J Korean Ophthalmol Soc.  2014 Jul;55(7):1030-1038.

Relationship among Water-Shed Zone, Nocturnal Dip and Visual Field Progression in Open Angle Glaucoma

• Seo HR
• Kim NY
• Rho SH

Abstract

PURPOSE
To investigate the influence of water-shed zone (WSZ) and nocturnal dip (ND) on the progression of the glaucomatous visual field (V/F) defects in open-angle glaucoma (OAG) patients when the intraocular pressure (IOP) was maintained under the target pressure.
METHODS
We performed fluorescence angiography (FAG), 24-hour ambulatory blood pressure monitoring (24-hr ABPM), and V/F tests. We examined the relationships among WSZ in early-FAG, ND over 10% (dip), and the progression of the glaucomatous V/F defects using chi-square, Fisher's exact, and multivariate logistic regression tests. A p-value < 0.05 was considered statistically significant.
RESULTS
When considering the correlation between WSZ and dip, statistical significance was found in OAG (p = 0.024, odds ratio (OR) = 3.308) and normal tension glaucoma (NTG) (p = 0.029, OR = 4.364) patients. In patients with dip, glaucomatous V/F defects significantly progressed (OAG: p = 0.003, OR = 5.938, NTG: p = 0.005, OR = 13.929). In patients with WSZ, the glaucomatous V/F defects progressed in all groups (OAG: p = 0.002, OR = 5.156, NTG: p = 0.024, OR = 4.750, primary open angle glaucoma (POAG): p = 0.021, OR = 8.750). In the patients with WSZ involving optic nerve head, the glaucomatous V/F defects had progressed in OAG (p = 0.004, OR = 5.958) and NTG (p = 0.009, OR = 8.333) groups. Based on binary logistic regression analysis, dip (p = 0.010, OR = 6.227) significantly affected V/F progression only in OAG patients.
CONCLUSIONS
In the OAG and NTG groups, ND over 10% influenced the progression of the glaucomatous V/F defects. The patients with WSZ tended to have ND over 10% in OAG and NTG groups and glaucomatous V/F defects progressed in all patients. Therefore, performing early FAG and 24-hr ambulatory blood pressure monitoring may be helpful for glaucoma patients with progressing glaucomatous V/F defects even when the IOP was maintained under the target pressure.

Keyword

Nocturnal dip; Progression of the glaucomatous visual field defects; Twenty-four-hour blood pressure monitoring; Vascular dysregulation; Water-shed zone

MeSH Terms

Blood Pressure Monitoring, Ambulatory
Fluorescein Angiography
Glaucoma
Glaucoma, Open-Angle*
Humans
Intraocular Pressure
Logistic Models
Low Tension Glaucoma
Odds Ratio
Optic Disk
Visual Fields*

Figure

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  Figure 1. The pattern of watershed zone in fluorescence angiography. (A) 65-year-old female NTG patient shows that watershed zone is not including the optic nerve head. (B) 72-year-old female POAG patient shows that watershed zone including the optic nerve head. NTG = normal tension glaucoma; POAG = primary open-angle glaucoma.

Reference

References

1. Armaly MF. Ocular pressure and visual fields. A ten-year follow-up study. Arch Ophthalmol. 1969; 81:25–40.

2. Levens RZ. Low tension glaucoma: a critical review and new material. Surv Ophthalmol. 1980; 24:621–64.

3. Perkins ES. The Bedford glaucoma survey. I. Long-term follow-up of boarderline cases. Br J Ophthalmol. 1973; 57:179–85.

4. Van Buskirk EM, Cioffi GA. Glaucomatous optic neuropathy. Am J Ophthalmol. 1992; 113:447–52.

5. Brubaker RF. Delayed functional loss in glaucoma. LII Edward Jackson Memorial Lecture. Am J Ophthalmol. 1996; 121:473–83.

6. Kim CS, Seong GJ, Lee NH, Song KC. Prevalence of primary open-angle glaucoma in central South Korea the Namil study. Ophthalmology. 2011; 118:1024–30.

7. Detry M, Boschi A, Ellinghaus G, de Plaen JF. Simultaneous 24-h monitoring of intraocular pressure and arterial blood pressure in patients with progressive and non-progressive primary open-angle glaucoma. Eur J Ophthalmol. 1996; 6:273–8.

8. Fechtner RD, Weinreb RN. Mechanisms of optice nerve damage in primary open angle glaucoma. Surv Ophthalmol. 1994; 39:23–42.

9. Juronen E, Tasa G, Veromann S, et al. Polymorphic glutathione S-transferase M1 is a risk factor of primary open-angle glaucoma among Estonians. Exp Eye Res. 2000; 71:447–52.

10. Araie M, Sekine M, Suzuki Y, Koseki N. Factors contributing to the progression of visual field damage in eyes with normal-tension glaucoma. Ophthalmology. 1994; 101:1440–4.

11. Beano F, Org ul S, Stumpfig D, et al. An evaluation of the effect of unoprostone isopropyl 0.15% on ocular hemodynamics in normal- tension glaucoma patients. Graefe's Arch Clin Exp Ophthalmol. 2001; 239:81–6.

12. Buckley C, Hadoke PWF, Henry E, O'Brien C. Systemic vascular endothelial cell dysfunction in normal pressure glaucoma. Br J Ophthalmol. 2002; 86:227–32.

13. Chung HS, Harris A, Kagemann L, Martin B. Peripapillary retinal blood flow in normal tension glaucoma. Br J Ophthalmol. 1999; 83:466–9.

14. The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma. Collaborative Normal-Tension Glaucoma Study Group. Am J Ophthalmol. 1998; 126:498–505.

15. Drance SM, Douglas GR, Wijsman K, et al. Response of blood flow to warm and cold in normal and low-tension glaucoma patients. Am J Ophthalmol. 1988; 105:35–9.

16. Drance S, Anderson DR, Schulzer M. Risk factors for progression of visual field abnormalities in normal-tension glaucoma. Am J Ophthalmol. 2001; 131:699–708.

17. Flammer J, Orgül S, Costa VP, et al. The impact of ocular blood flow in glaucoma. Pro Retin Eye Res. 2002; 21:359–93.

18. Flammer J, Pache M, Resink T. Vasospasm, its role in the pathogenesis of disease with particular reference to eye. Pro Retin Eye Res. 2001; 20:319–49.

19. Becker B. Diabetes mellitus and primary open-angle glaucoma. The XXVII Edward Jackson Memorial Lecture. Am J Ophthalmol. 1971; 71:1–16.

20. Mcleod SD, West SK, Quigley HA, Fozard JL. A longitudinal study of the relationship between intraocular and blood pressures. Invest Ophthalmol Vis Sci. 1990; 31:2361–6.

21. Armstrong JR, Daily RK, Dobson HL, Girard LJ. The incidence of glaucoma in diabetes mellitus. A comparison with the incidence of glaucoma in the general population. Am J Ophthalmol. 1960; 50:55–63.

22. Mitchell P, Lee AJ, Rochtchina E, Wang JJ. Open-angle glaucoma and systemic hypertension: the blue mountains eye study. J Glaucoma. 2004; 13:319–26.

23. Pradalier A, Hamard P, Sellem E, Bringer L. Migraine and glaucoma: an epidemiologic survey of French ophthalmologists. Cephalalgia. 1998; 18:74–6.

24. Broadway DC, Drance SM. Glaucoma and vasospasm. Br J Ophthalmol. 1998; 82:862–70.

25. Millar-Craig MW, Bishop CN, Raftery EB. Circadian variation of blood pressure. Lancet. 1978; 1:795–7.

26. Pickering T. Recommendations for the use of home (self) and ambulatory blood pressure monitoring. American Society of Hypertension Ad Hoc Panel. Am J Hypertens. 1996; 9:1–11.

27. Arend O, Remky A, Cantor LB, Harris A. Altitudinal visual field asymmetry is coupled with altered retinal circulation in patients with normal pressure glaucoma. Br J Ophthalmol. 2000; 84:1008–12.

28. Arend O, Remky A, Redbrake C, et al. Retinal hemodynamics in patients with normal pressure glaucoma. Quantification with digital laser scanning fluorescein angiography. Ophthalmologe. 1999; 96:24–9.

29. Flammer J, Orgül S. Optic nerve blood-flow abnormalities in glaucoma. Progr Ret Eye Res. 1998; 17:267–89.

30. Hayreh SS. The 1994 Von Sallman Lecture. The optic nerve head circulation in health and disease. Exp Eye Res. 1995; 61:259–72.

31. Plange N, Remky A, Arend O. Absolute filling defects of the optic disc in fluorescein angiograms in glaucoma–a retrospective clinical study. Klein Monatsbl Augenheilkd. 2001; 218:214–21.

32. Be'chetoille A, Bresson-Dumont H. Diurnal and nocturnal blood pressure drops in patients with focal ischemic glaucoma. Graefe's Arch Clin Exp Ophthalmol. 1994; 232:675–9.

33. Chumbley LC, Brubaker RF. Low-tension glaucoma. Am J Ophthalmol. 1976; 81:761–7.

34. Dielemans I, Vingerling JR, Algra D, et al. Primary open-angle glaucoma, intraocular pressure, and systemic blood pressure in the general elderly population. The Rotterdam Study. Ophthalmology. 1995; 102:54–60.

35. Drance SM, Wheeler C, Pattullo M. Uniocular open-angle glaucoma. Am J Ophthalmol. 1968; 65:891–902.

36. Francois J, Neetens A. The deterioration of the visual field in glaucoma and the blood pressure. Doc Ophthalmol. 1970; 28:70–132.

37. Geijssen HC. Systemic Vascular Risc Factors. In : Geijssen HC, editor. Studies on Normal Pressure Glaucoma. New York: Kugler Publications;1991. chap. 6.

38. Hayreh SS, Podhajsky P, Zimmermann MB. Role ofnocturnal arterial hypotension in optic nerve head ischemic disorders. Ophthal- mologica. 1999; 213:76–96.

39. Jampol LM, Board RJ, Maumenee AE. Systemic hypotension and glaucomatous changes. Am J Ophthalmol. 1978; 85:154–9.

40. Hayreh SS, Zimmerman MB, Podhaj sky P, Alward WL. Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders. Am J Ophthalmol. 1994; 117:603–24.

41. Seo HR, Ryu WY, Rho SH. Corrlelation between nocturnal dip and progression of glaucoma. J Korean Ophthalmol Soc. 2010; 51:1471–8.

42. Hayreh SS. In vivo choroidal circulation and its watershed zones. Eye (Lond). 1990; 4:273–89.

43. Hayreh SS. Segmental nature of the choroidal vasculature. Br J Ophthalmol. 1975; 59:631–48.

44. Hayreh SS. Inter-individual variation in blood supply of the optic nerve head. Its importance in various ischemic disorders of the optic nerve head, and glaucoma, low-tension glaucoma and allied disorders. Doc Ophthalmol. 1985; 59:217–46.

45. Hayreh SS. Posterior ciliary artery circulation in health and disease: the Weisenfeld lecture. Invest Ophthalmol Vis Sci. 2004; 45:749–57.

46. Hayreh SS, Ritch R, Shield MB, Krupin T. Blood supply of the anterior optic nerve. The glaucomas. St. Louis: C.V Mosby;1989. p. 133–61.

47. Huang P, Shi Y, Wang X, et al. Interocular Asymmetry of the Visual Field Defects in Newly Diagnosed Normal-tension Glaucoma, Primary Open-angle Glaucoma, and Chronic Angle-closure Glaucoma. J Glaucoma. 2013; Apr 29 [Epub ahead of print].

48. Aoyama A, Ishida K, Sawada A, Yamamoto T. Target intraocular pressure for stability of visual field loss progression in normal-tension glaucoma. Jpn J Ophthalmol. 2010; 54:117–23.

49. The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma. Collaborative Normal-Tension Glaucoma Study Group. Am J ophthalmol. 1998; 126:498–505.

50. Advanced Glaucoma Intervention Study. 2. Visual field test scoring and reliability. Ophthalmology. 1994; 101:1445–55.

51. Kim J, Dally LG, Ederer F, et al. The Advanced Glaucoma Intervention Study (AGIS): 14. Distinguishing progression of glaucoma from visual field fluctuations. Ophthalmology. 2004; 111:2109–16.

52. Wilkins MR, Fitzke FW, Khaw PT. Pointwise linear progression criteria and the detection of visual field change in a glaucoma trial. Eye (Lond). 2006; 20:98–106.

53. Zheng L, Sun Z, Li J, et al. Pulse pressure and mean arterial pressure in relation to ischemic stroke among patients with uncontrolled hypertension in rural areas of China. Stroke. 2008; 39:1932–7.

54. Plange N, Kaup M, Daneljan L, et al. 24-h blood pressure monitoring in normal tension glaucoma: night-time blood pressure variability. J Hum Hypertens. 2006; 20:137–42.

55. Graham SL, Drance SM, Wijsman K, et al. Ambulatory blood pressure monitoring in glaucoma. The nocturnal dip. Ophthalmology. 1995; 102:61–9.

56. Hirotsu C, Ohta E, Hirose N, Shimizu K. Profile analysis of 24-hours measurements of blood pressure. Biometrics. 2003; 59:907–15.

57. Choi J, Jeong J, Cho H, Kook MS. Effect of nocturnal blood pressure reduction on circadian fluctuation of mean ocular perfusion pressure: a risk factor for normal tension glaucoma. Invest Ophthalmol Vis Sci. 2006; 47:831–6.

58. Collignon N, Dewe W, Guillaume S, Collignon-Brach J. Ambulatory blood pressure monitoring in glaucoma patients. The nocturnal systolic dip and its relationship with disease progression. Int Ophthalmol. 1998; 22:19–25.

59. Hayreh SS. The blood supply of the optic nerve head and the evaluation of it - myth and reality. Prog Retin Eye Res. 2001; 20:563–93.

60. Gherghel D, Orgul S, Gugleta K, et al. Relationship between ocular perfusion pressure and retrobulbar blood flow in patients with glaucoma with progressive damage. Am J Ophthalmol. 2000; 130:597–605.

61. Sehi M, Flanagan JG, Zeng L, et al. Relative change in diurnal mean ocular perfusion pressure: a risk factor for the diagnosis of primary open-angle glaucoma. Invest Ophthalmol Vis Sci. 2005; 46:561–7.

62. Hayreh SS. Duke-elder lecture. Systemic arterial blood pressure and the eye. Eye (Lond). 1996; 10:5–28.

63. Harris A, Rechtman E, Siesky B, et al. The role of optic nerve blood flow in the pathogenesis of glaucoma. Ophthalmol Clin North Am. 2005; 18:345–53.

64. Xu W, Grunwald JE, Metelitsina TI, et al. Association of risk factors for choroidal neovascularization in age-related macular degeneration with decreased foveolar choroidal circulation. Am J Ophthalmol. 2010; 150:40–7.

65. Singh S, Dass R. The central artery of the retina. I. Origin and course. Br J Ophthalmol. 1960; 44:193–212.

66. Singh S, Dass R. The central artery of the retina. II. A study of its distribution and anastomosis. Br J Ophthalmol. 1960; 44:280–99.

67. Giuffre G. Main posterior watershed zone of the choroid. Variations of its position in normal subjects. Doc Ophthalmol. 1989; 72:175–80.

68. Onda E, Sato Y, Takahashi S, et al. Angiographic evaluation of watershed zone in the peripapillary choroid in glaucoma and non-glaucoma eyes. Invest Ophthalmol Vis Sci. 1996; 37:267.

69. Onda E, Cioffi GA, Bacon DR, van Buskirk EM. Microvasculature of the human optic nerve. Am J Ophthalmol. 1995; 120:92–102.

70. Sato Y1, Tomita G, Onda E, et al. Association between watershed zone and visual field defect in normal tension glaucoma. Jpn J Ophthalmol. 2000; 44:39–45.