Wave Reflection at the Origin of a First-Generation Branch Artery and Target Organ Protection: The AGES-Reykjavik Study.
Wave Reflection at the Origin of a First-Generation Branch Artery and Target Organ Protection: The AGES-Reykjavik Study.
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第一代分支动脉起源处的波反射和靶器官保护：AGES-Reykjavik研究。
DOI：
10.1161/hypertensionaha.120.16696
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发表时间：
2021-04
期刊：
影响因子：
8.3
通讯作者：
Mitchell, Gary F.
中科院分区：
文献类型：
--
作者：
Haidar, Michael A.;van Buchem, Mark A.;Sigurdsson, Sigurdur;Gotal, John D.;Gudnason, Vilmundur;Launer, Lenore J.;Mitchell, Gary F.
第一代分支动脉的过度压力和血流脉动与脑和肾等高血流器官的微血管损伤有关。然而，局部波反射和反射对微血管损伤的贡献仍然存在争议。对无中风、短暂性脑缺血发作或痴呆史的AGES-Reykjavik研究参与者（N=668, 378名女性，69 - 93岁）的主动脉流量、颈动脉压力、流量和水力、脑磁共振成像和认知评分进行评估。主动脉-颈动脉界面是一个明显不对称的分叉，有一个大的母血管（近端主动脉）分支成小的（颈动脉）和大的（远端主动脉）子血管。局部反射系数由主动脉和颈动脉特征阻抗计算。分支反射系数（决定两个子血管的压力放大）较低（0.06±0.03）。颈动脉血流传递系数低（0.11±0.04），与颈动脉与主动脉血流脉动性（波形SD， 7.2±2.0 vs. 98.7±21.8 mL/s， P<0.001）、脉动指数（1.8±0.5 vs. 4.5±0.6，P<0.001）和脉动功率百分比（10±4 vs. 25±5%，P<0.001）显著降低相关。与入射脉冲功率（19.0±9.8 mW vs. 35.9±17.8 mW， P<0.001）相比，透射脉冲功率在颈动脉内的反射（- 4.3±2.7 mW）和反射（- 12.5±8.1 mW）进一步降低。颈动脉血流脉动度越高，白质体积越小（R= - 0.130， P<0.001），记忆评分越低（R= - 0.161， P<0.001）。主动脉-支动脉分叉处特征阻抗的明显不对称限制了压力的放大，显著降低了传递到第一代分支动脉的流量和水力的绝对和相对脉动性，从而保护下游局部微循环免受脉动性损伤。第一代分支动脉分叉处明显的不对称限制了压力放大和全局功率反射，但在提供高平均流量的同时显着降低了分支动脉的脉动功率。低压传递系数（1 + Γ1 = 1.06）和高远端主动脉脉动流传递系数（1 - Γ3 = 0.82）结合低颈动脉脉动流传递系数（1 - Γ2 = 0.11）限制了脉动力向颈动脉的传递。
Excessive pressure and flow pulsatility in first-generation branch arteries are associated with microvascular damage in high-flow organs like brain and kidneys. However, the contribution of local wave reflection and rereflection to microvascular damage remains controversial. Aortic flow, carotid pressure, flow and hydraulic power, brain magnetic resonance images, and cognitive scores were assessed in AGES-Reykjavik study participants without history of stroke, transient ischemic attack or dementia (N=668, 378 women, 69 to 93 years of age). The aorta-carotid interface was generalized as a markedly asymmetric bifurcation, with a large parent vessel (proximal aorta) branching into small (carotid) and large (distal aorta) daughter vessels. Local reflection coefficients were computed from aortic and carotid characteristic impedances. The bifurcation reflection coefficient, which determines pressure amplification in both daughter vessels, was low (0.06±0.03). The carotid flow transmission coefficient was low (0.11±0.04) and associated with markedly lower carotid vs. aortic flow pulsatility (waveform SD, 7.2±2.0 vs. 98.7±21.8 mL/s, P<0.001), pulsatility index (1.8±0.5 vs. 4.5±0.6, P<0.001) and pulsatile power percentage (10±4 vs. 25±5%, P<0.001). Transmitted as compared to incident pulsatile power (19.0±9.8 mW vs. 35.9±17.8 mW, P<0.001) was further reduced by reflection (−4.3±2.7 mW) and rereflection (−12.5±8.1 mW) within the carotid. Higher carotid flow pulsatility correlated with lower white matter volume (R=−0.130, P<0.001) and lower memory scores (R=−0.161, P<0.001). Marked asymmetry of characteristic impedances at aorta-branch artery bifurcations limits amplification of pressure, markedly reduces absolute and relative pulsatility of transmitted flow and hydraulic power into first-generation branch arteries and thereby protects the downstream local microcirculation from pulsatile damage. Marked asymmetry at a first-generation branch artery bifurcation limits pressure amplification and global power reflection, but markedly reduces branch artery pulsatile power while delivering high mean flow. The low pressure transmission coefficient (1 + Γ1 = 1.06) and high distal aortic pulsatile flow transmission coefficient (1 – Γ3 = 0.82) combined with the low carotid pulsatile flow transmission coefficient (1 – Γ2 = 0.11) limits pulsatile power transmission into the carotids.