Vascular Dysfunction in Diabetes and Glaucoma
Chung et al reported significantly reduced blood flow throughout the peripapillary retina in patients with normal tension glaucoma). Similarly, while not focusing on the potential role diabetes may have in glaucoma progression, the Optical Coherence Tomography (OCT) Study investigated the use of Doppler OCT in studying retinal blood flow in patients with optic nerve and retinal disease. As seen in Table 1, patients with glaucoma, treated proliferative diabetic retinopathy, nonarteritic anterior ischemic optic neuropathy, and branch retinal vein occlusion showed significantly decreased retinal blood flow compared with normal patients (P<0.001). Although diabetes is known to produce vascular complications throughout the body, results regarding its effect on retinal blood flow are far from conclusive.
In a study comparing retinal blood flow velocity in normal patients to that of early diabetic patients without diabetic retinopathy, Burgansky-Eliash et al found an increase in velocity of arterial and venous flow in the latter, suggesting that irregularities in vessel function exist in diabetic eyes before the development of structural changes. Similarly, Patel et al concluded that patients with diabetic retinopathy have hyperperfusion through their retinal circulation compared with nondiabetics and diabetic patients with no diabetic retinopathy, which may be due to abnormal autoregulation of retinal circulation, hypertension, or hyperglycemia. However, other studies analyzing retinal hemodynamics suggest retinal blood flow is significantly decreased in patients with diabetes than without. The effect of plasma glucose levels on retinal blood flow may contribute to the contradictory findings involving blood flow during different stages of diabetes and diabetic retinopathy, making it difficult to ascertain a specific pathogenic mechanism involving diabetes and retinal blood flow.
The relationship between OAG and choroidal blood flow has also been analyzed. Given that fluctuations in oxygen supply to tissue often result in reperfusion damage and OAG patients have been shown to have higher choroidal blood flow variability, such patients may have an increased chance of infarction. This may explain why Yin et al discovered that peak choroidal filling was significantly delayed and choroidal thickness was significantly decreased in glaucoma patients compared with normal patients. Likewise, diabetes has been shown to alter choroidal blood flow. Dimitrova et al reported decreased EDV and increased RI in the posterior ciliary arteries of diabetic patients with and without diabetic retinopathy, which are responsible for the blood perfusion of the choroid. The increased posterior ciliary artery RI in nondiabetic retinopathy patients supports the probability that vessel function in the choroid is limited before evidence of diabetic retinopathy, suggesting choroid circulatory alteration may be one of the factors that leads to diabetic retinopathy. Even so, some results suggest that total choroidal perfusion is unaffected or decreased in diabetic patients. The exact association between OAG and diabetes with regards to choroidal blood flow remains unclear.
Blood flow in the retrobulbar region is another area impacted by glaucomatous activity. Zeitz et al displayed that progressive glaucoma correlates with decreased blood flow velocities in the retrobulbar vasculature supplying the optic nerve head, and results from Costa et al indicated that impairment of retrobulbar blood flow precedes the physical appearance of glaucomatous injury. Likewise, the development of diabetes has been shown to have an impact on retrobulbar hemodynamics. Shoshani and colleagues demonstrated that CRA PSV was 13.5% lower in diabetic patients (P=0.007) and OPP positively correlated with CRA and temporal posterior ciliary artery PSV and with CRA and nasal posterior ciliary artery RI. In addition, negative correlations between retrobulbar and retinal circulations were found only in diabetic OAG patients, implying these patients have lower retrobulbar flow in the CRA and higher retinal microcirculation. These findings are significant, as Galassi et al showed that in glaucoma patients with a RI of ≥0.78, the OR of a patient worsening in their glaucomatous progression was 6.61 (P=0.007), as defined by visual field deficits. Stated differently, glaucoma patients with an RI≥0.78 are >6 times more likely to experience visual field deterioration than glaucoma patients with an RI<0.78.
Some studies have even compared oxygen reactivity in the retrobulbar vessels between diabetic and normal patients, revealing that under hyperoxic conditions, normal patients had reduced retrobulbar blood flow to the eye, whereas diabetic patients experienced no change. These studies indicate that even diabetic patients with minimal or no retinopathy display altered hemodynamics in the major vessels of the eye. It has also been found that proliferative retinopathy correlates strongly with impaired flow in retrobulbar vessels. Although diabetes causes major vascular complications in the body, the specific compromise it places on retrobulbar blood flow and the potential for a corresponding risk of glaucoma warrants further research.
Blood Flow Abnormalities
Retinal Circulation
Chung et al reported significantly reduced blood flow throughout the peripapillary retina in patients with normal tension glaucoma). Similarly, while not focusing on the potential role diabetes may have in glaucoma progression, the Optical Coherence Tomography (OCT) Study investigated the use of Doppler OCT in studying retinal blood flow in patients with optic nerve and retinal disease. As seen in Table 1, patients with glaucoma, treated proliferative diabetic retinopathy, nonarteritic anterior ischemic optic neuropathy, and branch retinal vein occlusion showed significantly decreased retinal blood flow compared with normal patients (P<0.001). Although diabetes is known to produce vascular complications throughout the body, results regarding its effect on retinal blood flow are far from conclusive.
In a study comparing retinal blood flow velocity in normal patients to that of early diabetic patients without diabetic retinopathy, Burgansky-Eliash et al found an increase in velocity of arterial and venous flow in the latter, suggesting that irregularities in vessel function exist in diabetic eyes before the development of structural changes. Similarly, Patel et al concluded that patients with diabetic retinopathy have hyperperfusion through their retinal circulation compared with nondiabetics and diabetic patients with no diabetic retinopathy, which may be due to abnormal autoregulation of retinal circulation, hypertension, or hyperglycemia. However, other studies analyzing retinal hemodynamics suggest retinal blood flow is significantly decreased in patients with diabetes than without. The effect of plasma glucose levels on retinal blood flow may contribute to the contradictory findings involving blood flow during different stages of diabetes and diabetic retinopathy, making it difficult to ascertain a specific pathogenic mechanism involving diabetes and retinal blood flow.
Choroidal Circulation
The relationship between OAG and choroidal blood flow has also been analyzed. Given that fluctuations in oxygen supply to tissue often result in reperfusion damage and OAG patients have been shown to have higher choroidal blood flow variability, such patients may have an increased chance of infarction. This may explain why Yin et al discovered that peak choroidal filling was significantly delayed and choroidal thickness was significantly decreased in glaucoma patients compared with normal patients. Likewise, diabetes has been shown to alter choroidal blood flow. Dimitrova et al reported decreased EDV and increased RI in the posterior ciliary arteries of diabetic patients with and without diabetic retinopathy, which are responsible for the blood perfusion of the choroid. The increased posterior ciliary artery RI in nondiabetic retinopathy patients supports the probability that vessel function in the choroid is limited before evidence of diabetic retinopathy, suggesting choroid circulatory alteration may be one of the factors that leads to diabetic retinopathy. Even so, some results suggest that total choroidal perfusion is unaffected or decreased in diabetic patients. The exact association between OAG and diabetes with regards to choroidal blood flow remains unclear.
Retrobulbar Circulation
Blood flow in the retrobulbar region is another area impacted by glaucomatous activity. Zeitz et al displayed that progressive glaucoma correlates with decreased blood flow velocities in the retrobulbar vasculature supplying the optic nerve head, and results from Costa et al indicated that impairment of retrobulbar blood flow precedes the physical appearance of glaucomatous injury. Likewise, the development of diabetes has been shown to have an impact on retrobulbar hemodynamics. Shoshani and colleagues demonstrated that CRA PSV was 13.5% lower in diabetic patients (P=0.007) and OPP positively correlated with CRA and temporal posterior ciliary artery PSV and with CRA and nasal posterior ciliary artery RI. In addition, negative correlations between retrobulbar and retinal circulations were found only in diabetic OAG patients, implying these patients have lower retrobulbar flow in the CRA and higher retinal microcirculation. These findings are significant, as Galassi et al showed that in glaucoma patients with a RI of ≥0.78, the OR of a patient worsening in their glaucomatous progression was 6.61 (P=0.007), as defined by visual field deficits. Stated differently, glaucoma patients with an RI≥0.78 are >6 times more likely to experience visual field deterioration than glaucoma patients with an RI<0.78.
Some studies have even compared oxygen reactivity in the retrobulbar vessels between diabetic and normal patients, revealing that under hyperoxic conditions, normal patients had reduced retrobulbar blood flow to the eye, whereas diabetic patients experienced no change. These studies indicate that even diabetic patients with minimal or no retinopathy display altered hemodynamics in the major vessels of the eye. It has also been found that proliferative retinopathy correlates strongly with impaired flow in retrobulbar vessels. Although diabetes causes major vascular complications in the body, the specific compromise it places on retrobulbar blood flow and the potential for a corresponding risk of glaucoma warrants further research.
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