The relative contribution of metabolic and structural abnormalities to diastolic dysfunction in obesity

Background: Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. H...

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Published inInternational Journal of Obesity Vol. 42; no. 3; pp. 441 - 447
Main Authors Rayner, J J, Banerjee, R, Holloway, C J, Lewis, A J M, Peterzan, M A, Francis, J M, Neubauer, S, Rider, O J
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.03.2018
Nature Publishing Group
Subjects
59/57
692/499
692/699/75
Abnormalities
Adult
Body mass
Body Mass Index
Cardiovascular diseases
Cohort Studies
Diastole (Cardiac cycle)
Diastole - physiology
Epidemiology
Female
Health aspects
Health Promotion and Disease Prevention
Health risks
Heart diseases
Heart function
Humans
Hypertrophy
Internal Medicine
Intra-Abdominal Fat - diagnostic imaging
Intra-Abdominal Fat - physiopathology
Magnetic Resonance Imaging
Magnetic resonance spectroscopy
Male
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolism
Obesity
Obesity - diagnostic imaging
Obesity - epidemiology
Obesity - physiopathology
Original
original-article
Physiological aspects
Public Health
Risk analysis
Risk factors
Steatosis
Strain rate
Triglycerides
Triglycerides - blood
Ventricle
Ventricular Dysfunction, Left - diagnostic imaging
Ventricular Dysfunction, Left - physiopathology
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Abstract Background: Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown. Methods: Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4–53.0 kg m −2 ) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content. Results: Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r =−0.46, P =0.001). Myocardial triglyceride content (β=−0.2, P =0.008), PCr/ATP (β=−0.22, P =0.04) and LV mass:volume ratio (β=−0.61, P =0.04) all independently predicted peak diastolic strain rate (model R 2 0.36, P <0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling. Conclusions: Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.
AbstractList Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown. Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4-53.0 kg m ) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content. Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r=-0.46, P=0.001). Myocardial triglyceride content (β=-0.2, P=0.008), PCr/ATP (β=-0.22, P=0.04) and LV mass:volume ratio (β=-0.61, P=0.04) all independently predicted peak diastolic strain rate (model R 0.36, P<0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling. Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.
Background: Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown. Methods: Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4-53.0 kg m[sup.-2]) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content. Results: Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r=-0.46, P=0.001). Myocardial triglyceride content ([beta]=-0.2, P=0.008), PCr/ATP ([beta]=-0.22, P=0.04) and LV mass:volume ratio ([beta]=-0.61, P=0.04) all independently predicted peak diastolic strain rate (model R[sup.2] 0.36, P [less than] 0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling. Conclusions: Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity. International Journal of Obesity (2018) 42, 441-447; doi: 10.1038/ijo.2017.239; published online 24 October 2017
Background:Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown.Methods:Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4-53.0 kg m-2 ) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content.Results:Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r=-0.46, P=0.001). Myocardial triglyceride content (β=-0.2, P=0.008), PCr/ATP (β=-0.22, P=0.04) and LV mass:volume ratio (β=-0.61, P=0.04) all independently predicted peak diastolic strain rate (model R2 0.36, P<0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling.Conclusions:Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.
Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown. Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4-53.0 kg m[sup.-2]) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content. Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r=-0.46, P=0.001). Myocardial triglyceride content ([beta]=-0.2, P=0.008), PCr/ATP ([beta]=-0.22, P=0.04) and LV mass:volume ratio ([beta]=-0.61, P=0.04) all independently predicted peak diastolic strain rate (model R[sup.2] 0.36, P [less than] 0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling. Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.
Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown.BACKGROUNDObesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown.Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4-53.0 kg m-2) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content.METHODSEighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4-53.0 kg m-2) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content.Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r=-0.46, P=0.001). Myocardial triglyceride content (β=-0.2, P=0.008), PCr/ATP (β=-0.22, P=0.04) and LV mass:volume ratio (β=-0.61, P=0.04) all independently predicted peak diastolic strain rate (model R2 0.36, P<0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling.RESULTSIncreasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r=-0.46, P=0.001). Myocardial triglyceride content (β=-0.2, P=0.008), PCr/ATP (β=-0.22, P=0.04) and LV mass:volume ratio (β=-0.61, P=0.04) all independently predicted peak diastolic strain rate (model R2 0.36, P<0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling.Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.CONCLUSIONSMyocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.
Background: Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown. Methods: Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4–53.0 kg m −2 ) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content. Results: Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r =−0.46, P =0.001). Myocardial triglyceride content (β=−0.2, P =0.008), PCr/ATP (β=−0.22, P =0.04) and LV mass:volume ratio (β=−0.61, P =0.04) all independently predicted peak diastolic strain rate (model R 2 0.36, P <0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling. Conclusions: Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.
Audience Academic
Author Holloway, C J
Neubauer, S
Rayner, J J
Peterzan, M A
Lewis, A J M
Francis, J M
Rider, O J
Banerjee, R
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  email: oliver.rider@gmail.com
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/28974742$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
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Snippet Background: Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is...
Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined...
Background: Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is...
Background:Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is...
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SubjectTerms 59/57
692/499
692/699/75
Abnormalities
Adult
Body mass
Body Mass Index
Cardiovascular diseases
Cohort Studies
Diastole (Cardiac cycle)
Diastole - physiology
Epidemiology
Female
Health aspects
Health Promotion and Disease Prevention
Health risks
Heart diseases
Heart function
Humans
Hypertrophy
Internal Medicine
Intra-Abdominal Fat - diagnostic imaging
Intra-Abdominal Fat - physiopathology
Magnetic Resonance Imaging
Magnetic resonance spectroscopy
Male
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolism
Obesity
Obesity - diagnostic imaging
Obesity - epidemiology
Obesity - physiopathology
Original
original-article
Physiological aspects
Public Health
Risk analysis
Risk factors
Steatosis
Strain rate
Triglycerides
Triglycerides - blood
Ventricle
Ventricular Dysfunction, Left - diagnostic imaging
Ventricular Dysfunction, Left - physiopathology
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Title The relative contribution of metabolic and structural abnormalities to diastolic dysfunction in obesity
URI https://link.springer.com/article/10.1038/ijo.2017.239
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