Retinal and Choroidal Capillary Perfusion Are Reduced in Hypertensive Crisis Irrespective of Retinopathy

高血压危象期间,无论是否存在视网膜病变,视网膜和脉络膜毛细血管灌注均会减少。

阅读:1

Abstract

PURPOSE: Hypertensive crisis causes end-organ damage through small-vessel damage as described histologically. Noninvasive optical coherence tomography angiography (OCTA) makes it possible to image retinal and choroidal capillaries on a microscopic level in vivo. We quantified eye vessel perfusion changes in hypertensive crisis using OCTA. METHODS: Patients with hypertensive crisis (systolic blood pressure ≥180 mm Hg and/or diastolic blood pressure ≥110 mm Hg) and age-matched healthy controls were included in the study. OCTA en face 3 × 3-mm images of the superficial and deep retinal layers and the choriocapillaris were acquired. Outcome parameters included vessel density (VD) and vessel skeleton density (VSD) of the superficial and deep retinal layers, as well as flow voids of the choriocapillaris. RESULTS: Twenty-eight eyes of 17 patients and 31 age-matched control eyes of 18 healthy subjects were included. VD and VSD of the deep retinal layer were significantly reduced in hypertensive crisis (P ≤ 0.004). Choriocapillaris signal intensity was more heterogeneous in patients, and flow voids exhibited confluence with a larger average area and a lower absolute count (P ≤ 0.045). These changes were independent of time since onset of hypertensive crisis and of the presence and extent of retinopathy. Deep retinal changes were associated with renal end-organ failure (P = 0.045). CONCLUSIONS: Hypertensive crisis is associated with a significant reduction in retinal and choroidal capillary perfusion based on OCTA findings. These alterations are independent of retinopathy and related to end-organ damage. TRANSLATIONAL RELEVANCE: OCTA might help distinguish hypertensive urgency from hypertensive emergency earlier than currently possible.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。