant changes in echocardiographic measurements of the structure and functions of the left ventricle, left ventricular global longitudinal strain, left atrium, right ventricle and right ventricular global longitudinal strain compared with the control group. Body surface area and body mass index were important anthropometric features that correlated with the above echocardiographic changes, and should be routinely evaluated to assess cardiovascular risk in patients. Further larger studies are necessary to determine the clinical significance of the echocardiographic changes observed in obese individuals and their impact on health.
Introduction
The World Health Organisation (WHO) defines obesity as “abnormal or excessive fat accumulation that may impair health” and classifies obesity based on body mass index (BMI), with those with a BMI of 25–30 kg/m2 termed as overweight and those with BMI over 30 kg/m2 defined as obese.1,2 Obesity has reached pandemic levels in the last 50 years.3 One and a half billion people over the age of 20 in the world are thought to be overweight or obese.4 Obesity is associated with low-grade chronic inflammation leading to insulin resistance, which may progress to diabetes mellitus.5 Moreover, fatty liver disease, systemic hypertension and chronic kidney disease may be more prominent in this population, all of which are independent risk factors for cardiovascular morbidity and mortality.5–7
In a recent meta-analysis of 28 studies, Aune et al. found that high BMI and abdominal obesity, as measured by waist circumference (WC), are important risk factors for heart failure (HF).8 However, BMI is not an accurate parameter for all individuals, as some people, such as professional athletes in various sports who have increased muscle mass, may not be ‘obese’ even though they have an increased BMI.9,10 Recent studies have not demonstrated a direct significant relationship between BMI and cardiovascular disease (CVD), sometimes referred to as the obesity paradox.9,11,12 Therefore, it may be a suboptimal parameter to risk stratify individuals for cardiovascular disease. Other studies have found that waist-to-height ratio (WHtR), waist circumference (WC) and height, when raised to allometric power, may be more predictive of cardiovascular diseases.13–15 Similarly, neck circumference is known to have a positive correlation with the above parameters, in addition to an increased risk of hypertension, diabetes and hyperlipidaemia.16,17 Other parameters, such as body shape index (BSI) and body surface area (BSA), have not been validated so far. Moreover, it is unclear whether one or more of these factors may be predictive of the impact of obesity on cardiac structure and function, as assessed using transthoracic echocardiography, in otherwise healthy individuals.
Therefore, to understand the effects of obesity on cardiac structure and function in the absence of other confounding comorbid conditions, our study was performed to evaluate the correlation between various echocardiography and anthropometric parameters.
Materials and method
A prospective, cohort-matched, observational study was carried out at the outpatient cardiology department of Mashhad University of Medical Sciences Ghaem Hospital between 1 May 2019 and 31 September 2019. Patients aged 20 to 60 years referred to the cardiology clinic for various cardiovascular symptoms were considered for the study. Inclusion criteria comprised of patients with a normal clinical examination, sinus rhythm and no known cardiovascular risk factors and a BMI ≥25 kg/m2. Those individuals with new abnormal clinical findings or known history of cardiovascular disease (previous myocardial infarction, heart failure, valvular heart disease, overt cardiomyopathy and arrhythmias including atrial fibrillation), diabetes mellitus (fasting blood glucose >126 mg/dL), hypertension (systolic blood pressure [SBP] >140 mmHg and/or diastolic blood pressure [DBP] >90 mmHg), impaired renal or liver functions tests and thyroid diseases were excluded. The control group had participants who reported no history of cardiovascular disease and had normal BMI (18.5–24.9 kg/m2). Participants in the two groups were matched according to age and sex. The WC was measured in centimetres (cm) on a standing subject from the half-point of the lowest rib margin to the iliac crest. The WHtR was calculated by dividing the WC (cm) by height (cm). BMI, BSI (m11/6 kg–2/3) and BSA were calculated as weight/height(m)2, WC/BMI2/3 × height(cm)1/2 and [height(cm) × weight/3,600]1/2, respectively. All participants signed a consent form before commencing the study. Ethical approval for the study was granted by the local ethics committee. Transthoracic echocardiography (TTE) was performed by locally accredited echocardiologists using Siemens ACUSON SC2000 Ultrasound System with 4V1c Transducer (frequency bandwidth: 1.25–4.5 MHz). Standard views were obtained as per American Society of Echocardiography (ASE) guidelines.15 Statistical analysis was performed using SPSS v. 24.0. Quantitative data were described by mean and standard deviation (SD) and qualitative data were described by frequency and percentage. In the data analysis, t-test was used and, in the case of non-normality, the Mann-Whitney U test was used. Chi-square test was used for categorical data analysis, and in cases where more than 20% of the expected frequencies of the tables were less than five, Fisher’s exact test was used. The correlation of quantitative variables was analysed by Pearson correlation. A p value ≤0.05 was considered statistically significant for all analyses.
Results
A total of 196 participants, of which 51.5% were women, were recruited to the study. The average age for participants was 39.67 ± 10.55 years. Group 1 comprised 100 non-obese (BMI <25 kg/m2), healthy individuals while group 2 included 96 overweight and obese individuals (BMI ≥25 kg/m2). The study sample baseline characteristics can be found in table 1. The echocardiographic structural and functional measurements in relation to BMI are listed in table 2. Left atrial area (LAA), left atrial diameter (LAD), left atrial volume (LAV), left ventricular mass (LVM), mitral inflow E velocity, mitral inflow S velocity, Tei index, left ventricular global longitudinal strain (LVGLS), and right ventricular global longitudinal strain (RVGLS) were all significantly different in obese participants in comparison with the control group (table 2).
Table 1. Demographics and classifications of studied individuals
Sex | N | Mean age ± SD, years | Mean weight ± SD, kg | Mean height ± SD, cm | Mean heart rate ± SD, bpm | Mean BMI ± SD, kg/m2 | Mean WC ± SD, cm |
Control group (n=100) | |||||||
F | 51 | 38.29 ± 11.31 | 58.11 ± 6.58 | 162.98 ± 6.29 | 79.50 ± 12.17 | 21.90 ± 1.85 | 77.90 ± 5.13 |
M | 49 | 38.61 ± 11.56 | 71.52 ± 6.78 | 175.00 ± 6.08 | 74.63 ± 10.19 | 23.20 ± 1.44 | 90.77 ± 5.12 |
Case group (n=96) | |||||||
F | 50 | 42.10 ± 9.99 | 82.93 ± 12.49 | 161.26 ± 7.10 | 79.22 ± 10.32 | 32.10 ± 4.73 | 108.5 ± 8.23 |
M | 46 | 39.69 ± 9.02 | 89.67 ± 15.02 | 167.36 ± 7.87 | 76.10 ± 9.39 | 32.10 ± 5.08 | 108.89 ± 7.46 |
Control Group = patients without any pathologic finding and past medical history of cardiovascular disease and have normal BMI (18–24.9 kg/m2). Case Group = patients without any pathologic finding and past medical history of cardiovascular disease and have increased BMI (≥25 kg/m2). Key: BMI = body mass index; bpm = beats per minute; F = female; M = male; SD = standard deviation; WC = waist circumference |
Table 2. Comparison of various echocardiographic parameters between case and control groups as based on body mass index (BMI)
Parameter Mean ± SD |
Control group | Case group | p value |
LAA, cm2 | 16.47 ± 4.22 | 18.47 ± 2.42 | ≤0.001 |
LAD, cm | 3.21 ± 0.26 | 3.46 ± 0.46 | ≤0.001 |
LAV, ml | 45.70 ± 11.98 | 55.93 ± 7.88 | ≤0.001 |
LVM, g | 121.94 ± 37.43 | 138.91 ± 35.198 | 0.001 |
LVEDD, cm | 46.33 ± 3.83 | 48.97 ± 2.97 | ≤0.001 |
LVESD, cm | 28.41 ± 3.51 | 25.08 ± 3.39 | ≤0.001 |
LVEDV, ml | 97.26 ± 11.48 | 99.65 ± 18.13 | 0.271 |
LVESV, ml | 33.90 ± 5.25 | 37.97 ± 8.35 | ≤0.001 |
RVEDD, cm | 30.96 ± 2.02 | 30.05 ± 2.68 | 0.008 |
IVS, cm | 7.97 ± 1.32 | 8.26 ± 1.06 | 0.092 |
ASC, cm | 2.99 ± 0.35 | 3.02 ± 0.29 | 0.448 |
EF, % | 63.03 ± 3.90 | 61.96 ± 4.63 | 0.081 |
E’, cm/s | 74.64 ± 16.90 | 60.23 ± 12.19 | ≤0.001 |
A, cm/s | 61.32 ± 17.19 | 58.34 ± 18.74 | 0.248 |
Em, cm/s | 9.70 ± 1.89 | 7.62 ± 1.50 | ≤0.001 |
Sm, cm/s | 8.15 ± 1.01 | 7.39 ± 1.50 | ≤0.001 |
E/A | 1.29 ± 0.42 | 1.21 ± 0.66 | 0.276 |
E/Em | 7.68 ± 0.97 | 8.05 ± 1.92 | 0.092 |
Tei | 0.408 ± 0.02 | 0.45 ± 0.08 | ≤0.001 |
IVRT, ms | 80.14 ± 5.47 | 92.84 ± 13.61 | ≤0.001 |
STV | 12.10 ± 1.44 | 12.46 ± 2.05 | 0.152 |
LVGLS, % | 18.93 ± 0.78 | 21.05 ± 2.46 | ≤0.001 |
RVGLS, % | 20.78 ± 0.64 | 19.65 ± 1.76 | ≤0.001 |
Key: ASC = ascending aorta; EF = ejection fraction; IVRT = isovolumic relaxation time; IVS = interventricular septum; LAA = left atrial area; LAD = left atrial diameter; LAV = left atrial volume; LVEDD = left ventricle end diastolic diameter; LVESD = left ventricle end systolic diameter; LVEDV = left ventricle end diastolic volume; LVESV = left ventricle end systolic volume; LVGLS = left ventricular global longitudinal strain; LVM = left ventricle mass; RVEDD = right ventricle end diastolic diameter; RVGLS = right ventricular global longitudinal strain; STV = segmental thickness variability |
Left ventricular end diastolic diameter (LVEDD) had a significant correlation with BMI (p≤0.001), WC (p≤0.001), BSI (p=0.002) and BSA (p≤0.001), with a similar significant relationship of left ventricular end systolic diameter (LVESD) with these factors. Tei index, isovolumic relaxation time (IVRT), LVGLS and RVGLS all had significant correlation with all five anthropometric parameters. Both Tei index and IVRT had a negative correlation with BSI, while LVGLS and RVGLS had positive correlation with BSI. On the other hand, left ventricular ejection fraction (LVEF) had no significant correlation with any of the echocardiographic parameters analysed (table 3, available online).
Table 3. Correlation of anthropometric factors with structural and functional indicators of heart in population with BMI ≥25 kg/m2
Parameter | WC, cm Correlation (p value) |
BMI, kg/m2 Correlation (p value) |
WHtR, cm/m × 100 Correlation (p value) |
BSI, cm/(kg/m2)2/3×cm1/2 Correlation (p value) |
BSA, m2 Correlation (p value) |
LAA (cm2) | r=0.192 (p=0.060) | r=0.313 (p=0.002) | r=–0.170 (p=0.098) | r=0.001 (p=0.990) | r=0.713 (p≤0.001) |
LAD (cm) | r=0.259 (p=0.011) | r=0.377 (p≤0.001) | r=–0.143 (p=0.166) | r=–0.012 (p=0.907) | r=0.793 (p≤0.001) |
LAV (ml) | r=0.141 (p=0.169) | r=0.299 (p=0.003) | r=–0.205 (p=0.045) | r=–0.034 (p=0.744) | r=0.693 (p≤0.001) |
LVM (g) | r=0.634 (p≤0.001) | r=0.792 (p≤0.001) | r=0.382 (p≤0.001) | r=–0.487 (p≤0.001) | r=0.759 (p≤0.001) |
LVEDD (cm) | r=0.446 (p≤0.001) | r=0.626 (p≤0.001) | r=0.114 (p=0.267) | r=–0.306 (p=0.002) | r=0.825 (p≤0.001) |
LVESD (cm) | r=0.300 (p=0.003) | r=0.415 (p≤0.001) | r=0.121 (p=0.241) | r=–0.230 (p=0.024) | r=0.489 (p≤0.001) |
LVEDV (ml) | r=0.530 (p≤0.001) | r=0.603 (p≤0.001) | r=0.254 (p=0.013) | r=–0.250 (p=0.014) | r=0.699 (p≤0.001) |
LVESV (ml) | r=0.485 (p≤0.001) | r=0.552 (p≤0.001) | r=0.268 (p=0.008) | r=–0.263 (p=0.010) | r=0.575 (p≤0.001) |
RVEDD (cm) | r=0.632 (p≤0.001) | r=0.698 (p≤0.001) | r=0.352 (p≤0.001) | r=–0.308 (p=0.002) | r=0.735 (p≤0.001) |
IVS (cm) | r=0.664 (p≤0.001) | r=0.770 (p≤0.001) | r=0.500 (p≤0.001) | r=–0.515 (p≤0.001) | r=0.597 (p≤0.001) |
ASC (cm) | r=0.129 (p=0.209) | r=0.277 (p=0.006) | r=–0.020 (p=0.844) | r=–0.208 (p=0.042) | r=0.383 (p≤0.001) |
EF (%) | r=–0.151 (p=0.142) | r=–0.142 (p=0.168) | r=–0.172 (p=0.095) | r=0.111 (p=0.284) | r=–0.009 (p=0.930) |
E’ (cm/s) | r=–0.131 (p=0.202) | r=–0.114 (p=0.270) | r=–0.145 (p=0.159) | r=0.078 (p=0.452) | r=–0.012 (p=0.909) |
A (cm/s) | r=0.275 (p=0.007) | r=0.402 (p≤0.001) | r=0.283 (p=0.005) | r=–0.406 (p≤0.001) | r=0.176 (p=0.086) |
Em (cm/s) | r=–0.393 (p≤0.001) | r=–0.404 (p≤0.001) | r=–0.370 (p≤0.001) | r=0.281 (p=0.006) | r=–0.196 (p=0.056) |
Sm (cm/s) | r=–0.307 (p=0.002) | r=–0.248 (p=0.015) | r=–0.262 (p=0.010) | r=0.080 (p=0.437) | r=–0.149 (p=0.148) |
E/A | r=–0.183 (p=0.074) | r=–0.213 (p=0.037) | r=–0.205 (p=0.045) | r=0.197 (p=0.054) | r=–0.050 (p=0.631) |
E/EM | r=0.197 (p=0.054) | r=0.231 (p=0.023) | r=0.177 (p=0.084) | r=–0.179 (p=0.080) | r=0.141 (p=0.171) |
Tei | r=0.642 (p≤0.001) | r=0.782 (p≤0.001) | r=0.524 (p≤0.001) | r=–0.592 (p≤0.001) | r=0.551 (p≤0.001) |
IVRT (ms) | r=0.496 (p≤0.001) | r=0.536 (p≤0.001) | r=0.453 (p≤0.001) | r=–0.389 (p≤0.001) | r=0.295 (p=0.004) |
STV | r=–0.099 (p=0.336) | r=–0.156 (p=0.129) | r=–0.067 (p=0.515) | r=0.123 (p=0.234) | r=–0.121 (p=0.239) |
LVGLS (%) | r=–0.722 (p≤0.001) | r=–0.814 (p≤0.001) | r=–0.613 (p≤0.001) | r=0.584 (p≤0.001) | r=–0.531 (p≤0.001) |
RVGLS (%) | r=–0.611 (p≤0.001) | r=–0.664 (p≤0.001) | r=–0.526 (p≤0.001) | r=0.458 (p≤0.001) | r=–0.418 (p≤0.001) |
Key: ASC= ascending aorta; BMI = body mass index; BSA:= body surface area; BSI = body shape index; EF = ejection fraction; IVRT= isovolumic relaxation time; IVS = interventricular septum; LAA= left atrial area; LAD= left atrial diameter; LAV = left atrial volume; LVEDD = left ventricle end diastolic diameter; LVEDV = left ventricle end diastolic volume; LVESD = left ventricle end systolic diameter; LVESV = left ventricle end systolic volume; LVGLS = left ventricular global longitudinal strain; LVM = left ventricle mass; RVEDD = right ventricle end diastolic diameter; RVGLS = right ventricular global longitudinal strain; STV = S tricuspid valve; WC = waist circumference; WHtR = waist-to-height ratio |
Discussion
In this study, we evaluated the effects of obesity on echocardiographic structural and functional parameters, and better defined which anthropometric factors are best predictive of these changes. Our results show that in overweight and obese adults, who otherwise have no prior cardiovascular conditions, there is significant variation in cardiac structure, diastolic and systolic function. Additionally, of the anthropometric features, although BMI is most frequently correlated with such abnormalities, BSA is the strongest parameter to predict such abnormalities, with the proportional associated (r value) consistently higher for BSA than BMI for parameters where significant changes were detected (p<0.05). Only LVM, IVS, IVRT, Tei index, RVGLS and LVGLS had a greater r value for BMI than BSA (when p<0.05). Similar findings were also noted by Moukarzel et al., where BSA was most strongly associated with echocardiographic parameters in comparison with other anthropometric features.18
BMI ≥25 kg/m2 was associated with enlargement in left atrial dimensions, increase in LVEDD, LVESD, LVM, E mitral inflow velocity, S mitral inflow velocity, Tei index, and E/EM ratio, the latter two being reliable estimates of left ventricular diastolic pressures. Mehta et al. assessed the utility of WC and BMI in 49 children with abdominal obesity and noted significant changes in LA dimensions, as well as LV filling parameters.13 In patients with stable ischaemic heart disease or type 2 diabetes mellitus, obesity leads to impairment in left atrial volume and contractility, in comparison with non-obese individuals.19,20 Other studies showed that obese individuals have significantly increased LVEDD, septal wall thickness (SWT), left atrial diameter (LAD), LV end systolic volume (LVESV), left ventricular end diastolic volume (LVEDV) and IVRT.14,21,22 Our study showed similar findings with these parameters with significant differences between the two groups for LVEDD, LAD, LVESV and ISRT (p<0.05), although SWT and LVEDV were found to be non-significant. There was also a significant association between LVM and all five of the anthropometric parameters assessed. Daniels et al., in their study on children aged 6 to 17 years, found a statistically significant association between lean and fat body mass with LVM, although they determined that lean body mass had a stronger correlation with LVM than adiposity.23
Mehta et al. also noted that WC was the only anthropometric feature that had a significant negative association with septal, inferior wall and RV wall early and late peak velocities.13 Our results showed a significant correlation of early diastolic tissue velocity (EM) and systolic tissue velocity (SM) with BMI, WC and WHtR, although BSI was only significant for EM. These findings may be explained by the older age group of the participants, where the effects of obesity may be more prominent, although the duration of obesity in individual participants was not documented. Similarly, other studies on obese individuals found significantly reduced trans-mitral early-to-late velocity ratio and E mitral inflow velocity, findings also noted in our study.14,24 We also determined that WHtR, but not BSI, BSA and WC, had a significant association with this ratio.
Although this study could not find any significant relationship between LVEF and various anthropometric factors, a significant correlation of LVGLS and RVGLS was noted with obesity. LVGLS is now considered an important parameter for prognostication. In patients with acute heart failure, irrespective of ejection fraction (EF), a reduction in LVGLS was directly related to increase in cardiovascular outcomes.25 It is an important factor in patients with heart failure and preserved ejection fraction (HFpEF) where the EF value may not be helpful in identifying high-risk individuals.26–28 Similarly, other investigators determined significantly reduced tissue Doppler lateral peak velocities with significant differences in regional and global longitudinal strain in obese individuals in both adult and paediatric age groups, and including patients with type 2 diabetes mellitus.14,20,29–32 This may highlight the fact that obese individuals, who have no other known cardiovascular conditions, may be at high risk of developing heart failure.
The findings of predicting anthropometric measurements in the present study is supported by previous studies,12,13,33 in which BMI and BSA are better than other anthropometric measurements to predict cardiac remodelling and change of cardiac function. However, other parameters, such as height and waist circumference, may better predict events in obese individuals.15,34 These contradictory results may be explained by such differences between subjects enrolled in different studies: race, age, gender, duration of obesity, comorbid disease and family history.
The main limitation of this study is the small sample size, from a single institution, and that participants with BMI ≥25 kg/m2 were not further subdivided into different grades of obesity severity. Therefore, whether or not the findings would have been more significant as the degree of obesity progressed is unknown. Additionally, other important factors that may play a role in these findings, including leptin levels, presence of obstructive sleep apnoea, intravascular volume and invasive pulmonary and intrathoracic pressure, were not assessed. Nonetheless, our results must be interpreted with caution and larger studies with higher patient numbers should be carried out to confirm our findings.
We found that the presence of obesity in otherwise ‘healthy’ people affected most echocardiographic parameters of left atrial/ventricular and right ventricle chamber size and function. Whether this may lead to clinically significant abnormalities, including arrhythmias, such as atrial fibrillation (AF), is still not clear. However, such changes may be able to risk stratify patients that are at risk of developing heart failure at a later stage of life, and may be used as a motivation strategy in these patients to help them work on weight loss.
In summary, obesity can result in significant changes in cardiac structure, as well as alterations of systolic and diastolic function, as detected by transthoracic echocardiography. Although BMI most frequently correlates with such changes, BSA is the strongest parameter to predict abnormalities of cardiac structure, however, other anthropometric features, such as WC and BSI, may help further assist in predicting those individuals at higher risk of developing such features, and, therefore, should be routinely calculated in patients presenting to the cardiovascular team for assessment. Further studies need to be performed to assess whether such changes affect cardiovascular outcomes including heart failure, arrhythmias and mortality.
Key messages
- Obesity, in the absence of any other cardiovascular conditions, may result in significant changes in cardiac structure and function as assessed on transthoracic echocardiography
- Chamber dimensions, as well as systolic and diastolic parameters, may be significantly altered
- While there was no significant correlation of obesity with left ventricular ejection fraction (LVEF), association with other parameters of left ventricular systolic function, such as left ventricular global longitudinal strain (LVGLS), was noted, with the latter now considered an important prognostication parameter for heart failure
- Body surface area (BSA) is an important anthropometric factor for predicting abnormalities of cardiac structure, but other parameters such as body mass index (BMI) and body shape index (BSI) should also be considered in routine practice for more accurate patient assessment and can help identify at-risk individuals
Conflicts of interest
None declared.
Funding
None.
Study approval
All participants signed an informed consent form before commencing the study. Ethical approval for the study was granted by the local ethics committee (code: IR.IAU.MSHD.REC.1397.067).
Editors’ note
Table 3 is available online.
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