Ocular neovascularization with retinal vascular occlusion. II. Occurrence in central and branch retinal artery occlusion.

Sixty-one patients (64 eyes) with central retinal artery occlusion (CRAO) and 41 patients (44 eyes) with branch retinal artery occlusion (BRAO) were studied in detail clinically to find out the pathogenesis of their ocular neovascularization (NV). Ocular NV was seen in 12 eyes (11 patients) with CRAO: iris NV was seen in all 12 eyes, angle NV was seen with neovascular glaucoma (NVG) in ten of them, and no NV was seen in BRAO. Nine of ten patients with CRAO associated with NVG were old, having severe carotid artery disease (CAD) and severe generalized atherosclerotic arterial disease; in the remaining patient, NVG was caused by diabetes mellitus. Severe CAD results in chronic ocular ischemia, which, in turn, produces NV of the iris and angle and NVG; the latter, combined with poor perfusion pressure in the central retinal artery (caused by severe CAD), results in CRAO. Our study showed little evidence that CRAO, per se, is responsible for ocular NV. Various evidence in support of this hypothesis is presented. Our study also showed that the only eyes to recover good vision were those with transient CRAO for up to 11/2 hours, and no treatment helped.

Beta-blocker eyedrops and nocturnal arterial hypotension.

PURPOSE: To investigate the effects of topical beta-blocker eyedrops on nocturnal arterial hypotension and heart rate and on visual field deterioration. METHODS: We prospectively investigated 275 white patients, 161 with glaucomatous optic neuropathy and 114 with nonarteritic anterior ischemic optic neuropathy, by 24-hour ambulatory blood pressure monitoring and diurnal curve of intraocular pressure, in addition to detailed ophthalmic evaluation. Of the patients with glaucomatous optic neuropathy, 131 had normal-tension glaucoma and 30 had primary open-angle glaucoma. Of the 275 patients, 114 were using topical beta-blocker eyedrops twice daily (76 with normal-tension glaucoma, 26 with primary open-angle glaucoma, and 12 with anterior ischemic optic neuropathy). RESULTS: Hourly average blood pressure data analyses showed overall a drop in blood pressure as well as heart rate during sleep, and a significantly greater drop in mean diastolic blood pressure (P = .009) at night in normal-tension glaucoma than in anterior ischemic optic neuropathy. Also, patients using beta-blocker eyedrops experienced a significantly greater percentage drop in diastolic blood pressure at night (P = .028), lower minimum nighttime diastolic blood pressure (P = .072), and lower minimum nighttime heart rate (P = .002) than did those not using them. In normal-tension glaucoma, eyes receiving beta-blocker eyedrops showed visual field progression significantly (P = .0003) more often than those not receiving beta-blockers. CONCLUSIONS: The findings of our studies, as well as those of others, suggest that any factor that increases nocturnal arterial hypotension is a potential risk factor in vulnerable individuals with glaucomatous optic neuropathy or anterior ischemic optic neuropathy. The present study suggests that the use of beta-blocker eyedrops, by aggravating nocturnal arterial hypotension and reducing the heart rate, may be a potential risk factor in susceptible individuals.

Ocular manifestations of giant cell arteritis.

PURPOSE: To report the ocular manifestations of giant cell arteritis using the strict criterion of a positive temporal artery biopsy for diagnosis of giant cell arteritis. METHODS: In a prospective study from 1973 to 1995, we investigated 170 patients whose diagnosis of giant cell arteritis was confirmed on temporal artery biopsy. At the initial visit, all patients were questioned regarding systemic and ocular signs and symptoms of giant cell arteritis and underwent ophthalmic, erythrocyte sedimentation rate (Westergren), and C-reactive protein evaluations. Any patient with a high index of suspicion of giant cell arteritis was immediately started on systemic corticosteroid therapy and had temporal artery biopsy performed as soon as possible. RESULTS: Eighty-five (50.0%) of the 170 patients with giant cell arteritis proven by temporal artery biopsy presented with ocular involvement. Ocular symptoms in patients with ocular involvement were visual loss of varying severity in 83 (97.7%), amaurosis fugax in 26 (30.6%), diplopia in five (5.9%), and eye pain in seven (8.2%); ocular ischemic lesions consisted of arteritic anterior ischemic optic neuropathy in 69 (81.2%), central retinal artery occlusion in 12 (14.1%), cilioretinal artery occlusion in 12 (of 55 patients with satisfactory fluorescein angiography [21.8%]), posterior ischemic optic neuropathy in six (7.1%), and ocular ischemia in one (1.2%). In almost every patient with giant cell arteritis, fluorescein fundus angiography disclosed occlusive disease of the posterior ciliary arteries. CONCLUSION: Because giant cell arteritis is a potentially blinding disease and its early diagnosis is the key to preventing blindness, it is important to recognize its various ocular manifestations.

Occult giant cell arteritis: ocular manifestations.

PURPOSE: To report the incidence, visual symptoms, and ocular signs of occult giant cell arteritis in patients who initially presented with visual symptoms and ocular signs of giant cell arteritis. Occult giant cell arteritis was defined as ocular involvement by giant cell arteritis without any systemic symptoms and signs of giant cell arteritis. METHODS: In a prospective study from 1973 to 1995, we investigated 85 patients who had ocular involvement caused by giant cell arteritis and whose diagnosis of giant cell arteritis was confirmed on temporal artery biopsy. At the initial visit, patients were questioned specifically on systemic and ocular symptoms and signs of giant cell arteritis at or before the onset of visual disturbance. Erythrocyte sedimentation rate (Westergren) and C-reactive protein level were evaluated before the start of systemic corticosteroid therapy. RESULTS: Eighteen (21.2%) of 85 patients had occult giant cell arteritis. There was no significant difference in age and sex distribution between patients with and without systemic symptoms of giant cell arteritis. Although both groups of patients had abnormal erythrocyte sedimentation rate and C-reactive protein level, there was a significant difference in erythrocyte sedimentation rate (P < .0001) and C-reactive protein level (P=.0133), these being relatively lower in patients with occult giant cell arteritis. The ocular symptoms in the 18 patients with occult giant cell arteritis were visual loss of varying severity in 18 (100%), amaurosis fugax in six (33.3%), diplopia in two (11.1%), and eye pain in one (5.6%). Ocular ischemic lesions consisted of anterior ischemic optic neuropathy in 17 (94.4%), central retinal artery occlusion in two (11.1%), and cilioretinal artery occlusion in two (of 11 patients with satisfactory fluorescein angiography [18.2%]). The ocular symptoms and ischemic lesions were seen in a variety of combinations. CONCLUSIONS: Because occult giant cell arteritis is a potential cause of blindness, its early diagnosis is the key to preventing blindness; it is important to recognize that 21.2% of patients with giant cell arteritis and visual loss do not have any systemic symptoms of giant cell arteritis. Thus, in persons older than 55 years, amaurosis fugax or visual loss, development of an acute ocular ischemic lesion (particularly arteritic anterior ischemic optic neuropathy), and abnormal C-reactive protein level, with or without elevated erythrocyte sedimentation rate and systemic symptoms, should raise a high index of suspicion for giant cell arteritis.

Ocular and optic nerve head ischemic disorders and hearing loss.

PURPOSE: To investigate in an exploratory study whether any evidence suggests that ophthalmic ischemic disorders, particularly of the optic nerve head, are associated with hearing loss. METHODS: We investigated prospectively 583 consecutive patients in eight primary ocular diagnostic groups for associated hearing loss: nonarteritic anterior ischemic optic neuropathy (n = 81), normal-tension glaucoma (n = 36), primary open-angle glaucoma (n = 138), other types of glaucoma (n = 142), ocular arterial occlusive disorders (n = 22), retinal vein occlusion (n = 89), ocular vasculitis (n = 42), and a miscellaneous group (n = 33). The patients and their relatives were questioned in detail for any evidence of hearing loss in the patients. RESULTS: In the logistic regression model, with presence or absence of hearing loss as the dependent variable and gender, age, and diagnosis as independent variables, gender (P = .003) and age (P<.0001) were found to be significantly associated with hearing loss. No significant association was found with any of the ophthalmic disease groups evaluated in this study. Whenever any significant association with any ophthalmic disease group was seen, this result could be explained by examination of the association between diagnosis and age, which showed a significant (P<.001) association. CONCLUSIONS: This study showed that there is a significant (P<.001) relationship between hearing loss and aging-the older the population, the higher the incidence of hearing loss-but the study showed that there is no association between hearing loss and ocular and optic nerve head ischemic disorders. The two represent unrelated and independent disorders.

Incidence of various types of retinal vein occlusion and their recurrence and demographic characteristics.

We analyzed data on 1,108 patients (1,229 eyes) with various types of retinal vein occlusion. Retinal vein occlusion was classified into six distinct clinical types: (I) nonischemic and (II) ischemic central retinal vein occlusion, (III) nonischemic and (IV) ischemic hemicentral retinal vein occlusion, and (V) major and (VI) macular branch retinal vein occlusion. Retinal vein occlusion occurred more often in men than women. The age range of patients was between 14 and 92 years, with 570 of 1,108 patients (51%) 65 years or older; however, 99 of 620 (16%), 15 of 154 (10%), and 17 of 375 (5%) of the patients with central, hemicentral, and branch retinal vein occlusion, respectively, were younger than 45 years. The cumulative probability of developing a second episode of the same or a different type of retinal vein occlusion in the same eye was 0.9% within two years and 2.5% within four years, and in the fellow eye was 7.7% and 11.9%, respectively. The cumulative probability of conversion of nonischemic to ischemic central retinal vein occlusion at six months and 18 months was 13.2% and 18.6%, respectively, in persons 65 years of age or older and 6.7% and 8.1%, respectively, in persons 45 to 64 years of age.

Nonarteritic anterior ischemic optic neuropathy: time of onset of visual loss.

PURPOSE: To study time of day and seasonal variation of onset of visual loss in nonarteritic anterior ischemic optic neuropathy (AION). METHODS: From 1975 to 1995, we prospectively investigated the time of discovery of visual loss in 635 patients (871 eyes) with AION--a total of 925 episodes. Data were analyzed for two variables: time of day of discovery of visual loss for 544 episodes and seasonal variation of the onset of AION for 839 episodes. RESULTS: Of 544 episodes, time of day for discovery of visual loss was upon awakening from sleep in the morning or a nap in 282 (51.8%), during the first opportunity to use vision critically early in the morning in 117 (21.5%), and later in the day in 145 (26.7%). AION was significantly (P = .0030) more frequent in summer than winter. Estimated monthly onset rates were 82.7 episodes (95% confidence interval [CI], 71.3 to 95.8) in summer, 58.3 (95% CI, 48.9 to 69.6) in winter, 66.0 (95% CI, 55.9 to 77.9) in spring, and 72.7 (95% CI, 62.1 to 85.1) in fall. Onset significantly (P < .0001) occurred more during hot than cold months, with the estimated monthly rate of onset in hot months of 82.2 episodes (95% CI, 73.7 to 91.8) compared with 59.8 (95% CI, 53.3 to 67.1) in cold months. CONCLUSIONS: In at least 399 (73.3%) of 544 episodes of AION, patients discovered visual loss upon first awakening or at first opportunity to use vision critically after sleeping, suggesting that nocturnal arterial hypotension may play an important role. Also, AION developed more often in summer than in winter.

Ipsilateral recurrence of nonarteritic anterior ischemic optic neuropathy.

PURPOSE: To report the prevalence of recurrence of nonarteritic anterior ischemic optic neuropathy (NA-AION) in the same eye and possible contributing risk factors. DESIGN: Cohort study. SETTING: Institutional. STUDY POPULATION: The study includes 594 consecutive patients (829 eyes) with a diagnosis of NA-AION and follow-up of at least two months after the onset of NA-AION, examined in the Ocular Vascular Clinic since 1973. Simple progression of visual loss during an episode of NA-AION was not considered a fresh episode. INTERVENTION OR OBSERVATION PROCEDURES: Every patient had ophthalmic evaluation, including visual acuity, visual fields with a Goldmann perimeter, intraocular pressure, and slit lamp and ophthalmoscopic evaluation at initial visit and at each follow-up visit. The patients also had systemic evaluation; some patients had echocardiography (166 patients) and 24-hour ambulatory blood pressure (BP) monitoring-the latter was investigated in 80 patients (17 with and 63 without recurrence of NA-AION) who consented to participate in this study which was started in 1989. While optic disk edema was present, the patients were followed every 2 to 3 weeks. Once the optic disk edema resolved, they were followed up after 3 months, 6 months, and then at yearly intervals unless they had some new visual complaint. MAIN OUTCOME MEASURES: Prevalence of a fresh episode of NA-AION in the same eye, and comparison of ocular and systemic risk factors between patients with and without recurrence of NA-AION in the same eye. RESULTS: Of the 594 patients (829 eyes) in the study, recurrence of NA-AION in the same eye occurred in 45 patients (53 eyes) with a median follow-up of 3.1 years (range 2 months to 30.5 years) from the first onset of NA-AION. The Kaplan-Meier survival curve showed cumulative percentage of recurrence of NA-AION from first episode to second episode at three months 1.0%+/-0.4%(SE), at 6 months 2.7%+/-0.7%, at one year 4.1%+/-0.9%, and 2 years 5.8%+/-1.1%. There was no significant association between recurrence of NA-AION and the systemic conditions that were examined, except for nocturnal arterial hypotension. Overall patients with a recurrence of NA-AION had a significantly lower mean nighttime minimum diastolic BP (P =.003) and greater mean percentage drop during sleep in diastolic BP (P =.011) than those with no recurrence of NA-AION; all other measures of nocturnal hypotension were not significantly predictive. CONCLUSIONS: Recurrence of NA-AION in the same eye is uncommon (6.4%). Our study indicates that nocturnal diastolic arterial hypotension may be a risk factor; however, since this is a multifactorial disease, other so far unknown risk factors may also play a role. The role of various risk factors which may contribute to the recurrence of NA-AION is discussed.

Systemic diseases associated with various types of retinal vein occlusion.

PURPOSE: To investigate systemic diseases associated with various types of retinal vein occlusion. METHODS: We investigated prospectively in 1090 consecutive patients with retinal vein occlusion, almost all Caucasian (consistent with the racial pattern here), the prevalence of associated systemic disorders before or at the onset of various types of retinal vein occlusion. The patients were categorized into six types of retinal vein occlusion based on defined criteria: nonischemic and ischemic central retinal vein occlusion, nonischemic and ischemic hemi-central retinal vein occlusion, and major and macular branch retinal vein occlusion. The patients had a detailed ophthalmic and systemic evaluation according to our protocol. For data analysis, patients were divided into three age groups: young (younger than 45 years), middle-aged (45 to 64 years), and elderly (65 years or older). The observed prevalence rates of major systemic diseases were compared among central retinal vein occlusion, hemi-central retinal vein occlusion, and branch retinal vein occlusion using a polytomous logistic regression analysis adjusting for gender and age. Logistic regression adjusting for age and gender was also used to compare the observed prevalence of systemic disease between nonischemic and ischemic in central retinal vein occlusion and hemi-central retinal vein occlusion and between major and macular branch retinal vein occlusion. These observed prevalence rates were also compared with those expected in a gender-matched and age-matched control population from estimates from the US National Center for Health Statistics. RESULTS: There was a significantly higher prevalence of arterial hypertension in branch retinal vein occlusion compared with central retinal vein occlusion (P < .0001) and hemi-central retinal vein occlusion (P = .028). Branch retinal vein occlusion also had a significantly higher prevalence of peripheral vascular disease (P = .0002), venous disease (P = .011), peptic ulcer (P = .031), and other gastrointestinal disease (P < .0001) compared with central retinal vein occlusion. The proportion of patients with branch retinal vein occlusion with cerebrovascular disease was also significantly (P = .049) greater than that of the combined group of patients with central retinal vein occlusion and patients with hemi-central retinal vein occlusion. There was no significant difference in prevalence of any systemic disease between central retinal vein occlusion and hemi-central retinal vein occlusion. A significantly greater prevalence of arterial hypertension (P = .025) and diabetes mellitus (P = .011) was present in the ischemic central retinal vein occlusion compared with the nonischemic central retinal vein occlusion. Similarly, arterial hypertension (P = .0002) and ischemic heart disease (P = .048) were more prevalent in major branch retinal vein occlusion than in macular branch retinal vein occlusion. Relative to the US white control population, the combined group of patients with central retinal vein occlusion and patients with hemi-central retinal vein occlusion had a higher prevalence of arterial hypertension (P < .0001), peptic ulcer (P < .0001), diabetes mellitus (in ischemic type only, P < .0001), and thyroid disorder (P < .0001). The patients with branch retinal vein occlusion showed a greater prevalence of arterial hypertension (P < or = .005), cerebrovascular disease (P = .007), chronic obstructive pulmonary disease (P = .012), peptic ulcer (P < .0001), diabetes (in young only, P = .0005), and thyroid disorder (P = .003) compared with the US white control population. CONCLUSIONS: The findings of our study revealed that a variety of systemic disorders may be present in association with different types of retinal vein occlusion and in different age groups, and that their relative prevalence differs significantly, so that the common practice of generalizing about these disorders for the entire group of patients with retinal vein occlusion can be misleading. The presence of a particular associated systemic disease does not necessarily imply a cause-and-effect relationship with that type of retinal vein occlusion; the particular disease may or may not be one of the risk factors in a multifactorial scenario predisposing an eye to develop a particular type of retinal vein occlusion. Based on our study, we think that apart from a routine medical evaluation, an extensive and expensive workup for systemic diseases is unwarranted in the vast majority of patients with retinal vein occlusion.

Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders.

We measured 24-hour ambulatory blood pressure monitoring and diurnal curve of the intraocular pressure in 166 white patients with anterior ischemic optic neuropathy, normal-tension glaucoma, primary open-angle glaucoma, and other optic nerve head disorders. Hourly average blood pressure data analyses showed a significant (P < .0001) decrease in mean systolic (26%) and diastolic (33%) blood pressure measurements at night. A significantly (P = .0028) lower nighttime mean diastolic blood pressure and a significantly (P = .0044) greater mean percentage decrease in diastolic blood pressure were noted in normal-tension glaucoma than in anterior ischemic optic neuropathy. Patients with arterial hypertension taking oral hypotensive therapy showed a significant association between progressive visual field deterioration and nocturnal hypotension, particularly in anterior ischemic optic neuropathy. Intraocular pressure showed no significant correlation with visual field deterioration in any of these conditions. Our findings suggest that nocturnal hypotension, in the presence of other vascular risk factors, may reduce the optic nerve head blood flow below a critical level, and thereby may play a role in the pathogenesis of anterior ischemic optic neuropathy and glaucomatous optic neuropathy; that is, nocturnal hypotension may be the final insult in a multifactorial situation. The same mechanisms may be true of a number of other ocular ischemic disorders. This finding opens a new dimension in the understanding and management of these visually disabling diseases.

Giant cell arteritis: validity and reliability of various diagnostic criteria.

PURPOSE: To ascertain the validity, reliability, sensitivity, and specificity of various signs and symptoms of and diagnostic tests for early diagnosis of giant cell arteritis. METHODS: From 1973 to 1994, we studied 363 patients who had temporal artery biopsy for suspected giant cell arteritis. All patients underwent detailed clinical evaluation and had erythrocyte sedimentation rates determined; since 1985, 223 patients had their C-reactive protein values estimated. Erythrocyte sedimentation rate and C-reactive protein levels were also estimated in 749 and 138 control subjects, respectively. Signs and symptoms of giant cell arteritis, erythrocyte sedimentation rate, and C-reactive protein levels among patients with positive and negative biopsies were compared. RESULTS: Of the 363 patients, temporal artery biopsy was positive in 106 and negative in 257. The odds of a positive biopsy were 9.0 times greater with jaw claudication (P < .0001), 3.4 times greater with neck pain (P = .0085), 2.0 times greater with an erythrocyte sedimentation rate of 47 to 107 mm/hour (P = .0454), 3.2 times greater with C-reactive protein above 2.45 mg/dl (P = .0208), and 2.0 times greater for age 75 years or more (P = .0105). CONCLUSIONS: Clinical criteria most strongly suggestive of giant cell arteritis include jaw claudication, C-reactive protein above 2.45 mg/dl, neck pain, and an erythrocyte sedimentation rate of 47 mm/hour or more, in that order. C-reactive protein was more sensitive (100%) than erythrocyte sedimentation rate (92%) for detection of giant cell arteritis; erythrocyte sedimentation rate combined with C-reactive protein gave the best specificity (97%).

Systemic diseases associated with nonarteritic anterior ischemic optic neuropathy.

PURPOSE: We investigated, in nonarteritic anterior ischemic optic neuropathy, the prevalence of various systemic diseases before or at its onset and the incidence of subsequent morbidity and mortality. METHODS: We investigated prospectively the presence of systemic diseases before or at the onset of nonarteritic anterior ischemic optic neuropathy in 406 patients. The information was obtained by complete medical history and physical examination. The prevalence rates of systemic diseases in young, middle-aged, and elderly groups were compared with those in the general population. We also analyzed the influence of systemic diseases on subsequent morbidity and mortality. RESULTS: Compared with the prevalences reported in the general population, our patients in each of the three age groups showed a significantly higher prevalence of arterial hypertension (P < or = .02), diabetes mellitus (P < .01), and gastrointestinal ulcer (P < or = .02). Also, middle-aged and elderly patients showed a significantly higher prevalence of ischemic heart disease (P < .01) and thyroid disease (P < .01). Middle-aged patients had significantly higher rates of chronic obstructive pulmonary disease and cerebrovascular disease (P < or = .01). After onset of anterior ischemic optic neuropathy, patients with both arterial hypertension and diabetes mellitus had a significantly higher incidence of cerebrovascular disease (P < .01). CONCLUSIONS: Nonarteritic anterior ischemic optic neuropathy is a multifactorial disease in which some systemic diseases may act as predisposing factors and others as precipitating factors. Patients with anterior ischemic optic neuropathy show no significant increase in mortality, but those with both arterial hypertension and diabetes mellitus have significantly (P < .01) increased incidence of cerebrovascular disease.

Aspirin therapy in nonarteritic anterior ischemic optic neuropathy.

PURPOSE: To determine the benefit of aspirin in reducing the risk of nonarteritic anterior ischemic optic neuropathy in the fellow eye following its occurrence in the first eye. METHODS: A retrospective cohort study was conducted on 431 patients, 153 of whom were and 278 of whom were not prescribed aspirin following the development of unilateral nonarteritic anterior ischemic optic neuropathy. RESULTS: The 2-year cumulative probability of nonarteritic anterior ischemic optic neuropathy in the fellow eye was 7% in the aspirin group and 15% in the no-aspirin group, and 5-year cumulative probabilities were 17% and 20%, respectively. Compared with the no-aspirin group, the rate ratio for nonarteritic anterior ischemic optic neuropathy in the fellow eye in the aspirin-user group was 0.43 (95% confidence interval, 0.19 to 0.92) over the first 2 years and 0.68 (95% confidence interval, 0.36 to 1.26) over the 5-year period. The overall calculated 5-year risk was 19%; however, if none of the patients with incomplete follow-up developed nonarteritic anterior ischemic optic neuropathy in the fellow eye, then the 5-year risk would be about 12%. CONCLUSIONS: The 5-year risk of nonarteritic anterior ischemic optic neuropathy occurring in the second eye is far lower than that reported by previous studies. Our results suggest a possible short-term but little or no long-term benefit to aspirin in reducing the risk of nonarteritic anterior ischemic optic neuropathy in the fellow eye. However, this finding must be viewed with caution because this study was not conducted prospectively with a controlled protocol.

Seasonal variations in the onset of retinal vein occlusion.

Seasonal variation in the development of retinal vein occlusion in 1003 consecutive patients with various types of retinal vein occlusion was studied prospectively from 1973 to 1990. No seasonal variation in the onset of any type or combination of types of retinal vein occlusion was found. This refutes previous reports of such seasonal variation, which were based on small retrospective series.

Role of thrombocytosis in diagnosis of giant cell arteritis and differentiation of arteritic from non-arteritic anterior ischemic optic neuropathy.

PURPOSE: To investigate the role of thrombocytosis in the diagnosis of giant cell arteritis (GCA), and differentiation of arteritic (A-AION) from non-arteritic (NA-AION) anterior ischemic optic neuropathy; and comparison of the sensitivity and specificity of platelet count to that of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and some other hematologic variables in the diagnosis of GCA. METHODS: This retrospective study is based on 121 temporal artery biopsy confirmed GCA patients and 287 patients with NA-AION seen in our clinic. For inclusion in this study, all GCA patients, at their initial visit, prior to the initiation of corticosteroid therapy, must have had ESR (Westergren), platelet count and complete blood count, and temporal artery biopsy. From 1985 onwards CRP estimation was done. For inclusion in this study, all NA-AION patients at the initial visit must have undergone evaluation similar to that described above for GCA, except for temporal artery biopsy. Wilcoxon rank-sum test and the two-sample t-test were used to compare hematologic variables between GCA patients with and without visual loss, between those with and without systemic symptoms, and also between GCA and NA-AION patients. Pearson correlation coefficient was computed to measure the association of platelet counts and the other hematologic variables with ESR. Receiver operating characteristic (ROC) curves were constructed for ESR, CRP, platelet count, combinations of ESR and platelet count, and CRP and platelet count, hemoglobin, hematocrit, and white blood cell (WBC) count and the area under the curve (AUC) were compared. RESULTS: Comparison of ESR, CRP, and hematologic variables of GCA patients and of A-AION with the NA-AION group, showed significantly (p <0.0001) higher median levels of ESR, CRP, platelet count, and WBC count and lower levels of hemoglobin and hematocrit in the GCA patients and A-AION than in NA-AION. Comparing AUC of the ROC curve between ESR and platelet count, ESR was a better predictor of GCA compared to platelet count (AUC of 0.946 vs. 0.834). There was a slight improvement in prediction of GCA using the combination of ESR and platelet count (AUC=0.953). The other hematologic variables had an AUC that was smaller than platelet count (0.854 for hemoglobin; 0.841 for hematocrit), with WBC being the least predictive of GCA (AUC=0.666). The AUC of the ROC curve for CRP was 0.978. There was no improvement in prediction of GCA using platelet count in combination with CRP (AUC=0.976). CONCLUSIONS: Patients with GCA had significantly (p <0.0001) higher values of platelet count, ESR, CRP and WBC but lower values for hemoglobin and hematocrit compared to the NA-AION group. Predictive ability of an elevated platelet count did not surpass elevated ESR or CRP as a diagnostic marker for GCA. Thrombocytosis may complement ESR. Hemoglobin, hematocrit and WBC were much less predictive of GCA. Elevated CRP had a greater predictive ability for GCA compared to ESR or the other hematologic parameters; thrombocytosis in combination with CRP did not yield an improvement in prediction of GCA.

Argon laser scatter photocoagulation in treatment of branch retinal vein occlusion. A prospective clinical trial.

The objective of this prospective study was to ascertain whether scatter argon laser photocoagulation to the involved sector in major branch retinal vein occlusion and ischemic hemicentral retinal vein occlusion (a) prevents development of retinal and/or optic disk neovascularization and vitreous hemorrhage, and (b) affects visual acuity, visual fields and macular retinal lesions. The study was done in 271 eyes allocated to either treated (n = 61 eyes) or untreated (n = 210) groups. In this study, on an average follow-up of 3.6 years, the laser treatment (1) significantly reduced the risk of development of retinal neovascularization and vitreous hemorrhage, (2) did not affect the visual acuity and macular retinal lesions, and (3) produced a significant worsening in the peripheral visual fields compared to the untreated eyes. In view of our findings, we recommend that argon laser photocoagulation treatment should be given only when neovascularization is seen and not otherwise, because in the latter case, its detrimental effects may outweigh its beneficial ones.

Ocular ischemic syndrome.

PURPOSE: The purpose of the study is to investigate the clinical features and management of ocular ischemic syndrome (OIS) and factors influencing its development. INTERVENTION: The following interventions were used: detailed medical and ocular histories, complete ophthalmic evaluation including fluorescein angiography, internal carotid artery evaluation by duplex ultrasonography, and/or aortic arch angiography, management, and follow-up. MAIN OUTCOME MEASURES: The following outcome measures were considered: visual acuity, visual fields, intraocular pressure, anterior segment neovascularization and other abnormalities, lens, optic disc, retinal and choroidal changes, carotid artery stenosis or occlusion, diabetes mellitus, arterial hypertension, coronary artery disease, and cerebrovascular disease. RESULTS: Mean age of the 32 patients (39 eyes) with OIS was 68 +/- 8 years. Presenting visual symptoms included amaurosis fugax (15%) and/or gradual (28%) or sudden (41%) visual loss. At initial visit, eyes with OIS had visual acuity less than or equal to 20/400 in 64%, iris neovascularization (NV) in 87%, angle NV in 59%, intraocular pressure from 4 to 60 mmHg (median 18 mmHg), optic disc pale (40%) and/or cupped (19%) or edematous (8%), disc NV (13%), retinal NV (3%), marked retinal circulatory stasis (21%), and retinal hemorrhages (24%). Associated systemic diseases in these patients included diabetes mellitus (56%), arterial hypertension (50%), coronary artery disease (38%), and previous stroke or transient ischemic attack (31%); the incidence of diabetes, coronary artery disease, and cerebrovascular disease was much higher in patients with OIS than in the comparable general population, especially that of diabetes. Occlusion or severe stenosis (80%-99%) of the internal carotid artery was seen in 74% on the side of OIS. CONCLUSIONS: Ocular ischemic syndrome has a poor visual prognosis. However, the ophthalmologist's diagnosis may be crucial to the health of these patients, because OIS may be the presenting sign of serious cerebrovascular and ischemic heart diseases.

Role of nocturnal arterial hypotension in optic nerve head ischemic disorders.

OBJECTIVE: To investigate the role of nocturnal arterial hypotension, intraocular pressure (IOP) and heart rate in optic nerve head (ONH) ischemic disorders, and the effects of systemic factors and topical beta-blocker eye-drops on nocturnal arterial hypotension and heart rate. METHODS: We investigated prospectively, by 24-hour ambulatory blood pressure (BP) monitoring and diurnal curve of the IOP, 275 white patients with anterior ischemic optic neuropathy (AION - 114), normal tension glaucoma (NTG - 131) and primary open angle glaucoma (POAG - 30). RESULTS: Hourly average BP data analyses showed a significantly greater drop in mean diastolic BP (p < 0.009) at night in NTG than AION. Cases with visual field deterioration had significantly (p = 0.05) lower minimum nighttime diastolic BP. Arterial hypertensives on oral hypotensive therapy showed a significantly lower mean nighttime systolic BP (p = 0.006) and larger mean percentage drop in systolic (p < 0.0001), diastolic (p = 0.0009) and mean (p < 0.0001) BPs. Normotensives and hypertensives without therapy had no such difference. IOP showed no significant correlation with visual field deterioration in any of these conditions. Patients using beta-blocker eyedrops, compared with those not using them, had greater percentage drop in diastolic BP (p = 0.028), lower minimum nighttime diastolic BP (p = 0.072) and lower minimum nighttime heart rate (p = 0.002). CONCLUSIONS: Findings of our study suggest that nocturnal hypotension, by reducing the ONH blood flow below a crucial level during sleep in a vulnerable ONH, may play a role in the pathogenesis of AION and glaucomatous optic neuropathy (GON) and progression of visual loss in them. Thus, nocturnal hypotension may be the final insult in a multifactorial situation.

Electroretinography in central retinal vein occlusion. Correlation of electroretinographic changes with pupillary abnormalities.

In 149 eyes with central retinal vein occlusion (CRVO), we prospectively investigated the role of routine, clinical electroretinography (ERG) in differentiating ischemic (60 eyes) from nonischemic CRVO (89 eyes). Single-flash photopic and scotopic ERGs were recorded. Data for the amplitudes and implicit times of a- and b-waves and for the b-/a-wave amplitude ratio were analyzed in detail. The study revealed that the best ERG parameter (for both photopic and scotopic ERG) for differentiating ischemic from nonischemic CRVO was a subnormal b-wave amplitude (reduced to less than or equal to 60% or by greater than or equal to 1 SD from the normal mean value, or less than or equal to 64%-69% of that in the fellow normal eye), with a sensitivity of 80%-90% and a specificity of 70%-80%. ERG findings were correlated with the relative afferent pupillary defect (RAPD). An RAPD of greater than or equal to 0.7 log units showed a sensitivity of 88% and a specificity of 90% in differentiating ischemic from nonischemic CRVO. ERG and RAPD findings showed a good correlation. The combined ERG and RAPD tests could differentiate 97%-100% of ischemic from nonischemic CRVO cases, with a specificity of about 70%.