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Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound
Published on: December 2, 2014
Associations between circulating resistin concentrations and left ventricular mass are not accounted for by effects
Glenda Norman1, Gavin R Norton2, Vernice Peterson1
1Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand Medical School, 7 York Road, Parktown, Johannesburg, 2193, South Africa.
Insights
Resistin, an adipokine, impacts left ventricular mass (LVM) and may contribute to heart failure. This study found resistin
Area of Science:
- Cardiovascular Endocrinology
- Renal Physiology
- Cardiac Remodeling
Background:
- Resistin, an adipokine, is implicated in heart failure, potentially via effects on left ventricular mass (LVM).
- The role of resistin's impact on aortic stiffness and renal function in this association remains unclear.
Purpose of the Study:
- To investigate the relationship between circulating resistin concentrations and LVM.
- To determine if aortic stiffness (pulse wave velocity, PWV) or renal function (estimated glomerular filtration rate, eGFR) mediate the effects of resistin on LVM.
Main Methods:
- Cross-sectional study of 647 community participants.
- Echocardiography measured LVM index (LVMI) and inappropriate LVM (LVMinappr).
- Assessed relationships between resistin, LVMI, LVMinappr, LVH, PWV, and eGFR using regression analysis.
Main Results:
- Resistin concentrations were independently associated with LVMI, LVMinappr, LVH, PWV, and eGFR.
- LVMI, LVMinappr, and LVH were independently associated with PWV and eGFR.
- Adjustments for PWV or eGFR did not alter the association between resistin and LVM measures.
Conclusions:
- The association between resistin and LVM is not explained by ventricular-vascular coupling or renal dysfunction.
- Resistin likely exerts direct effects on the myocardium contributing to LVM.
Background:
Although, in-part through an impact on left ventricular mass (LVM), resistin (an adipokine) may contribute to heart failure, whether this is explained by the adverse effects of resistin on aortic stiffness and renal function is unknown.
Methods:
Relationships between circulating resistin concentrations and LVM index (LVMI), and LVM beyond that predicted by stroke work (inappropriate LVM [LVMinappr]) (echocardiography) were determined in 647 randomly selected community participants, and in regression analysis, the extent to which these relations could be explained by aortic pulse wave velocity (PWV) or estimated glomerular filtration rate (eGFR) was evaluated.
Results:
Independent of confounders, resistin concentrations were independently associated with LVMI, LVMinappr, LV hypertrophy (LVH), PWV and eGFR. Furthermore, independent of confounders, LVMI, LVMinappr and LVH were independently associated with PWV and eGFR. However, adjustments for either PWV or eGFR failed to modify the relationships between resistin concentrations and LVMI, LVMinappr or LVH. Moreover, in multivariate regression analysis neither PWV nor eGFR significantly modified the contribution of resistin to LVMinappr or LVMI.
Conclusions:
Independent relationships between circulating concentrations of the adipocytokine resistin and LVM are not explained by the impact of resistin on ventricular-vascular coupling or renal dysfunction. Resistin's effects on LVM are therefore likely to be through direct actions on the myocardium.
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