Effects of sarcopenia, body mass indices, and sarcopenic obesity on diastolic function and exercise capacity in Koreans

Obesity induces left ventricular diastolic dysfunction and ultimately causes heart failure. Sarcopenic obesity is common in heart failure with preserved ejection fraction (HFpEF). However, the precise mechanism by which sarcopenic obesity is related to HFpEF is poorly understood. We aimed to evaluat...

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Published inMetabolism, clinical and experimental Vol. 97; pp. 18 - 24
Main Authors Jung, Mi-Hyang, Ihm, Sang-Hyun, Park, Sang Min, Jung, Hae Ok, Hong, Kyung-Soon, Baek, Sang Hong, Youn, Ho-Joong
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.08.2019
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Abstract Obesity induces left ventricular diastolic dysfunction and ultimately causes heart failure. Sarcopenic obesity is common in heart failure with preserved ejection fraction (HFpEF). However, the precise mechanism by which sarcopenic obesity is related to HFpEF is poorly understood. We aimed to evaluate the combined effect of sarcopenia (SP) and obesity on left ventricular diastolic function and exercise capacity. This study included 733 healthy subjects who underwent health check-ups in a tertiary hospital in Korea. All participants were categorized into four groups: non-SP/non-obese, SP/non-obese, non-SP/obese, and SP/obese. Comprehensive echocardiography with cardiopulmonary exercise testing was performed. Diastolic dysfunction was defined as an E/e' ratio ≥ 10. Across SP and obesity groups, a gradual decrease in e' velocity and an increase in the E/e' ratio was noted after adjustment for age and sex. Furthermore, a gradual decrease in percent-predicted peak VO2 was observed across the groups. In the multivariate logistic regression analysis, the SP/obese group had the highest risk for diastolic dysfunction (OR 4.27, 95% CI 2.41–7.57), followed by the non-SP/obese group (OR 2.88, 95% CI 1.57–5.29) and the SP/non-obese group (OR 1.90, 95% CI 1.01–3.56) compared with the reference (non-SP/non-obese) group even after controlling for various confounders. Sarcopenic obesity was associated with impaired diastolic function and decreased exercise capacity, suggesting a possible mechanism by which sarcopenic obesity contributes to the development of HFpEF. •Sarcopenic obesity was associated with impaired diastolic function and exercise intolerance.•The present study highlighted the importance of measuring body composition in the reclassification of obese populations.•Our data implied the possibility of both obesity and sarcopenia as targets for the prevention of HFpEF.
AbstractList Obesity induces left ventricular diastolic dysfunction and ultimately causes heart failure. Sarcopenic obesity is common in heart failure with preserved ejection fraction (HFpEF). However, the precise mechanism by which sarcopenic obesity is related to HFpEF is poorly understood. We aimed to evaluate the combined effect of sarcopenia (SP) and obesity on left ventricular diastolic function and exercise capacity.AIMSObesity induces left ventricular diastolic dysfunction and ultimately causes heart failure. Sarcopenic obesity is common in heart failure with preserved ejection fraction (HFpEF). However, the precise mechanism by which sarcopenic obesity is related to HFpEF is poorly understood. We aimed to evaluate the combined effect of sarcopenia (SP) and obesity on left ventricular diastolic function and exercise capacity.This study included 733 healthy subjects who underwent health check-ups in a tertiary hospital in Korea. All participants were categorized into four groups: non-SP/non-obese, SP/non-obese, non-SP/obese, and SP/obese. Comprehensive echocardiography with cardiopulmonary exercise testing was performed. Diastolic dysfunction was defined as an E/e' ratio ≥ 10.METHODSThis study included 733 healthy subjects who underwent health check-ups in a tertiary hospital in Korea. All participants were categorized into four groups: non-SP/non-obese, SP/non-obese, non-SP/obese, and SP/obese. Comprehensive echocardiography with cardiopulmonary exercise testing was performed. Diastolic dysfunction was defined as an E/e' ratio ≥ 10.Across SP and obesity groups, a gradual decrease in e' velocity and an increase in the E/e' ratio was noted after adjustment for age and sex. Furthermore, a gradual decrease in percent-predicted peak VO2 was observed across the groups. In the multivariate logistic regression analysis, the SP/obese group had the highest risk for diastolic dysfunction (OR 4.27, 95% CI 2.41-7.57), followed by the non-SP/obese group (OR 2.88, 95% CI 1.57-5.29) and the SP/non-obese group (OR 1.90, 95% CI 1.01-3.56) compared with the reference (non-SP/non-obese) group even after controlling for various confounders.RESULTSAcross SP and obesity groups, a gradual decrease in e' velocity and an increase in the E/e' ratio was noted after adjustment for age and sex. Furthermore, a gradual decrease in percent-predicted peak VO2 was observed across the groups. In the multivariate logistic regression analysis, the SP/obese group had the highest risk for diastolic dysfunction (OR 4.27, 95% CI 2.41-7.57), followed by the non-SP/obese group (OR 2.88, 95% CI 1.57-5.29) and the SP/non-obese group (OR 1.90, 95% CI 1.01-3.56) compared with the reference (non-SP/non-obese) group even after controlling for various confounders.Sarcopenic obesity was associated with impaired diastolic function and decreased exercise capacity, suggesting a possible mechanism by which sarcopenic obesity contributes to the development of HFpEF.CONCLUSIONSarcopenic obesity was associated with impaired diastolic function and decreased exercise capacity, suggesting a possible mechanism by which sarcopenic obesity contributes to the development of HFpEF.
Obesity induces left ventricular diastolic dysfunction and ultimately causes heart failure. Sarcopenic obesity is common in heart failure with preserved ejection fraction (HFpEF). However, the precise mechanism by which sarcopenic obesity is related to HFpEF is poorly understood. We aimed to evaluate the combined effect of sarcopenia (SP) and obesity on left ventricular diastolic function and exercise capacity. This study included 733 healthy subjects who underwent health check-ups in a tertiary hospital in Korea. All participants were categorized into four groups: non-SP/non-obese, SP/non-obese, non-SP/obese, and SP/obese. Comprehensive echocardiography with cardiopulmonary exercise testing was performed. Diastolic dysfunction was defined as an E/e' ratio ≥ 10. Across SP and obesity groups, a gradual decrease in e' velocity and an increase in the E/e' ratio was noted after adjustment for age and sex. Furthermore, a gradual decrease in percent-predicted peak VO2 was observed across the groups. In the multivariate logistic regression analysis, the SP/obese group had the highest risk for diastolic dysfunction (OR 4.27, 95% CI 2.41–7.57), followed by the non-SP/obese group (OR 2.88, 95% CI 1.57–5.29) and the SP/non-obese group (OR 1.90, 95% CI 1.01–3.56) compared with the reference (non-SP/non-obese) group even after controlling for various confounders. Sarcopenic obesity was associated with impaired diastolic function and decreased exercise capacity, suggesting a possible mechanism by which sarcopenic obesity contributes to the development of HFpEF. •Sarcopenic obesity was associated with impaired diastolic function and exercise intolerance.•The present study highlighted the importance of measuring body composition in the reclassification of obese populations.•Our data implied the possibility of both obesity and sarcopenia as targets for the prevention of HFpEF.
Obesity induces left ventricular diastolic dysfunction and ultimately causes heart failure. Sarcopenic obesity is common in heart failure with preserved ejection fraction (HFpEF). However, the precise mechanism by which sarcopenic obesity is related to HFpEF is poorly understood. We aimed to evaluate the combined effect of sarcopenia (SP) and obesity on left ventricular diastolic function and exercise capacity. This study included 733 healthy subjects who underwent health check-ups in a tertiary hospital in Korea. All participants were categorized into four groups: non-SP/non-obese, SP/non-obese, non-SP/obese, and SP/obese. Comprehensive echocardiography with cardiopulmonary exercise testing was performed. Diastolic dysfunction was defined as an E/e' ratio ≥ 10. Across SP and obesity groups, a gradual decrease in e' velocity and an increase in the E/e' ratio was noted after adjustment for age and sex. Furthermore, a gradual decrease in percent-predicted peak VO was observed across the groups. In the multivariate logistic regression analysis, the SP/obese group had the highest risk for diastolic dysfunction (OR 4.27, 95% CI 2.41-7.57), followed by the non-SP/obese group (OR 2.88, 95% CI 1.57-5.29) and the SP/non-obese group (OR 1.90, 95% CI 1.01-3.56) compared with the reference (non-SP/non-obese) group even after controlling for various confounders. Sarcopenic obesity was associated with impaired diastolic function and decreased exercise capacity, suggesting a possible mechanism by which sarcopenic obesity contributes to the development of HFpEF.
Author Baek, Sang Hong
Park, Sang Min
Jung, Mi-Hyang
Ihm, Sang-Hyun
Youn, Ho-Joong
Hong, Kyung-Soon
Jung, Hae Ok
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Keywords Heart failure
Obesity
OR
Diastole
CI
LV
HFpEF
BP
ANCOVA
HOMA-IR
Sarcopenia
ANOVA
Exercise tolerance
BIA
BMI
Language English
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Snippet Obesity induces left ventricular diastolic dysfunction and ultimately causes heart failure. Sarcopenic obesity is common in heart failure with preserved...
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SubjectTerms Body Mass Index
Diastole
Diastole - physiology
Exercise - physiology
Exercise Test - methods
Exercise tolerance
Exercise Tolerance - physiology
Female
Heart failure
Heart Failure - physiopathology
Humans
Male
Middle Aged
Obesity
Obesity - physiopathology
Oxygen Consumption - physiology
Republic of Korea
Retrospective Studies
Sarcopenia
Sarcopenia - physiopathology
Stroke Volume - physiology
Ventricular Dysfunction, Left - physiopathology
Ventricular Function, Left - physiology
Title Effects of sarcopenia, body mass indices, and sarcopenic obesity on diastolic function and exercise capacity in Koreans
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0026049519300952
https://dx.doi.org/10.1016/j.metabol.2019.05.007
https://www.ncbi.nlm.nih.gov/pubmed/31125536
https://www.proquest.com/docview/2232101822
Volume 97
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