Vascular aspects in the pathophysiology of glaucomatous optic neuropathy

Hak Sung Chung, Alon Harris, David W. Evans, Larry Kagemann, Hanna J. Garzozi, Bruce Martin

Research output: Contribution to journalArticle

155 Citations (Scopus)

Abstract

Glaucoma remains a major eye illness with unknown etiology. Although elevated intraocular pressure is clearly a major risk factor, vascular deficits may contribute to initiation and progression of glaucoma. When intraocular pressure is acutely elevated in healthy individuals, the resistance index (derived from the peak systolic and end-diastolic velocities and an indirect index of vascular resistance distal to the site of measurement) in the central retinal and posterior ciliary arteries increases progressively. This result implies that mechanical and vascular factors may be coupled in such a way that perfusion of the retina and optic nerve head may be influenced by changes in the intraocular pressure. Further, at night, when ophthalmic artery flow velocities fall as arterial blood pressure falls in glaucoma patients, the risk of disease progression may be increased. The constancy of these same flow velocities in age-matched healthy individuals points to a possible vascular autoregulatory defect in glaucoma. In addition, in normal-tension glaucoma, vasodilation (CO2 inhalation) normalizes retrobulbar arterial flow velocities, hinting that some vascular deficits in glaucoma may be reversible. Finally, Ca2+ channel blockade improves contrast sensitivity in patients with normal-tension glaucoma, who also show increased retrobulbar vessel flow velocities, a result suggesting that visual function loss may be linked to ocular ischemia. Emerging evidence points to a role of ischemia in the pathogenesis of glaucoma, suggesting that treatments designed to improve ocular blood flow may benefit glaucoma patients.

Original languageEnglish
JournalSurvey of Ophthalmology
Volume43
Issue number6 SUPPL.
DOIs
StatePublished - Jun 1999

Fingerprint

Optic Nerve Diseases
Glaucoma
Blood Vessels
Intraocular Pressure
Low Tension Glaucoma
Ischemia
Ciliary Arteries
Ophthalmic Artery
Contrast Sensitivity
Optic Disk
Vasodilation
Vascular Resistance
Inhalation
Disease Progression
Retina
Arterial Pressure
Perfusion

Keywords

  • Autoregulation
  • Ca channel blocker
  • Intraocular pressure
  • Ischemia
  • Nocturnal ocular blood flow
  • Vasospasm

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Vascular aspects in the pathophysiology of glaucomatous optic neuropathy. / Chung, Hak Sung; Harris, Alon; Evans, David W.; Kagemann, Larry; Garzozi, Hanna J.; Martin, Bruce.

In: Survey of Ophthalmology, Vol. 43, No. 6 SUPPL., 06.1999.

Research output: Contribution to journalArticle

Chung, Hak Sung ; Harris, Alon ; Evans, David W. ; Kagemann, Larry ; Garzozi, Hanna J. ; Martin, Bruce. / Vascular aspects in the pathophysiology of glaucomatous optic neuropathy. In: Survey of Ophthalmology. 1999 ; Vol. 43, No. 6 SUPPL.
@article{0e1e42f446ad4adc912de4a361bb8664,
title = "Vascular aspects in the pathophysiology of glaucomatous optic neuropathy",
abstract = "Glaucoma remains a major eye illness with unknown etiology. Although elevated intraocular pressure is clearly a major risk factor, vascular deficits may contribute to initiation and progression of glaucoma. When intraocular pressure is acutely elevated in healthy individuals, the resistance index (derived from the peak systolic and end-diastolic velocities and an indirect index of vascular resistance distal to the site of measurement) in the central retinal and posterior ciliary arteries increases progressively. This result implies that mechanical and vascular factors may be coupled in such a way that perfusion of the retina and optic nerve head may be influenced by changes in the intraocular pressure. Further, at night, when ophthalmic artery flow velocities fall as arterial blood pressure falls in glaucoma patients, the risk of disease progression may be increased. The constancy of these same flow velocities in age-matched healthy individuals points to a possible vascular autoregulatory defect in glaucoma. In addition, in normal-tension glaucoma, vasodilation (CO2 inhalation) normalizes retrobulbar arterial flow velocities, hinting that some vascular deficits in glaucoma may be reversible. Finally, Ca2+ channel blockade improves contrast sensitivity in patients with normal-tension glaucoma, who also show increased retrobulbar vessel flow velocities, a result suggesting that visual function loss may be linked to ocular ischemia. Emerging evidence points to a role of ischemia in the pathogenesis of glaucoma, suggesting that treatments designed to improve ocular blood flow may benefit glaucoma patients.",
keywords = "Autoregulation, Ca channel blocker, Intraocular pressure, Ischemia, Nocturnal ocular blood flow, Vasospasm",
author = "Chung, {Hak Sung} and Alon Harris and Evans, {David W.} and Larry Kagemann and Garzozi, {Hanna J.} and Bruce Martin",
year = "1999",
month = "6",
doi = "10.1016/S0039-6257(99)00050-8",
language = "English",
volume = "43",
journal = "Survey of Ophthalmology",
issn = "0039-6257",
publisher = "Elsevier USA",
number = "6 SUPPL.",

}

TY - JOUR

T1 - Vascular aspects in the pathophysiology of glaucomatous optic neuropathy

AU - Chung, Hak Sung

AU - Harris, Alon

AU - Evans, David W.

AU - Kagemann, Larry

AU - Garzozi, Hanna J.

AU - Martin, Bruce

PY - 1999/6

Y1 - 1999/6

N2 - Glaucoma remains a major eye illness with unknown etiology. Although elevated intraocular pressure is clearly a major risk factor, vascular deficits may contribute to initiation and progression of glaucoma. When intraocular pressure is acutely elevated in healthy individuals, the resistance index (derived from the peak systolic and end-diastolic velocities and an indirect index of vascular resistance distal to the site of measurement) in the central retinal and posterior ciliary arteries increases progressively. This result implies that mechanical and vascular factors may be coupled in such a way that perfusion of the retina and optic nerve head may be influenced by changes in the intraocular pressure. Further, at night, when ophthalmic artery flow velocities fall as arterial blood pressure falls in glaucoma patients, the risk of disease progression may be increased. The constancy of these same flow velocities in age-matched healthy individuals points to a possible vascular autoregulatory defect in glaucoma. In addition, in normal-tension glaucoma, vasodilation (CO2 inhalation) normalizes retrobulbar arterial flow velocities, hinting that some vascular deficits in glaucoma may be reversible. Finally, Ca2+ channel blockade improves contrast sensitivity in patients with normal-tension glaucoma, who also show increased retrobulbar vessel flow velocities, a result suggesting that visual function loss may be linked to ocular ischemia. Emerging evidence points to a role of ischemia in the pathogenesis of glaucoma, suggesting that treatments designed to improve ocular blood flow may benefit glaucoma patients.

AB - Glaucoma remains a major eye illness with unknown etiology. Although elevated intraocular pressure is clearly a major risk factor, vascular deficits may contribute to initiation and progression of glaucoma. When intraocular pressure is acutely elevated in healthy individuals, the resistance index (derived from the peak systolic and end-diastolic velocities and an indirect index of vascular resistance distal to the site of measurement) in the central retinal and posterior ciliary arteries increases progressively. This result implies that mechanical and vascular factors may be coupled in such a way that perfusion of the retina and optic nerve head may be influenced by changes in the intraocular pressure. Further, at night, when ophthalmic artery flow velocities fall as arterial blood pressure falls in glaucoma patients, the risk of disease progression may be increased. The constancy of these same flow velocities in age-matched healthy individuals points to a possible vascular autoregulatory defect in glaucoma. In addition, in normal-tension glaucoma, vasodilation (CO2 inhalation) normalizes retrobulbar arterial flow velocities, hinting that some vascular deficits in glaucoma may be reversible. Finally, Ca2+ channel blockade improves contrast sensitivity in patients with normal-tension glaucoma, who also show increased retrobulbar vessel flow velocities, a result suggesting that visual function loss may be linked to ocular ischemia. Emerging evidence points to a role of ischemia in the pathogenesis of glaucoma, suggesting that treatments designed to improve ocular blood flow may benefit glaucoma patients.

KW - Autoregulation

KW - Ca channel blocker

KW - Intraocular pressure

KW - Ischemia

KW - Nocturnal ocular blood flow

KW - Vasospasm

UR - http://www.scopus.com/inward/record.url?scp=0038824378&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0038824378&partnerID=8YFLogxK

U2 - 10.1016/S0039-6257(99)00050-8

DO - 10.1016/S0039-6257(99)00050-8

M3 - Article

C2 - 10416746

AN - SCOPUS:0038824378

VL - 43

JO - Survey of Ophthalmology

JF - Survey of Ophthalmology

SN - 0039-6257

IS - 6 SUPPL.

ER -