Abstract
Purpose
To investigate the effect of nocturnal dip influence on the progression of glaucomatous visual field defect.
Methods
We performed 24hr ABPM and V/F tests on patients diagnosed with NTG (140 patients, 280 eyes) and POAG (84 patients, 168 eyes). Nocturnal dips below 10% were classified as non-dippers, and those above 10% were noted as dippers. The correlations among nocturnal dip, progression of glaucomatous visual field defect, and hypertension treatment were examined.
Results
In NTG, dippers in both systolic and diastolic blood pressure furthered glaucomatous visual field defects, with a relative risk of approximately three times that of non-dippers. Hypertension treatment was not influenced by the progression of glaucomatous visual field defect but was influenced by dips in the systolic and diastolic pressures in NTG and in diastolic pressure in POAG. Nocturnal dips were more frequent in the group with progression of the visual field compared to those in the group with non-progression of the visual field in NTG.
Conclusions
Dipper caused a progression of glaucomatous visual field defects in NTG and was influenced by hypertension treatment in NTG and POAG. Performing 24hr ABPM should be helpful for glaucoma patients with progression of a glaucomatous visual field defect even when the IOP is less than the target pressure. In addition, hypertension treatment should be considered an important factor in the treatment of glaucoma.
References
2. Levene RZ. Low tension glaucoma: a critical review and new material. Surv Ophthalmol. 1980; 24:621–64.
3. Flammer J, Orgul S. Optic nerve blood-flow abnormalities in glaucoma. Prog Retin Eye Res. 1998; 17:267–89.
4. Leske MC, Heijl A, Hussein M, et al. Early Manifest Glaucoma Trial Group. Factors for glaucoma progression and the effect of treatment: the early manifest glaucoma trial. Arch Ophthalmol. 2003; 121:48–56.
5. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol. 1998; 126:487–97.
6. Lichter PR, Musch DC, Gillespie BW, et al. CIGTS Study Group. Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology. 2001; 108:1943–53.
7. The Advanced Glaucoma Intervention Study Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000; 130:429–40.
9. Mcleod SD, West SK, Quigley HA, Fozard JL. A longitudinal study of the relationship between intraocular and blood pressure. Invest Ophthalmol Vis Sci. 1990; 31:2361–6.
10. Bonomi L, Marchini G, Marraffa M, et al. Vascular risk factor for primary open angle glaucoma: The Egna-Neumarkt Study. Ophthalmology. 2000; 107:1287–93.
11. 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.
12. Gasser P, Flammer J. Blood-cell velocity in the nailfold capillaries of patients with normal-tension and high-tension glaucoma. Am J Ophthalmol. 1991; 111:585–8.
13. Pradalier A, Hamard P, Sellem E, Bringer L. Migraine and glaucoma: an epidemiologic survey of French ophthalmologists. Cephalalgia. 1998; 18:74–6.
15. Leske MC. Ocular perfusion pressure and glaucoma: clinical trial and epidemiologic findings. Curr Opin Ophthalmol. 2009; 20:73–8.
16. Hayreh SS. Progress in the understanding of the vascular etiology of glaucoma. Curr Opin Ophthalmol. 1994; 5:26–35.
17. Flammer J, Orgül S, Costa VP, et al. The impact of ocular blood flow in glaucoma. Prog Retin Eye Res. 2002; 21:359–393.
18. Kaiser HJ, Schoetzau A, Stümpfig D, Flammer J. Blood-flow ve-locities of the extraocular vessels in patients with high-tension and normal-tension primary open-angle glaucoma. Am J Ophthalmol. 1997; 123:320–7.
19. 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.
20. 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.
21. Gherghel D, Orgül 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.
22. 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; 46:561–6.
23. Hayreh SS. Duke-elder Lecture. Systemic arterial blood pressure and the eye. Eye. 1996; 10:5–28.
24. Millar-Craig MW, Bishop CN, Raftery EB. Circadian variation of blood pressure. Lancet. 1978; 1:795–7.
25. Pickering T. Recommendation for use of home (self) and ambulatory blood-pressure monitoring. Am J Hypertens. 1996; 9:1–11.
26. Joe SG, Park SB, Kook MS, et al. Twenty-four hour blood pressure pattern in patients with normal tension glaucoma in the habitual position. Korean J Ophthalmol. 2009; 23:32–9.
27. Osusky R, Rohr P, Schotzau A, Flammer J. Nocturnal dip in the optic nerve head perfusion. Jpn J Ophthalmol. 2000; 44:128–31.
28. Mozaffarieh M, Grieshaber MC, Flammer J. Oxygen and blood flow: players in the pathogenesis of glaucoma. Molecular Vision. 2008; 14:224–33. sure reduction on circadian fluctuation of mean ocular perfusion pressure: a risk factor for normal tension glaucoma. Invest Ophthalmol Vis Sci 2006;47:831–6.
30. Choi J, Kim KH, Jeong J, et al. Circadian fluctuation of mean ocular perfusion pressure is a consistent risk factor for normal tension glaucoma. Invest Ophthalmol Vis Sci. 2007; 48:104–11.
31. 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.
32. Graham SL, Drance SM, Wijsman K, et al. Ambulatory blood pressure monitoring in glaucoma. The nocturnal dip. Ophthalmology. 1995; 102:61–9.
33. Hirotsu C, Ohta E, Hirose N, Shimizu K. Profile analysis of 24-hours measurements of blood pressure. Biometrics. 2003; 59:907–15.
34. 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.
35. The Advanced Glaucoma Intervention Study Investigators. Advanced Glaucoma Intervention Study. 2. Visual field test scoring and reliability. Ophthalmology. 1994; 101:1445–55.
36. Kim J, Dally LG, Ederer F, et al. The Advanced Glaucoma Intervention Study Investigators. The Advanced Glaucoma Intervention Study (AGIS): 14. Distinguishing progression of glaucoma from visual field fluctuations. Ophthalmology. 2004; 111:2109–16.
37. Deokule S, Weinreb RN. Relationships among systemic blood pressure, intraocular pressure, and open-angle glaucoma. Can J Ophthalmol. 2008; 43:302–7.
38. Leske MC, Heijl A, Hyman L, et al. EMGT Group. Predictors of long-term progression in the early manifest glaucoma trial. Ophthalmology. 2007; 114:1965–72.
39. Leske MC, Wu SY, Hennis A, et al. BESs Study Group. Risk factors for incident open-angle glaucoma: the Barbados Eye Studies. Ophthalmology. 2008; 115:85–93.
40. Leske MC, Wu SY, Nemesure B, Hennis A. Incident open-angle glaucoma and blood pressure. Arch Ophthalmol. 2002; 120:954–9.
41. Tielsch JM, Katz J, Sommer A, et al. Hypertension, perfusion pressure, and primary open-angle glaucoma. A population-based assessment. Arch Ophthalmol. 1995; 113:216–21.
42. Punjabi OS, Stamper RL, Bostrom AG, Lin SC. Does treated systemic hypertension affect progression of optic nerve damage in glaucoma suspects? Curr Eye Res. 2007; 32:153–160.
43. Topouzis F, Coleman AL, Harris A, et al. Association of blood pressure status with the optic disc structure in nonglaucoma subjects: the Thessaloniki Eye Study. Am J Ophthalmol. 2006; 142:60–7.
44. Hulsman CA, Vingerling JR, Hofman A, et al. Blood pressure, arterial stiffness, and open-angle glaucoma: the Rotterdam study. Arch Ophthalmol. 2007; 125:805–12.
45. Riccadonna M, Covi G, Pancera P, et al. Autonomic system activity and 24-hour blood pressure variations in subjects with normal- and high-tension glaucoma. J Glaucoma. 2003; 12:156–63.
46. Yazici B, Usta E, Erturk H, Dilek K. Comparison of ambulatory blood pressure values in patients with glaucoma and ocular hypertension. Eye. 2003; 17:593–8.
47. Tokunaga T, Kashiwagi K, Tsumura T, et al. Association between nocturnal blood pressure reduction and progression of visual field defect in patients with primary open-angle glaucoma or normal tension glaucoma. Jpn J Ophthalmol. 2004; 48:380–5.
48. Graham SL, Drance SM. Nocturnal hypotension role in glaucoma progression. Surv Ophthalmol. 1999; 43:S10–6.
49. Kashiwagi K, Hosaka O, Kashiwagi F, et al. Systemic circulatory parameters: comparison between patients with normal tension glaucoma and normal subjects using ambulatory monitoring. Jpn J Ophthalmol. 2001; 45:388–96.
50. Kida T, Liu JHK, Weinreb RN. Effect of aging on nocturnal blood flow in optic nerve head and macula in healthy human eyes. J Glaucoma. 2008; 17:366–71.
51. Gherghel D, Orgül S, Gugleta K, Flammer J. Retrobulbar blood flow in glaucoma patients with nocturnal over-dipping in systemic blood pressure. Am J Ophthalmol. 2001; 132:641–7.
52. Fuchsjäger-Mayrl G, Wally B, Georgopoulos M, et al. Ocular blood flow and systemic blood pressure in patients with primary open-angle glaucoma and ocular hypertension. Invest Ophthalmol Vis Sci. 2004; 45:834–9.
53. Emre M, Orgül S, Gugleta K, Flammer J. Ocular blood flow alteration in glaucoma is related to systemic vascular dysregulation. Br J Ophthalmol. 2004; 88:662–6.
54. Hennis A, Wu SY, Nemesure B, Leske MC. Barbados Eye Studies Group. Hypertension, diabetes, and longitudinal changes in intraocular pressure. Ophthalmology. 2003; 110:908–14.
55. Girkin CA, Kannel WB, Friedman DS, Weinreb RN. Glaucoma risk factor assessment and prevention: lessons from coronary heart disease. Am J Ophthalmol. 2004; 138:S11–8.
56. Grieshaber MC, Mozaffarieh M, Flammer J. What is the link between vascular dysregulation and glaucoma? Surv Ophthalmol. 2007; 52:S144–54.
57. von Känel R, Jain S, Mills PJ, et al. Relation of nocturnal blood pressure dipping to cellular adhesion, inflammation and hemo-stasis. J Hypertens. 2004; 22:2087–93.
Table 1.
| NTG | POAG | p value |
---|---|---|---|
M: F (n) | 114: 166 | 92: 76 | 0.479* |
Mean age (yrs) | 56.17 ± 14.84 | 58.23 ± 13.89 | 0.676† |
Mean IOP (mmHg) | 12.98 ± 2.47 | 14.31 ± 3.50 | 0.244† |
Mean deviation of visual field (dB) | −4.18 ± 5.25 | −8.43 ± 8.74 | 0.128† |
Mean SBP (mmHg) | 115.95 ± 11.02 | 120.63 ± 13.24 | 0.481† |
Mean DBP (mmHg) | 72.94 ± 7.36 | 76.37 ± 10.22 | 0.278† |
Mean nocturnal dip of SBP (%) | 7.98 ± 5.54 | 8.41 ± 6.17 | 0.118† |
Mean nocturnal dip of DBP (%) | 8.89 ± 6.93 | 9.22 ± 7.16 | 0.180† |
Hypertension (n) | 112 | 61 | 0.374* |
Mean period of hypertension medication (yrs) | 7.33 ± 4.28 | 7.03 ± 3.47 | 0.614† |
Table 2.
|
V/F progression |
Chi-square test |
|||
---|---|---|---|---|---|
Yes | No | p value* | Odd ratio | Relative risk | |
SBP in NTG | | | <0.000 | | |
Dipper | 27 | 67 | | 4.951 | 3.816 |
Non-dipper | 14 | 172 | | (CI†: 2.448∼10.015) | (CI†: 2.103∼6.925) |
DBP in NTG | | | 0.002 | | |
Dipper | 30 | 112 | | 3.093 | 2.650 |
Non-dipper | 11 | 127 | | (CI†: 1.481∼6.456) | (CI†: 1.384∼5.077) |
SBP in POAG | | | 0.116 | | |
Dipper | 11 | 51 | | 2.071 | 1.881 |
Non-dipper | 10 | 96 | | (CI†: 0.824∼5.202) | (CI†: 0.848∼4.173) |
DBP in POAG | | | 0.128 | | |
Dipper | 13 | 65 | | 2.050 | 1.875 |
Non-dipper | 8 | 82 | | (CI†: 0.802∼5.242) | (CI†: 0.82∼4.287) |
Table 3.
|
V/F progression |
Chi-square test |
|||
---|---|---|---|---|---|
Yes | No | p value* | Odd ratio | Relative risk | |
NTG | | | 0.112 | | |
HTN Treatment group | 21 | 91 | | 1.708 | 1.575 |
Normal BP group | 20 | 148 | | (CI†: 0.878∼3.323) | (CI†: 0.896∼2.768) |
POAG | | | 0.249 | | |
HTN Treatment group | 10 | 51 | | 1.711 | 1.595 |
Normal BP group | 11 | 96 | | (CI†: 0.681∼4.299) | (CI†: 0.719∼3.537) |
Table 4.
|
Dipper |
Chi-square test |
|||
---|---|---|---|---|---|
Yes | No | p value* | Odd ratio | Relative risk | |
SBP in NTG | | | 0.001 | | |
HTN treatment group | 51 | 61 | | 2.430 | 1.779 |
Normal BP group | 43 | 125 | | (CI†: 1.462∼4.040) | (CI†: 1.282∼2.469) |
DBP in NTG | | | <0.000 | | |
HTN treatment group | 80 | 32 | | 10.625 | 3.750 |
Normal BP group | 62 | 106 | | (CI†: 6.054∼18.647) | (CI†: 2.688∼5.232) |
SBP in POAG | | | 0.068 | | |
HTN treatment group | 28 | 33 | | 1.822 | 1.445 |
Normal BP group | 34 | 73 | | (CI†: 0.953∼3.481) | (CI†: 0.979∼2.131) |
DBP in POAG | | | <0.000 | | |
HTN treatment group | 33 | 28 | | 3.170 | 1.996 |
Normal BP group | 45 | 62 | | (CI†: 1.639∼6.132) | (CI†: 1.355∼2.940) |
Table 5.
|
The mean of nocturnal dip (%) |
The mean of blood pressure (mmHg) |
||||
---|---|---|---|---|---|---|
V/F progression |
p value* |
V/F progression |
p value* | |||
Yes | No | Yes | No | |||
SBP in NTG | | | 0.001 | | | 0.392 |
Dipper | 15.66 ± 4.02 | 13.21 ± 2.70 | | 118.27 ± 11.05 | 121.28 ± 10.77 | |
Non-dipper | 3.63 ± 5.42 | 5.10 ± 3.55 | | 115.28 ± 10.93 | 113.56 ± 10.38 | |
DBP in NTG | | | <0.000 | | | 0.245 |
Dipper | 16.57 ± 4.23 | 14.07 ± 3.30 | | 73.84 ± 8.11 | 74.40 ± 7.15 | |
Non-dipper | 1.81 ± 3.54 | 3.11 ± 3.94 | | 75.11 ± 8.69 | 71.25 ± 6.97 | |
SBP in POAG | | | 0.144 | | | 0.175 |
Dipper | 18.03 ± 5.23 | 13.93 ± 3.45 | | 122.30 ± 8.51 | 123.15 ± 19.10 | |
Non-dipper | 3.25 ± 3.06 | 4.91 ± 3.84 | | 126.51 ± 11.88 | 118.49 ± 9.11 | |
DBP in POAG | | | 0.104 | | | 0.139 |
Dipper | 18.03 ± 5.48 | 14.90 ± 3.71 | | 81.25 ± 3.16 | 79.55 ± 11.74 | |
Non-dipper | 2.75 ± 3.24 | 3.95 ± 4.35 | | 76.55 ± 10.44 | 73.07 ± 8.52 | |