INSERM, U970, Department of Epidemiology, Paris Cardiovascular Research Center (PARCC), Team 4 Cardiovascular Epidemiology and Sudden Death, Paris Descartes University, 56 rue Leblanc, 75015, Paris, France.
Menzies Institute for Medical Research, College of Health and Medicine, University of Tasmania, Hobart, TAS, Australia.
Eur J Appl Physiol. 2018 Nov;118(11):2455-2463. doi: 10.1007/s00421-018-3972-2. Epub 2018 Aug 29.
It is widely thought that excess pulsatile pressure from increased stiffness of large central arteries (macro-vasculature) is transmitted to capillary networks (micro-vasculature) and causes target organ damage. However, this hypothesis has never been tested. We sought to examine the association between macro- and micro-vasculature waveform features in patients with type 2 diabetes (i.e., those with elevated stiffness; T2D) compared with non-diabetic controls.
Among 13 T2D (68 ± 6 years, 39% male) and 15 controls (58 ± 11 years, 40% male) macro-vascular stiffness was determined via aortic pulse wave velocity (aPWV) and macro-vascular waveforms were measured using radial tonometry. Forearm micro-vascular waveforms were measured simultaneously with macro-vascular waveforms via low power laser Doppler fluxmetry. Augmentation index (AIx) was derived on macro- and micro-vascular waveforms. Target organ damage was assessed by estimated glomerular filtration rate (eGFR) and central retinal artery equivalent (CRAE).
aPWV was higher among T2D (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 macro-vasculature pressure waveforms. In all subjects, macro- and micro-vasculature AIx were significantly related (r = 0.43, p = 0.005). In T2D alone, micro-vasculature AIx was associated with eGFR (r = - 0.63, p = 0.037), whereas in controls, macro-vasculature AIx and AP were associated with CRAE (r = - 0.58, p = 0.025 and r = - 0.61, p = 0.015).
Macro- and micro-vasculature waveform features are related; however, micro-vasculature features are more closely related to markers of target organ damage in T2D. These findings are suggestive of a possible interaction between the macro- and micro-circulation.
人们普遍认为，大动脉（宏观血管）僵硬增加导致的脉动压力过大会传递到毛细血管网络（微观血管），并导致靶器官损伤。然而，这一假说从未得到过验证。我们试图在 2 型糖尿病患者（即那些存在僵硬升高的患者；T2D）和非糖尿病对照者之间，检查宏观和微观血管波形特征之间的关联。
在 13 例 T2D（68±6 岁，39%男性）和 15 例对照者（58±11 岁，40%男性）中，通过主动脉脉搏波速度（aPWV）确定大血管僵硬程度，并使用桡动脉张力测量法测量大血管波形。同时通过低功率激光多普勒通量测量法在大血管波形测量时测量前臂微血管波形。在宏观和微观血管波形上得出增强指数（AIx）。通过估算肾小球滤过率（eGFR）和中央视网膜动脉等效（CRAE）评估靶器官损伤。
T2D 患者的 aPWV 更高（9.3±2.5 比 7.5±1.4 m/s，p=0.046）。存在与大血管压力波形具有明显相似的脉动微血管波形。在所有受试者中，宏观和微观血管 AIx 显著相关（r=0.43，p=0.005）。在 T2D 患者中，微血管 AIx 与 eGFR 相关（r=-0.63，p=0.037），而在对照组中，大血管 AIx 和 AP 与 CRAE 相关（r=-0.58，p=0.025 和 r=-0.61，p=0.015）。
宏观和微观血管波形特征相关；然而，微血管特征与 T2D 靶器官损伤标志物的关系更为密切。这些发现提示宏观和微循环之间可能存在相互作用。
