Relationship Between Nocturnal Dip, Carotid Artery Blood Flow, Brain Ischemic Change in Open Angle Glaucoma.
10.3341/jkos.2013.54.9.1386
- Author:
Hong Ryung SEO
1
;
Sang Wook JIN
;
Sae Heun RHO
Author Information
1. Department of Ophthalmology, Dong-A University Medical Center, Dong-A University College of Medicine, Busan, Korea. shrho@donga.ac.kr
- Publication Type:Original Article
- Keywords:
Brain ischemia;
Carotid artery blood flow;
Dipper;
Progression of visual field defect;
24-hour blood pressure monitoring
- MeSH:
Blood Pressure Monitoring, Ambulatory;
Brain;
Brain Ischemia;
Carotid Arteries;
Glaucoma;
Glaucoma, Open-Angle;
Humans;
Low Tension Glaucoma;
Salicylates;
Visual Fields
- From:Journal of the Korean Ophthalmological Society
2013;54(9):1386-1394
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To investigate the effect of nocturnal dip, carotid artery blood flow, and brain ischemic change on the progression of glaucomatous visual field defect in open-angle glaucoma (OAG) when IOP is less than the target pressure. METHODS: We classified OAG patients (74 patients, 148 eyes) who maintained IOP less than the target pressure as normal tension glaucoma (NTG; 52 patients, 104 eyes) or primary OAG (POAG; 22 patients, 44 eyes). Additionally, we performed 24-hr ambulatory blood pressure monitoring (24-hr ABPM), carotid artery color Doppler U/S (CAD), brain MRI, and visual field (V/F) tests on the patients. Nocturnal dips less than 10% were classified as non-dippers, and dips greater than 10% as dippers. The relationships among nocturnal dip, carotid artery blood flow, brain ischemic change, and progression of glaucomatous V/F defect were examined. RESULTS: In the case of dippers, glaucomatous V/F defects were aggravated, with a relative risk of approximately 1.74 (NTG) and 2.91 (POAG) times that of non-dippers. In NTG, decreased carotid artery blood flow and brain ischemic change furthered glaucomatous V/F defects, with a relative risk of approximately 2.40 and 2.54 times that of normal carotid artery blood flow and brain MRI findings, respectively. However, in POAG, decreased carotid artery blood flow and brain ischemic change were not influenced by the progression of glaucomatous V/F defects. CONCLUSIONS: In dippers, decreased carotid artery blood flow and brain ischemic change caused a progression of glaucomatous V/F defects in NTG and POAG patients. Thus, performing 24-hr ABPM, CAD, and brain MRI should be helpful for glaucoma patients with progression of glaucomatous V/F defects even when the IOP is less than the target pressure. In addition, this analysis provides useful information regarding glaucoma diagnosis and treatment.
