Author + information
- Keiichiro Yoshinaga,
- Yoichi Ito,
- Satoshi Fujii,
- Saori Nishio,
- Noriki Ochi,
- Katoh Chietsugu,
- Mamiko Inoue,
- Mutsumi Nishida,
- Osamu Manabe and
- Nagara Tamaki
Background: Simple arterial function measurements can be used to estimate atherosclerosis risk. Recently we developed a novel modality, an automated oscillometric method to measure brachial artery vascular elastic modulus (VE), possibly linked to endothelial dysfunction associated with chronic kidney disease (CKD). We sought molecular determinants of VE in CKD.
Methods: Twelve CKD patients (eGFR 25.9±23.5 mL/min/1.73m2) and 15 controls were studied. An automated oscillometric detector measured rest VE. VE was defined as [VE =ΔPressure/ (100XΔarea/Area) mmHg/%]. Using ultrasound, we measured the brachial artery's reactive hyperemia [flow mediated dilatation (FMD)]. Endogenous inhibitors of nitric oxide synthase, symmetric dimethylarginine (SDMA), and arginine (Arg) were measured by HPLC. Galectin-3 (Gal-3), regulator of vascular fibrosis expressed in endothelium, was measured by ELISA.
Results: CKD patients had lower FMD (4.86±3.37 vs 9.05±2.98 %, P=0.003) and higher VE than did controls (1.08±0.26 vs 0.83±0.17 mmHg/%, P=0.002). On multivariate analysis, decreased %FMD (P=0.0099), eGFR (P=0.0052), increased SDMA (P=0.0037), Arg (P=0.048), and Gal-3 (P=0.0022) were predictors for attenuated VE.
Conclusions: Attenuated vascular elasticity detected by this approach correlated with reduced FMD in CKD. Molecular determinants of the attenuated VE were SDMA, Arg, and Gal-3. Therefore, this simple measurement may reflect endothelial dysfunction and vascular fibrosis.
Poster Hall, Hall C
Sunday, March 19, 2017, 9:45 a.m.-10:30 a.m.
Session Title: Vascular Medicine: Aortic and Peripheral Artery Diseases
Abstract Category: 40. Vascular Medicine: Non Coronary Arterial Disease
Presentation Number: 1298-358
- 2017 American College of Cardiology Foundation