J Obes Metab Syndr 2025; 34(1): 54-64
Published online January 30, 2025 https://doi.org/10.7570/jomes24027
Copyright © Korean Society for the Study of Obesity.
Jin Kyung Oh1, Yuri Seo2, Wonmook Hwang1, Sami Lee2, Yong-Hoon Yoon1, Kyupil Kim2, Hyun Woong Park1, Jae-Hyung Roh1, Jae-Hwan Lee1, Minsu Kim1,*
1Division of Cardiology, Department of Internal Medicine, Chungnam National University Sejong Hospital, Chungnam National University College of Medicine, Sejong; 2Department of Family Medicine, Chungnam National University Sejong Hospital, Sejong, Korea
Correspondence to:
Minsu Kim
https://orcid.org/0000-0001-9230-3137
Division of Cardiology, Department of Internal Medicine, Chungnam National University Sejong Hospital, Chungnam National University College of Medicine, 20 Bodeum 7-ro, Sejong 30099, Korea
Tel: +82-44-995-5691
Fax: +82-44-995-5698
E-mail: mskimep80@gmail.com
The first two authors contributed equally to this study.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background: Although the presence of both obesity and reduced muscle mass presents a dual metabolic burden and additively has a negative effect on a variety of cardiometabolic parameters, data regarding the associations between their combined effects and left ventricular diastolic function are limited. This study investigated the association between the ratio of skeletal muscle mass to visceral fat area (SVR) and left ventricular diastolic dysfunction (LVDD) in patients with preserved ejection fraction using random forest machine learning.
Methods: In total, 1,070 participants with preserved left ventricular ejection fraction who underwent comprehensive health examinations, including transthoracic echocardiography and bioimpedance body composition analysis, were enrolled. SVR was calculated as an index of sarcopenic obesity by dividing the appendicular skeletal muscle mass by the visceral fat area.
Results: In the random forest model, age and SVR were the most powerful predictors of LVDD. Multivariate logistic regression analysis demonstrated that older age (adjusted odds ratio [OR], 1.11; 95% confidence interval [CI], 1.07 to 1.15) and lower SVR (adjusted OR, 0.08; 95% CI, 0.01 to 0.57) were independent risk factors for LVDD. SVR showed a significant improvement in predictive performance and fair predictability for LVDD, with the highest area under the curve noted in both men and women, with statistical significance. In non-obese and metabolically healthy individuals, the lowest SVR tertile was associated with a greater risk of LVDD compared to the highest SVR tertile.
Conclusion: Decreased muscle mass and increased visceral fat were significantly associated with LVDD compared to obesity, body fat composition, and body muscle composition indices.
Keywords: Intra-abdominal fat, Muscle, Skeletal, Body composition, Ventricular dysfunction, Left, Random forest
The prevalence of overweightness and obesity has increased in modern communities, posing a significant health burden due to the heightened risk of cardiovascular disease.1,2 Obesity induces several changes in cardiac structure and function, including increased left ventricular (LV) mass and impaired LV systolic and diastolic function.3-5 Left ventricular diastolic dysfunction (LVDD) is characterized by impaired relaxation and deteriorated filling properties of the left ventricle and is commonly detected in otherwise healthy and asymptomatic patients.6-9 Its influence on diastolic function and hemodynamics seems to be multifactorial, stemming from elevated inflammation and oxidative stress associated with obesity10 as well as from related conditions like diabetes mellitus (DM), dyslipidemia, and hypertension (HTN).11
Body mass index (BMI) is a common metric for assessing obesity; however, its efficacy is limited as it fails to distinguish between fat mass and lean body mass and overlooks variations in body fat distribution.12 Sarcopenic obesity is the coexistence of sarcopenia and visceral obesity. As loss of skeletal muscle mass and increase in body fat are associated with increased morbidity and mortality, both obesity and reduced muscle mass may present a dual metabolic burden and collectively affect various cardiometabolic parameters.13-16 However, the association between these combined effects and LV diastolic function remains unclear. Therefore, this study aimed to evaluate the ratio of skeletal muscle mass to visceral fat area (SVR) as an index of skeletal muscle mass corrected by visceral fat area (VFA) and comprehensively assess LVDD in patients with preserved ejection fraction using random forest machine learning.
We screened 1,554 participants aged >18 years who underwent comprehensive health examinations, including transthoracic echocardiography and bioimpedance body composition analysis, at the Chungnam National University Sejong Hospital’s Healthcare Center, Republic of Korea, from July 1, 2020 to December 31, 2023. We excluded 281 patients with left ventricular ejection fraction (LVEF) of <50% and 152 patients with atrial fibrillation at baseline. Additionally, patients with significant valve disease, previous valve surgery, congenital heart disease, hypertrophic or restrictive cardiomyopathy, or renal insufficiency were excluded. A total of 1,070 participants (521 men and 549 women) were finally included in this study (Supplementary Fig. 1). The study protocol was approved by the Institutional Review Board and Ethics Committee of Chungnam National University Sejong Hospital (no. 2021-03-003), which waived the need for informed consent for this retrospective study. The study was conducted in accordance with the principles of the Declaration of Helsinki.
Transthoracic echocardiography was performed using commercially available echocardio-graphic systems (Epiq CVx [Philips Healthcare] or Vivid E95 [GE Healthcare]). Subsequently, the stored images were reviewed and analyzed by a single experienced echocardiographic specialist, JKO, to evaluate diastolic function. LV and left atrium (LA) chamber quantification was performed according to the recommendations of the American Society of Echocardiography,17 and a modified biplanar method was used to calculate the LVEF. LV and LA volumes were assessed from apical four- and two-chamber views using Simpson’s biplane method and indexed by body surface area. LV diastolic function was analyzed using the mitral inflow pattern. From an apical four-chamber view, the transmitral flow was sampled using pulsed-wave Doppler at the level of the mitral valve leaflet tips. The early mitral inflow peak velocity (E) and late mitral inflow peak velocity (A) were measured, and their ratio (E/A) was calculated.18 Doppler tissue interrogation of the early diastolic mitral annular relaxation velocity (E′) and late diastolic velocity (A′) were recorded at the septal annulus, and the E/E′ ratio was calculated as an index of LV filling pressures. LVDD with normal LVEF was defined by an LVEF of >50% and present if three or four variables met the following cutoff values: (1) average E/E′ ratio >14; (2) septal E’ velocity <7 cm/sec or lateral E′ velocity <10 cm/sec; (3) tricuspid regurgitation velocity >2.8 m/sec; and (4) LA volume index >34 mL/m2.18
All participants’ body compositions were analyzed using dual bioelectrical impedance measurements (Inbody 970; Biospace) on the same day as echocardiography. According to the instructions provided by the manufacturer, the participants stood upright and comfortably on the analyzer’s footplate barefoot, with their legs and arms apart. The lean body mass of the arms and legs, appendicular skeletal muscle mass (ASM), fat-free mass, total body fat percentage, and VFA were measured.19 The ASM was estimated as the sum of the muscle mass estimated individually for each arm and leg.20 Absolute ASM was converted to skeletal muscle mass index (SMI) by dividing the value by the square of the height in meters (kg/m2),21 and SVR (kg/cm2) was calculated as an index of sarcopenic obesity by dividing the ASM (kg) by VFA (cm2).
Random forest, a classic machine learning algorithm,22 was applied to identify associations between body composition assessment data and LVDD (as defined above). For the initial random forest model development, we included 20 variables (nine demographic/comorbidities, three laboratory data, and eight body composition assessment data) (Supplementary Table 1). From the random forest model including 20 variables, the important predictors of LVDD were identified using the R package ‘Boruta,’23 which is a feature-selection method paired with random forest and selects features that have discriminating importance scores (Z-scores) greater than randomly permuted features (shadow matrixes). The proportion of missing values was minimal, and these were imputed using the ‘miss Forest’ algorithm before model development.
Continuous variables are presented as mean±standard deviation or median (interquartile range) values, whereas categorical variables are presented as numbers and percentages. Group comparisons were evaluated using the chi-squared or Fisher’s exact test for categorical variables and Student’s t-test or the Mann–Whitney U-test for continuous variables, as appropriate. Univariate logistic regression analyses were performed to evaluate the predictive values of each variable, and significant variables entered a multiple logistic regression model. Multivariable models included significant univariate variables and known clinical risk factors like age, sex, systolic blood pressure (SBP), HTN, DM, dyslipidemia, hemoglobin, estimated glomerular filtration rate (eGFR), fasting plasma glucose, total cholesterol, BMI, waist-hip ratio, SVR, and SMI. Odds ratios (ORs) and 95% confidence intervals (CIs) were reported. To evaluate the prognostic utility of SVR in predicting LVDD, the receiver operating characteristic (ROC) curve was plotted, and the area under the ROC curve (AUC) was calculated. The incremental value of SVR was assessed in a series of logistic models, in which the first model consisted of fitting the clinical data entered as a block (age, sex, HTN, DM, dyslipidemia, SBP, hemoglobin, glucose, and eGFR) in the test group. The χ2 values were compared across models. We also calculated the integrated discrimination improvement and continuous net reclassification improvement for the prediction of LVDD, following the methodology of Pencina et al.24,25 All reported P-values were two-sided, and statistical significance was set at P<0.05. All analyses were performed using SPSS version 21.0 (IBM Corporation) and R version 3.6.0 (R Foundation for Statistical Computing).
The baseline demographic and clinical characteristics of the patients according to the presence of LVDD are shown in Table 1. The patients were divided into a normal LV diastolic function group (n=997) and an LVDD group (n=73). When comparing the two groups, patients with LVDD were older and included greater proportions of women and individuals with HTN, DM, dyslipidemia, or a history of cerebrovascular disease. Among the laboratory findings, hemoglobin, eGFR, total cholesterol, and low-density lipoprotein cholesterol levels were lower, while fasting glucose was higher, in the group with LVDD. Following echocardiography, it was revealed that the LVDD group had a greater LA volume index and LV mass index and higher early and late mitral inflow peak velocities (E and A), early diastolic mitral annular relaxation velocity (E′), E/E′ ratio, and tricuspid regurgitation peak velocity, respectively, than the normal LV diastolic function group. LV dimensions and LVEF were not significantly different between the two groups.
Table 1 presents the comparison of body composition assessment using bioelectrical impedance measurements of the patients according to the presence of LVDD. In the LVDD group, the mean values of BMI, percentage body fat, VFA, and SVR were 25.6 kg/m², 33.4%, 165.3 cm2, and 0.19 kg/cm2, respectively. The mean waist circumference and waist-hip ratio were 71.8 cm and 1.02, respectively. Significant differences were observed in body fat and muscle composition between the two groups. The body surface area, waist circumference, waist-hip ratio, and VFA were greater and the body fat percentage and SVR were higher in the LVDD group than in the normal diastolic function group. However, SMI and appendicular muscle mass were significantly lower in the LVDD group. BMI and fat-free mass index were not statistically different between the two groups.
Fig. 1 displays the important variables contributing to the risk of LVDD, as identified by random forest, with the 20 variables ranked by relative importance. In the random forest model, age was the most important predictor of LVDD. SBP, HTN, diastolic blood pressure, history of cardiovascular disease, and eGFR emerged as important clinical risk factors. However, other comorbidities, such as DM, dyslipidemia, and a history of coronary artery disease, had relatively low importance, indicating little predictive value. Regarding the body composition assessment data, SVR was the second most powerful predictor among all variables. VFA, body fat percentage, waist-hip ratio, waist circumference, and SMI were also predictors with greater importance. However, BMI, a more commonly recognized obesity index, offered comparatively little predictive importance.
Table 2 shows the results of the logistic regression analysis performed to reveal the relationship between the variables and LVDD prediction. On univariate logistic regression analysis, body fat percentage, waist circumference, waist-hip ratio, VFA, SVR, and SMI showed significant associations with LVDD. In multivariate analyses, age (adjusted OR, 1.11; 95% CI, 1.07 to 1.15; P<0.001) and SVR (adjusted OR, 0.08; 95% CI, 0.01 to 0.57; P=0.027) showed a significant association with LVDD among the parameters significant in the univariate analysis. The results indicated that older age and lower SVR are independent risk factors for LVDD after adjusting for age, sex, SBP, HTN, DM, dyslipidemia, smoking, alcohol consumption, hemoglobin level, eGFR, fasting plasma glucose level, cholesterol level, BMI, waist-hip ratio, SVR, and SMI (Supplementary Table 2). To reduce multicollinearity between the data, body fat percentage, VFA, and arm muscle circumference were not simultaneously entered into the multivariate logistic regression model.
The prognostic performances of SVR, waist-hip ratio, BMI, and SMI are shown in Fig. 2. Model 1, including clinical variables (age, sex, HTN, DM, dyslipidemia, SBP, hemoglobin, fasting plasma glucose, cholesterol, and eGFR), yielded an overall χ2 value of 100.6. Model 2 adjustments included the factors in model 1 and SMI, whereas model 3 considered the adjusted factors in model 1 and BMI. In model 4, which incorporated the waist-hip ratio into model 1, the χ2 value increased from 100.6 to 109.4 (P=0.003). When SVR was added to model 1, the value increased from 100.6 to 117.6 in model 5 (P<0.001) (Fig. 2). The waist-hip ratio and SVR provided incremental prognostic values; however, the addition of SVR increased the prediction performance more than the combination of clinical data and SMI, BMI, and waist-hip ratio. Adding SVR showed a significant improvement in predictive performance (C-statistic=0.853 [95% CI, 0.814 to 0.892; P=0.014]; net classification index=0.411 [95% CI, 0.188 to 0.634; P<0.001]; and integrated discrimination improvement=0.016 [95% CI, 0.005 to 0.028; P=0.006]).
ROC analysis revealed the strength of the univariate relationship between different indices of body composition assessment (SVR, waist-hip ratio, BMI, and SMI) and LVDD in men and women (Fig. 3). The AUC for waist-hip ratio, BMI, and SMI were 0.57 (95% CI, 0.47 to 0.67) in men and 0.67 (95% CI, 0.59 to 0.75) in women, 0.52 (95% CI, 0.39 to 0.64) in men and 0.64 (95% CI, 0.55 to 0.72) in women, and 0.64 (95% CI, 0.55 to 0.72) in men and 0.52 (95% CI, 0.44 to 0.61) in women, respectively. SVR showed fair predictability for LVDD, with the highest AUC noted for men (AUC=0.69; 95% CI, 0.61 to 0.77) and women (AUC=0.71; 95% CI, 0.64 to 0.78) with statistical significance. The whole patient population was divided into sex-specific SVR tertiles (Q), as follows: Q1, <0.29 kg/cm2; Q2, 0.29–0.41 kg/cm2; Q3, >0.41 kg/cm2 in men and Q1, <0.17 kg/cm2; Q2, 0.17–0.26 kg/cm2; and Q3, >0.26 kg/cm2 in women. According to study findings, the prevalence of LVDD decreased with increasing SVR. In subgroup analysis, women had a greater prevalence of LVDD than men. Among men, the prevalence rates of LVDD in the Q1, Q2, and Q3 tertiles were 7.8%, 2.0%, and 0%, respectively. Among women, the prevalence rates of LVDD in the Q1, Q2, and Q3 levels were 18.7%, 6.35%, and 3.8%, respectively (P<0.05). In non-obese (adjusted OR, 3.5) and metabolically healthy patients (OR, 17.8), the lowest SVR tertile had a higher OR compared to the highest SVR tertile (Fig. 4). All individuals were considered metabolically healthy,26 as characterized by the absence of DM, HTN, or dyslipidemia diagnoses.
In this study, we explored the association between SVR and LVDD in a Korean population with preserved LVEF. SVR emerged as an independent factor associated with impaired LV diastolic function, with a lower SVR significantly elevating the risk of LVDD, even after adjusting for clinical risk factors and other body composition indices. Notably, SVR exhibited a greater predictive capacity for LVDD compared to BMI, VFA, and SMI. Moreover, lower SVR was significantly associated with LVDD in non-obese and metabolically healthy individuals.
As aging is related to a gradual loss of skeletal muscle mass and an increased incidence of obesity, several studies have shown that a reduction in muscle mass and an increase in fat mass contribute independently to mobility impairment in the elderly.5,13,14 Additionally, as individuals age, intra-abdominal fat tends to increase progressively due to the redistribution of body fat, even among healthy individuals who maintain a relatively stable BMI.27,28 Although BMI is the most widely used index for defining obesity, it does not provide information on the distribution of fat, such as visceral (around organs) versus subcutaneous (under the skin) fat, which contributes more significantly to an increased risk of cardiovascular disease.29 BMI tends to reflect overall body weight, which includes both lean body mass (muscles, bones, and organs) and fat mass. This is because the formula for BMI does not differentiate between these two components. Individuals with similar BMIs may have different body compositions, leading to variations in muscle mass and fat mass. Thus, to obtain a more comprehensive assessment of an individual’s body composition related to excess body fat, additional measures such as waist circumference, body fat percentage, and imaging techniques are needed.
Obesity can have diverse impacts on the structure and function of the LV. Obesity is associated with an overall increase in body mass, leading to an increase in LV mass.30 Interestingly, recent studies have investigated the association between adipose tissue distribution and cardiac function and have consistently demonstrated a robust association between visceral adiposity and LVDD. The visceral fat is metabolically active and releases inflammatory mediators. These bioactive substances can directly affect the myocardium, leading to alterations in LV diastolic function. Additionally, metabolic, hormonal, and hemodynamic factors are involved in these mechanisms and participate in complex interplay.31,32
Some studies have suggested that an appropriate ratio of healthy body fat to muscle mass may positively impact LV mass and diastolic function. Optimal lean body mass can reduce the load on the heart and enhance diastolic function. Additionally, it can improve insulin sensitivity and contribute to inflammatory suppression, thereby reducing the likelihood of cardiovascular and vascular diseases.33-35 Thus, a combined consideration of skeletal muscle mass and visceral fat provides a more comprehensive understanding of cardiac function. VFA calculation by computed tomography (CT) imaging is considered the gold-standard measure for assessing visceral adiposity owing to its accurate and direct quantification of visceral fat. However, its use is limited by factors, such as exposure to ionizing radiation, cost considerations, and requirements for specialized equipment.36,37 Thus, this study explored the association between SVR and LVDD in a large Korean population, using bioelectrical impedance measurements to assess skeletal muscle mass and VFA. The findings corroborate previous research, highlighting SVR as a more robust independent predictor of LVDD compared to BMI, SMI, or VFA, even among individuals who are metabolically healthy and not obese. As an index of sarcopenic obesity, SVR may be associated with LVDD through several mechanisms, including metabolic influences, inflammatory modulation, hormonal regulation, insulin sensitivity, and potential hemodynamic effects. The skeletal muscle is a metabolically active tissue that plays a crucial role in glucose metabolism and insulin sensitivity. Increased skeletal muscle mass may improve glucose metabolism and insulin sensitivity; however, visceral fat accumulation is associated with insulin resistance. Skeletal muscles secrete myokines, which are known to have anti-inflammatory effects. Conversely, visceral fat is associated with the release of pro-inflammatory adipokines. The balance achieved through SVR, with higher skeletal muscle and lower visceral fat, may contribute to an anti-inflammatory environment that potentially mitigates inflammation-related cardiac dysfunction.
The strengths of our study include its large sample size and accurate assessment of LV diastolic function according to the current guidelines. However, this study had several limitations. First, our study was a single-center retrospective analysis, and the limited data may have affected the statistical validity of BMI, VFA, SMI, and SVR. Second, a dual bioelectrical impedance analyzer was used to measure the VFA. Abdominal CT imaging is the gold standard for visceral adiposity assessment; however, a previous study revealed an obvious correlation between VFA measurements obtained through CT imaging and a dual bioelectrical impedance analyzer.38 Finally, given potential ethnic disparities in body composition, uncertainty remains about whether our findings in the Korean population can be extrapolated to other ethnic groups. Therefore, multicenter prospective studies are needed to obtain more significant results on this issue.
In conclusion, our study demonstrated that decreased muscle mass and increased visceral fat are significantly associated with LVDD in patients with preserved LVEF. Lower SVR level is an independent predictor of LVDD compared to other obesity, body fat composition, and body muscle composition indices. The combined consideration of skeletal muscle mass and visceral fat provided a more effective means of predicting LVDD, even in non-obese and metabolically healthy individuals.
Supplementary materials can be found online at https://doi.org/10.7570/jomes24027.
The authors declare no conflict of interest.
This work was supported by the research fund of Chungnam National University Hospital.
Study concept and design: JKO, YS, and MK; acquisition of data: WH, SL, YHY, and KK; analysis and interpretation of data: JKO and YS; drafting of the manuscript: JKO; critical revision of the manuscript: HWP, JHR, and JHL; obtained funding: JKO; and study supervision: MK.
Baseline characteristics of the study population according to the presence of left ventricular diastolic dysfunction
Characteristic | LVDD | P | |
---|---|---|---|
No (n=997) | Yes (n=73) | ||
Demographics | |||
Age (yr) | 54.9 ± 12.5 | 67.8 ± 8.8 | < 0.001 |
Male sex | 499 (50.1) | 22 (30.1) | 0.001 |
Hemodynamics | |||
SBP (mmHg) | 128.2 ± 16.1 | 134.8 ± 15.8 | 0.001 |
DBP (mmHg) | 77.2 ± 11.8 | 74.4 ± 10.4 | 0.036 |
Heart rate (bpm) | 77.2 ± 12.6 | 74.5 ± 13.6 | 0.109 |
History of disease data | |||
Hypertension | 347 (34.8) | 45 (61.6) | < 0.001 |
Diabetes mellitus | 132 (13.2) | 22 (30.1) | < 0.001 |
Dyslipidemia | 322 (32.3) | 35 (47.9) | 0.010 |
History of coronary heart disease | 66 (6.6) | 8 (11.0) | 0.154 |
History of cerebrovascular disease | 23 (2.3) | 5 (6.8) | 0.037 |
Smoking | 0.916 | ||
Never | 722 (74.0) | 53 (72.6) | |
Past | 174 (17.8) | 13 (17.8) | |
Current | 80 (8.2) | 7 (9.6) | |
Alcohol consumption | 0.621 | ||
None | 444 (46.1) | 36 (52.2) | |
Moderate | 440 (45.7) | 28 (40.6) | |
Heavy | 79 (8.2) | 5 (7.2) | |
Biochemical markers | |||
Hemoglobin (mmol/L) | 14.2 ± 1.4 | 13.4 ± 1.5 | < 0.001 |
Serum creatinine (µmol/L) | 0.8 ± 0.3 | 0.9 ± 1.3 | 0.324 |
eGFR (mL/min) | 94.2 ± 19.2 | 89.1 ± 23.5 | 0.032 |
Fasting plasma glucose (mmol/L) | 104.2 ± 31.3 | 115.2 ± 36.4 | 0.005 |
Total cholesterol (mmol/L) | 190.7 ± 44.6 | 169.8 ± 44.7 | < 0.001 |
HDL cholesterol (mmol/L) | 53.4 ± 12.6 | 50.3 ± 11.4 | 0.057 |
LDL cholesterol (mmol/L) | 116.5 ± 40.6 | 96.1 ± 39.0 | < 0.001 |
Triglycerides (mmol/L) | 145.3 ± 109.7 | 142.3 ± 111.3 | 0.825 |
Echocardiographic data | |||
LV end-systolic diameter (mm) | 38.3 ± 10.2 | 39.1 ± 10.4 | 0.539 |
LV end-diastolic diameter (mm) | 37.8 ± 13.5 | 37.3 ± 9.8 | 0.737 |
LA volume index (mL/m2) | 24.2 ± 4.8 | 32.3 ± 9.0 | < 0.001 |
LV mass index (g/m2) | 72.1 ± 15.2 | 84.0 ± 16.5 | < 0.001 |
LV ejection fraction (%) | 60.9 ± 2.4 | 60.5 ± 2.4 | 0.171 |
Mitral E velocity (cm/sec) | 60.3 ± 16.4 | 66.2 ± 16.6 | 0.003 |
Mitral A velocity (cm/sec) | 65.4 ± 16.8 | 66.2 ± 16.6 | < 0.001 |
E/A ratio | 1.0 ± 0.4 | 0.9 ± 0.7 | 0.013 |
Mitral E/e’ ratio | 7.7 ± 2.0 | 13.6 ± 3.3 | < 0.001 |
Septal E’ (cm/sec) | 8.1 ± 2.3 | 5.3 ± 1.3 | < 0.001 |
TR peak velocity (m/sec) | 2.3 ± 0.2 | 2.6 ± 0.3 | < 0.001 |
Body composition assessment | |||
Body height (m) | 164.0 ± 8.9 | 157.6 ± 9.5 | < 0.001 |
Body weight (kg) | 67.1 ± 13.1 | 63.7 ± 11.4 | 0.016 |
Body mass index (kg/m2) | 24.8 ± 3.5 | 25.6 ± 3.6 | 0.091 |
Body surface area (m2) | 1.7 ± 0.3 | 1.7 ± 0.2 | 0.002 |
Body fat composition | |||
Body fat mass (kg) | 20.3 ± 3.4 | 21.2 ± 5.8 | 0.194 |
Percentage body fat (%) | 30.2 ± 6.9 | 33.4 ± 6.8 | < 0.001 |
Fat-free mass (kg) | 46.8 ± 10.1 | 42.4 ± 6.9 | < 0.001 |
Fat-free mass index | 17.2 ± 2.3 | 16.9 ± 2.1 | 0.171 |
Waist circumference (cm) | 60.0 ± 42.9 | 71.8 ± 37.7 | 0.022 |
Waist-hip ratio | 0.91 ± 0.20 | 1.02 ± 0.22 | < 0.001 |
Visceral fat area (cm2) | 114.7 ± 94.8 | 165.3 ± 106.4 | < 0.001 |
SVR (kg/cm2) | 0.4 ± 0.5 | 0.2 ± 0.1 | < 0.001 |
Body muscle composition | |||
Skeletal muscle mass (kg) | 25.8 ± 6.1 | 22.9 ± 5.3 | < 0.001 |
Skeletal muscle mass index | 7.1 ± 1.1 | 6.7 ± 1.0 | 0.003 |
Segmental lean analysis (kg) | |||
Right arm muscle mass | 2.5 ± 0.7 | 2.3 ± 0.6 | 0.001 |
Left arm muscle mass | 2.5 ± 0.7 | 2.2 ± 0.6 | 0.003 |
Trunk muscle mass | 21.3 ± 4.5 | 19.4 ± 3.9 | < 0.001 |
Right leg muscle mass | 7.2 ± 1.7 | 6.2 ± 1.6 | < 0.001 |
Left leg muscle mass | 7.1 ± 1.7 | 6.2 ± 1.6 | < 0.001 |
Arm muscle circumference (cm) | 26.9 ± 2.8 | 26.3 ± 2.5 | 0.059 |
Values are presented as mean±standard deviation or number (%).
LVDD, left ventricular diastolic dysfunction; SBP, systolic blood pressure; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LV, left ventricle; LA, left atrium; TR, tricuspid regurgitation; SVR, ratio of skeletal muscle mass to visceral fat area.
Univariate and multivariable logistic regression analyses for left ventricular diastolic dysfunction
Variable | Univariate analysis | Multivariable analysis | ||
---|---|---|---|---|
OR (95% CI) | P | Adjusted OR (95% CI) | P | |
Age (yr) | 1.13 (1.09–1.16) | < 0.001 | 1.11 (1.07–1.15) | < 0.001 |
Male sex | 0.43 (0.26–0.72) | 0.001 | 0.35 (0.11–1.40) | 0.081 |
SBP (mmHg) | 1.03 (1.01–1.04) | 0.001 | 1.01 (0.99–1.02) | 0.523 |
Hypertension | 3.01 (1.85–4.91) | < 0.001 | 1.34 (0.72–2.50) | 0.351 |
Diabetes mellitus | 2.83 (1.66–4.81) | < 0.001 | 1.26 (0.60–2.66) | 0.539 |
Dyslipidemia | 1.93 (1.20–3.11) | 0.007 | 0.98 (0.55–1.76) | 0.946 |
Smoking | 1.19 (0.52–2.71) | 0.675 | 2.25 (0.77–6.62) | 0.140 |
Alcohol consumption | 0.78 (0.30–2.05) | 0.615 | 2.69 (0.80–9.08) | 0.111 |
Hemoglobin (mmol/L) | 0.70 (0.59–0.82) | < 0.001 | 0.81 (0.64–1.03) | 0.090 |
eGFR (mL/min) | 0.99 (0.97–0.99) | 0.031 | 1.00 (0.99–1.02) | 0.754 |
Fasting plasma glucose (mmol/L) | 1.01 (1.00–1.01) | 0.007 | 1.00 (0.99–1.01) | 0.469 |
Total cholesterol (mmol/L) | 0.99 (0.98–0.99) | < 0.001 | 0.99 (0.99–1.00) | 0.115 |
Body mass index (kg/m2) | 1.06 (0.99–1.13) | 0.084 | 0.97 (0.84–1.12) | 0.659 |
Waist-hip ratio | 8.20 (3.02–22.28) | < 0.001 | 0.72 (0.09–5.85) | 0.757 |
SVR (kg/cm2) | 0.01 (0.01–0.04) | < 0.001 | 0.08 (0.01–0.57) | 0.027 |
Skeletal muscle mass index | 0.72 (0.57–0.90) | 0.004 | 1.36 (0.70–2.63) | 0.364 |
Percentage body fat, visceral fat area, and arm muscle circumference were not included in the multivariable model due to multicollinearity with body mass index and skeletal muscle mass index.
OR, odds ratio; CI, confidence interval; SBP, systolic blood pressure; eGFR, estimated glomerular filtration rate; SVR, ratio of skeletal muscle mass to visceral fat area.
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