| Summary: | Objectives: It is widely thought that excess pulsatile pressure energy from increased stiffness of large central arteries (macro-vasculature) is transmitted to capillary networks (micro-vasculature) and causes end-organ damage (i.e. kidneys). However, this hypothesis has never been tested, and we sought to achieve this by examining people with increased macro-vascular stiffness (patients with type 2 diabetes T2DM) compared with non-diabetic controls.
Methods: Among 13 T2DM (68±6 years) and 15 controls (58±11 years) macro-vascular function was measured by aortic stiffness and radial artery waveforms by tonometry. Forearm micro-vascular waveforms were simultaneously measured via low power laser Doppler flowmetry, with augmentation index (AIx) and augmented pressure (AP) derived on all waveforms. Kidney function was assessed by estimated glomerular filtration rate (eGFR).
Results: Aortic stiffness was higher among T2DM (9.3±2.5 vs 7.5±1.4 m/s, p=0.046). There was an obvious pulsatile micro-vascular waveform, with qualitative features similar to radial waveforms. Macro-vasculature AIx and AP were significantly related to micro-vasculature AIx (r=0.428. p=0.005 and r=0.545, p=0.004 respectively). Micro-vascular (but not macro-vascular) AIx was associated with eGFR in T2DM (r=−0.632, p=0.037).
Conclusions: This is the first in-human evidence of pulsatile pressure interaction between the macro-vasculature and micro-vasculature, and provides potential explanation for accelerated kidney dysfunction.
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