Retrobulbar blood flow in glaucoma patients with nocturnal over-dipping in systemic blood pressure

doi:10.1016/S0002-9394(01)01193-X

American Journal of Ophthalmology

Volume 132, Issue 5, November 2001, Pages 641-647

https://doi.org/10.1016/S0002-9394(01)01193-X Get rights and content

Abstract

PURPOSE: To evaluate the relationship between the circadian blood pressure rhythm and the retrobulbar blood flow in glaucoma patients.

DESIGN: Cross-sectional study.

METHODS: Circadian blood pressure measurements and color Doppler imaging (CDI) in the ophthalmic artery as well as the central retinal artery of one randomly selected eye were obtained in 193 primary open-angle glaucoma patients. CDI parameters were compared by means of analysis of covariance between patients with a nocturnal decrease in mean systemic blood pressure (MBP) below 20% of the average daytime MBP (over-dippers), patients with a decrease between 10% to 20% (dippers), and patients with a decrease of less than 10% (nondippers), using age, intraocular pressure (IOP), and MBP during color Doppler measurement as covariates.

RESULTS: An analysis of covariance disclosed, after correcting for age, IOP, and MBP during color Doppler imaging, a significantly lower EDV (P = .0096) and a significantly higher RI (P = .033) in the central artery of over-dipping glaucoma patients compared with nondippers or dippers. This effect seemed independent of the use of vasoactive drugs.

CONCLUSIONS: Glaucoma patients with a marked drop in nocturnal systemic blood pressure seem to have altered retrobulbar blood flow parameters, suggesting that an abnormal systemic blood pressure profile may be the manifestation of some kind of systemic vascular dysregulation relevant for the ocular circulation.

Section snippets

Patients and methods

We evaluated 193 consecutive patients (115 women and 78 men) with primary open-angle glaucoma (mean ±SD age: 67.34 ± 14.54 years) in a cross-sectional study during the period between 1996 to 1999. All procedures conformed to the Declaration of Helsinki. Patients with closed iridocorneal angles, evidence of secondary glaucoma, pseudoexfoliation, pigmentary dispersion, a history of intraocular surgery, any form of retinal or neuroophthalmologic disease that could result in visual field defects,

Results

The characteristics of the study patients and p-values before correction for multiple comparison are given in Table 1 (the latter p-values are provided here for the sake of completeness). There were no statistically significant differences between groups in age, visual field defect, and average diurnal IOP (Table 1). Although significant differences were observed in systemic blood pressure (Table 1), blood pressure during the CDI procedure, or average day-time blood pressure levels, did not

Discussion

Circadian blood pressure measurements and color Doppler imaging in the ophthalmic artery and the central retinal artery of one randomly selected eye were obtained in 193 primary open-angle glaucoma patients. After correcting for age, intraocular pressure, and mean blood pressure during retrobulbar blood flow measurements, a lower end diastolic velocity and a higher resistivity index were found in the central retinal artery of glaucoma patients showing a decrease in mean blood pressure during

References (35)

M.T Nicolela et al.
Color Doppler imaging in patients with asymmetric glaucoma and unilateral visual field loss
Am J Ophthalmol
(1996)
H.J Kaiser et al.
Blood-flow velocities of the extraocular vessels in patients with high-tension and normal-tension primary open-angle glaucoma
Am J Ophthalmol
(1997)
O Findl et al.
Assessment of optic disk blood flow in patients with open-angle glaucoma
Am J Ophthalmol
(2000)
D.R Anderson
Introductory comments on blood flow autoregulation in the optic nerve head and vascular risk factors in glaucoma
Surv Ophthalmol
(1999)
D Gherghel et al.
Relationship between ocular perfusion pressure and retrobulbar blood flow in patients with glaucoma with progressive damage
Am J Ophthalmol
(2000)
S.S Hayreh et al.
Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders
Am J Ophthalmol
(1994)
S.L Graham et al.
Ambulatory blood pressure monitoring in glaucoma. The nocturnal dip
Ophthalmology
(1995)
J.A Staessen et al.
Mean and range of the ambulatory pressure in normotensive subjects from a meta-analysis of 23 studies
Am J Cardiol
(1991)
S.D Pierdomenico et al.
Circadian blood pressure changes and myocardial ischemia in hypertensive patients with coronary artery disease
J Am Coll Cardiol
(1998)
S.S Hayreh et al.
Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders
Am J Ophthalmol
(1994)

J Flammer et al.

Optic nerve blood-flow abnormalities in glaucoma

Prog Ret Eye Res

(1998)

H.J Kaiser et al.

Blood-flow velocities in the extraocular vessels in normal volunteers

Am J Ophthalmol

(1996)

J.S Floras

Antihypertensive treatment, myocardial infarction, and nocturnal myocardial ischemia

Lancet

(1988)

S.L Graham et al.

Nocturnal hypotensionrole in glaucoma progression

Surv Ophthalmol

(1999)

Y Yamazaki et al.

The relationship between progression of visual field defects and retrobulbar circulation in patients with glaucoma

Am J Ophthalmol

(1997)

J Schumann et al.

Interocular difference in progression of glaucoma correlates with interocular differences in retrobulbar circulation

Am J Ophthalmol

(2000)

P Rojanapongpun et al.

Ophthalmic artery flow velocity in glaucomatous and normal subjects

Br J Ophthalmol

(1993)

Cited by (67)

Is “normal tension glaucoma” glaucoma?
2019, Medical Hypotheses
Citation Excerpt :
Studies also reported that the retinal vessels of the optic nerve head were less shifted to the nasal side in a number of patients with either Flammer syndrome or NTG [31]. Thus, Flammer syndrome induce GON in NTG cases mainly due to low blood pressure, increased retinal venous pressure and improper autoregulation, resulting in ocular blood flow (OBF) instability [15,32]. (2) Migraine is the most well-known vasospastic clinical entity, and a number of investigations reported that the migraine was associated with NTG.
Primary open angle glaucoma (POAG) represents a distinct disease entity with elevated intraocular pressure (IOP) as the main risk factor, even though the reasons for why the IOP is elevated remains to be elucidated. It is considered that normal tension glaucoma (NTG) is a subtype of POAG, comprising a special form of glaucomatous neurodegeneration or glaucomatous optic neuropathy (GON) almost exactly the same as that seen in POAG, but the IOP, as named, remains in the statistically normal range. Actually the disease entity of NTG has been a profound confusion and it is difficult to be accurately conceptualized. One of the reasons is that the IOP is closely linked to the occurrence of GON in POAG but not in NTG, and for the latter, it seems that GON is secondary to a number of local or systemic disorders. In recent years, increasing evidences suggest that NTG or IOP independent GON is a non-glaucomatous disease with different disease entities from POAG and with more diverse and complex etiologies. Here we hypothesized that NTG, at least for those with recognizable primary diseases, is not a glaucomatous disease; instead, it represents a group of disorders with GON as a characteristic clinical feature or phenotype.
Vascular factors in glaucoma
2015, Journal Francais d'Ophtalmologie
La physiopathologie exacte du glaucome n’est pas parfaitement élucidée. La compréhension de la physiopathogénie vasculaire du glaucome nécessite : de bien connaître les techniques de mesure du flux sanguin oculaire, et de caractériser la topographie de l’atteinte vasculaire et les mécanismes impliqués dans cette neuropathie. Une diminution de la pression de perfusion moyenne et une perte de l’autorégulation vasculaire sont incriminées dans la pathologie glaucomateuse. Une diminution précoce du flux sanguin oculaire, contribuant à la progression de la neuropathie optique, a été identifiée dans le glaucome primitif à angle ouvert et dans le glaucome à pression normale. L’atteinte vasculaire associée au glaucome est présente dans les différents lits vasculaires oculaires (de l’artère ophtalmique jusqu’à la rétine) et se caractérise par une diminution du flux sanguin basal associée à un dysfonctionnement de la vasorégulation.
The exact pathophysiology of glaucoma is not fully understood. Understanding of the vascular pathophysiology of glaucoma requires: knowing the techniques for measuring ocular blood flow and characterizing the topography of vascular disease and the mechanisms involved in this neuropathy. A decreased mean ocular perfusion pressure and a loss of vascular autoregulation are implicated in glaucomatous disease. Early decrease in ocular blood flow has been identified in primary open-angle glaucoma and normal pressure glaucoma, contributing to the progression of optic neuropathy. The vascular damage associated with glaucoma is present in various vascular territories within the eye (from the ophthalmic artery to the retina) and is characterized by a decrease in basal blood flow associated with a dysfunction of vasoregulation.
Calcium channels and their blockers in intraocular pressure and glaucoma
2014, European Journal of Pharmacology
Citation Excerpt :
Among various IOP-independent factors assumed to be associated with glaucoma, impaired ocular perfusion is probably the only factor for which the contribution to POAG incidence and/or progression was confirmed by population-based or prospective cohort studies (Bonomi et al., 2000; Leske et al., 1995; Leske et al., 2007, 2008, 2001; Tielsch et al., 1995). Ocular circulation is impaired in glaucoma and ocular hypertension patients (Ciancaglini et al., 2001; Evans et al., 1999; Galassi et al., 2003; Gherghel et al., 2001; Liu et al., 1999; Yaoeda et al., 2003) and compromised local circulation is probably correlated with visual field deterioration (Satilmis et al., 2003; Schumann et al., 2000; Yamazaki and Drance, 1997). Thus, improvement of local ocular circulation may be beneficial in the treatment of glaucomatous optic neuropathy.
Several factors besides high intraocular pressure assumed to be associated with the development and progression of glaucoma, and calcium channel blockers (CCBs) have been an anticipated option for glaucoma treatment by improving ocular perfusion and/or exerting neuroprotective effects on retinal ganglion cells with safety established in wide and long-term usage. Decrease in IOP has been reported after topical application of CCBs, however, the effect is much smaller and almost negligible after systemic application. Various CCBs have been reported to increase posterior ocular blood flow in vivo and to exert direct neuroprotection in neurons in vitro. Distribution of the drug at a pharmacologically active concentration in the posterior ocular tissues across the blood–brain barrier or blood–retina barrier, especially in the optic nerve head and retina where the ganglion cells mainly suffer from glaucomatous damage, is essential for clinical treatment of glaucoma. Improved visual functions such as sensitivity in the visual field test have been reported after administration of CCBs, but evidences from the randomized studies have been limited and effects of CCBs on blood flow and direct neuroprotection are hardly distinguished from each other.
The Correlation of Body Mass Index to the Level of Intraocular Pressure in Non-Glaucomatous Iraqi Subjects
2024, Oftalmologija. Vostochnaja Evropa
Optical coherence tomography and optical coherence tomography angiography: essential tools for detecting glaucoma and disease progression
2023, Frontiers in Ophthalmology
Treatment of glaucoma patients with flammer syndrome
2021, Journal of Clinical Medicine

View all citing articles on Scopus

^☆: Supported by a grant of the Swiss National Foundation (32-059094.99).

View full text

Retrobulbar blood flow in glaucoma patients with nocturnal over-dipping in systemic blood pressure☆

Abstract

Section snippets

Patients and methods

Results

Discussion

Am J Ophthalmol

Am J Ophthalmol

Am J Ophthalmol

Surv Ophthalmol

Am J Ophthalmol

Am J Ophthalmol

Ophthalmology

Am J Cardiol

J Am Coll Cardiol

Am J Ophthalmol

Prog Ret Eye Res

Am J Ophthalmol

Lancet

Surv Ophthalmol

Am J Ophthalmol

Am J Ophthalmol

Ophthalmic artery flow velocity in glaucomatous and normal subjects

Br J Ophthalmol