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Multicenter Study
. 2018 Aug;20(8):1191-1201.
doi: 10.1002/ejhf.1188. Epub 2018 Apr 16.

Adiposity, body composition and ventricular-arterial stiffness in the elderly: the Atherosclerosis Risk in Communities Study

Affiliations
Multicenter Study

Adiposity, body composition and ventricular-arterial stiffness in the elderly: the Atherosclerosis Risk in Communities Study

Miguel M Fernandes-Silva et al. Eur J Heart Fail. 2018 Aug.

Abstract

Aim: Weight gain appears to accelerate age-related ventricular-arterial stiffening, which has been implicated in the development of heart failure (HF), but it is unclear whether body fat accumulation underpins this association. We evaluated the relationship of adiposity, using measures of body composition, with ventricular-arterial stiffness among the elderly in the community.

Methods and results: Adiposity was accessed through body mass index (BMI), waist circumference, and body fat percentage. We studied the association of these measures with carotid-femoral pulse wave velocity (cfPWV), arterial elastance index (EaI), left ventricular (LV) end-systolic elastance index (EesI) and LV end-diastolic elastance index (EedI) in 5520 community-based, elderly Atherosclerosis Risk in Communities (ARIC) Study participants, who underwent echocardiography between 2011 and 2013. BMI and waist circumference were directly associated with EaI, EedI and EesI even after adjusting for age, sex, race, hypertension, diabetes mellitus, heart rate, prevalent coronary heart disease and HF. After further adjustment for BMI, body fat percentage demonstrated significant independent linear relationships with EaI [standardized beta coefficient (β)=0.17, P<0.001], EesI (β=0.08, P=0.003) and EedI (β=0.20, P<0.001), and significant non-linear relationships with cfPWV (P=0.033).

Conclusion: In this biracial community-based cohort, increased adiposity was associated with increased ventricular-arterial stiffness among the elderly and suggests a potential mechanism by which obesity might contribute to the development of HF.

Keywords: Adiposity; Aging; Arterial stiffness; Obesity; Ventricular stiffness.

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Conflict of interest statement

CONFLICTS OF INTEREST

None declared.

Figures

Figure 1:
Figure 1:. Association between body fat and ventricular-arterial stiffness, after adjusting for body mass index and other potential confounders in all participants
cfPWV – carotid-femoral pulse wave velocity; EaI – Arterial elastance indexed by body surface area, TACI – total arterial compliance indexed by body surface area; LV EedI – left ventricle end-diastolic elastance indexed by body surface area, LV EesI - left ventricle end-systolic elastance indexed by body surface area Adjusted plot for age, sex, race, body mass index, hypertension, use of anti-hypertensive medications at visit 5, diabetes mellitus, heart rate and prevalence of coronary heart disease or heart failure. For cfPWV, mean arterial pressure was included in the model. Dashed lines show 95% prediction bands. The x-axis was truncated at the 1st and 99th percentiles of the empirical distribution of the exposure of interest. However, all data from the exposure of interest was used to fit the model. The truncation affected only the graphical display.
Figure 2:
Figure 2:. Association between body fat and ventricular-arterial stiffness, after adjusting for body mass index and other potential confounders among metabolic healthy participants
cfPWV – carotid-femoral pulse wave velocity; EaI – Arterial elastance indexed by body surface area, TACI – total arterial compliance indexed by body surface area; LV EedI – left ventricle end-diastolic elastance indexed by body surface area, LV EesI - left ventricle end-systolic elastance indexed by body surface area Adjusted plot for age, sex, race and body mass index. Participants with history of coronary heart disease or heart failure were excluded from this analysis. For cfPWV, mean arterial pressure was included in the model. Dashed lines show 95% prediction bands. The x-axis was truncated at the 1st and 99th percentiles of the empirical distribution of the exposure of interest. However, all data from the exposure of interest was used to fit the model. The truncation affected only the graphical display.

Comment in

  • In need of signalling pathway data.
    Pizard A. Pizard A. Eur J Heart Fail. 2018 Aug;20(8):1202-1204. doi: 10.1002/ejhf.1219. Epub 2018 Jun 12. Eur J Heart Fail. 2018. PMID: 29893008 No abstract available.

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