脈搏壓與收縮壓對正常眼壓型青光眼結構變化之影響

研究目的 本研究旨在探討脈搏壓與收縮壓對於正常眼壓型青光眼 ( Normal Tension Glaucoma, NTG )患者視網膜神經纖維層 ( Retinal Nerve Fiber Layer, RNFL ) 厚度、黃斑部血管密度 ( Macular Vessel Density, MVD )、視神經盤周圍區域血管密度 ( Peripapillary Vessel Density, PVD ) 以及眼部生理結構的影響。 研究方法 本回溯性研究納入2020年10月至2023年2月期間於新店耕莘眼科確診93 位正常眼壓型青光眼患者的164隻眼資料。脈搏壓 ( Pulse Pressure, PP ) 以隧道式血壓計測量並依照數值分為低 ( ≤ 40 mmHg )、中 ( 41-60 mmHg )、高 ( > 60 mmHg ) 三組，以眼部光學斷層掃描儀血管造影術 ( Optical Coherence Tomography Angiography, OCT-A ) 評估黃斑部周圍血管密度及視神經盤周圍血管密度，並以血壓參數；統計分析部分以迴歸模型分析評估三組收縮壓對於上述結構與MVD和PVD之相關性。 研究結果 與低、中脈搏壓組相比，高脈搏壓組的視神經盤周圍平均、上側、下側、區域神經纖維層厚度顯著較薄 ( p < 0.001 )；且相較於中脈搏壓組，高脈搏壓組的鼻側區域神經纖維層厚度顯著較薄 ( p = 0.012 )，下側區域黃斑部周圍神經節細胞層厚度也顯著較薄 ( p = 0.032 )。與低脈搏壓組相比，高脈搏壓組的黃斑部周圍上側、鼻側與下側區域血管密度也顯著較低 ( p < 0.05 )。 在單變量迴歸模型分析中，高脈搏壓組之收縮壓每增加一個單位，視神經盤周圍平均神經纖維層厚度會減少0.388 µm ( ß = -0.388, p = 0006 )、顳側區域黃斑部周圍血管密度會減少0.339 % area ( ß = -0.339, p = 0.017 )、上側區域黃斑部周圍血管密度則會減少0.567 % area ( ß = -0.567, p < 0.001 )；在控制等價球面度數、中央角膜厚度、眼壓以及眼軸長度等四個變項之後，收縮壓每增加一個單位，視神經盤周圍平均神經纖維層厚度會減少0.335 µm ( ß = -0.335, p = 0.014 )、顳側區域黃斑部周圍血管密度會減少0.298 % area ( ß = -0.298, p = 0.033 )、上側區域黃斑部周圍血管密度則會減少0.557 % area ( ß = -0.557, p <0.001 )。 結論 本研究發現，在高脈搏壓組NTG患者中，收縮壓升高與特定區域的黃斑部周圍血管密度和視神經盤周圍神經纖維層厚度下降有關，並且這樣的結構變化也反映出較高的視覺功能惡化。這顯示血流動力學因素可能加速眼部特定區域微血管以及神經纖維層退化。未來臨床管理中，不僅需要控制眼壓，也應針對NTG患者的異常血壓變化進行評估，以全面預防與治療NTG。

Purpose This study aims to investigate the effects of pulse pressure (PP) and systolic blood pressure (SBP) on retinal nerve fiber layer (RNFL) thickness, macular vessel density (MVD), peripapillary vessel density (PVD), and ocular structural parameters in patients with NTG. Methods NTG subjects who met inclusion and exclusion criteria were evaluated retrospectively. One hundred sixty-four eyes of 93 patients were enrolled at Cardinal Tien Hospital Xindian Ophthalmology Department between October 2020 and February 2023. Based on pulse pressure (PP), patients were categorized into three groups: low (≤ 40 mmHg), medium (41–60 mmHg), and high (> 60 mmHg). Optical Coherence Tomography Angiography (OCT-A) was used to measure macular and peripapillary vessel densities, while blood pressure parameters were obtained using an oscillometric blood pressure monitor. Regression models were applied for analyzing the impact of systolic blood pressure (SBP) on structural parameters, as well as on MVD and PVD. Results Compared to the low and medium pulse pressure (PP) groups, the high PP group exhibited significantly thinner average, superior, and inferior peripapillary retinal nerve fiber layer (RNFL) thicknesses (p < 0.001). Additionally, the nasal RNFL thickness was significantly thinner in the high PP group compared to the medium PP group (p = 0.012), and the inferior macular ganglion cell layer thickness was also significantly reduced (p = 0.032). Furthermore, the high PP group showed significantly lower vessel density in the superior, nasal, and inferior regions of the macular area compared to the low PP group. In the univariable regression analysis within the high pulse pressure (PP) group, each 1 mmHg increase in systolic blood pressure (SBP) was associated with a decrease of 0.388 µm in average peripapillary RNFL thickness (ß = -0.388, p = 0.006), a decrease of 0.339 % area in temporal macular vessel density (ß = -0.339, p = 0.017), and a decrease of 0.567 % area in superior macular vessel density (ß = -0.567, p < 0.001). After adjusting for spherical equivalent, central corneal thickness, intraocular pressure, and axial length, each 1 mmHg increase in SBP remained significantly associated with a reduction of 0.335 µm in average peripapillary RNFL thickness (ß = -0.335, p = 0.014), 0.298 % area in temporal macular vessel density (ß = -0.298, p = 0.033), and 0.557 % area in superior macular vessel density (ß = -0.557, p < 0.001). Conclusion This study found that in NTG patients with high pulse pressure, higher systolic blood pressure was associated with decreased macular vessel density and peripapillary retinal nerve fiber layer thickness in certain retinal regions, the structural change also reflects a deterioration in visual field. It suggests that hemodynamic factors may accelerate microvascular and nerve fiber degeneration in specific ocular regions. Regarding to clinical management, it is important not only to control intraocular pressure but also to monitor abnormal blood pressure fluctuations in NTG patients to ensure an efficient follow-up to prevent visual field loss and guartee the effect of treatment.