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Epidemiology |

Ten-Year Incidence of Retinal Vein Occlusion in an Older Population:  The Blue Mountains Eye Study FREE

Sudha Cugati, MS; Jie Jin Wang, MMed, PhD; Elena Rochtchina, MApplStat; Paul Mitchell, MD, PhD
[+] Author Affiliations

Section Editor: Leslie Hyman,, PhD
Author Affiliations: Centre for Vision Research, Department of Ophthalmology, University of Sydney, Westmead Hospital, Westmead, Australia.

More Author Information
Arch Ophthalmol. 2006;124(5):726-732. doi:10.1001/archopht.124.5.726.
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Published online

Objective  To assess the 10-year incidence of retinal vein occlusion (RVO) and its predictors in an older population.

Methods  The Blue Mountains Eye Study examined 3654 residents aged 49 years and older (82.4% response) from 1992 to 1994, reexamined 2335 residents (75.1% of survivors) from 1997 to 1999, and reexamined 1952 residents (75.6% of survivors) from 2002 to 2004. Incident RVO was assessed from stereoscopic retinal photographs. Kaplan-Meier cumulative 10-year incidence was calculated.

Results  After excluding 47 residents with RVO at baseline and 171 residents with no photographs at either follow-up examination, 2346 residents were considered at risk of developing RVO. The cumulative 10-year incidence of RVO was 1.6%. Age was significantly associated with the incidence of RVO (P = .03, Mantel-Haenszel χ2 test for trend). Factors predicting the incidence of RVO included mean arterial blood pressure (age-adjusted odds ratio [OR], 1.41 per 10–mm Hg increase), ocular perfusion pressure (OR, 1.71 per 10–mm Hg increase), obesity (OR, 2.16), and presence of retinal arteriolar wall signs (focal narrowing: OR, 3.37; arteriovenous nicking: OR, 4.09; and opacification: OR, 4.89).

Conclusions  Older age (≥70 years), increasing mean arterial blood pressure, and atherosclerotic retinal vessel signs were significant predictors of incident RVO.

Figures in this Article

Retinal vein occlusion (RVO) is an important cause of unilateral vision loss1,2 and has been associated with an increased risk of cardiovascular mortality and stroke.35 Central RVO, even when unilateral, may be associated with reduced vision-related quality of life.6

Most reported studies of RVO are derived from hospital-based samples,5,712 with few population-based studies providing data on the prevalence of RVO and its associated risk factors.1315 The frequency of RVO in a hospital-based sample was 1.5%.16 The prevalence of RVO among older population-based samples has ranged from 0.3% in the Atherosclerosis Risk in Communities Study (12 642 persons aged 51-70 years) and the Cardiovascular Health Study (2824 persons aged 73 years and older)15 to 1.6% in the Blue Mountains Eye Study (3654 persons aged 49 years and older).13 The Beaver Dam Eye Study reported a 0.7% prevalence of RVO.14 The substantially lower prevalence of RVO among subjects in the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study is likely because only 1 single-eye nonmydriatic photograph was taken of each participant in those studies.15,17

In Hiroshima, Japan, the 5-year incidence of RVO was 0.6% at a general outpatient clinic but was 4.2% in the glaucoma clinic.18 The 4-year incidence of RVO in an Israeli study1 of persons aged 40 years and older was 2.14 cases (0.2%) per 1000 people. In the Beaver Dam Eye Study14 population, the 5-year incidence of RVO was 0.8%. In a Japanese cohort study,19 245 (19.6%) of 1250 baseline participants 40 years and older were reexamined after 10 years, and 1 patient (0.41%) had developed incident branch RVO; this study had substantial participant losses during follow-up. To our knowledge, there are no other reports of 10-year incidence data of RVO from large well-conducted population-based cohort studies.

Systemic risk factors associated with RVO include hypertension,5,1214,2022 diabetes mellitus,5,14,20,21 cerebrovascular disease,5,13 cardiovascular disease,21 increased body mass index,21 reduced high-density lipoprotein cholesterol levels,21 smoking,22 thyroid disorder,5 and peptic ulcer.5 Ocular risk factors associated with RVO include glaucoma or ocular hypertension,2023 shorter axial length,13,24 and focal arteriolar narrowing and arteriovenous (AV) nicking.14,15 A recent meta-analysis25 of RVO and thrombophilic factors indicated that hyperhomocysteinuria and cardiolipin antibodies may be associated with RVO. Other hematologic factors reportedly associated with RVO include elevated erythrocyte sedimentation rates20,26 and elevated hematocrits.26

A 1.6% prevalence of RVO was previously reported among an older Australian population.13 The objective of this study was to assess the 10-year incidence of RVO and its predictors in the same older Australian population.

The Blue Mountains Eye Study is a population-based cohort study of a suburban Australian population aged 49 years and older at baseline. The study was approved by the Western Sydney Area Human Ethics Committee and was conducted in accord with the principles of the Declaration of Helsinki. The survey methods and procedures were described previously.27,28 Of 4433 eligible residents, baseline examinations (1992-1994) were performed on 3654 individuals (82.4% participation rate). The surviving baseline participants were invited to attend follow-up examinations after 5 years (1997-1999) and after 10 years (2002-2004). At each visit, the participants were examined in the same order as at baseline using the same procedures and equipment.

Face-to-face interviews were conducted and comprehensive eye examinations, including retinal photography, were performed at each visit. Stereoscopic 30° retinal photographs (Zeiss FF3 fundus camera; Carl Zeiss, Oberkochen, Germany) of diabetic retinopathy study fields 1 (optic disc) and 2 (macula) and nonstereoscopic photographs of fields 3 (temporal), 4 and 5 (upper and lower vascular arcades), and 6 (nasal to the optic disc edge) were taken of both eyes. Diabetic retinopathy study fields 4 and 5 were modified slightly to place the vascular arcades slightly closer to the center of the photograph.29 All photographs were graded for the presence of RVO by a grader who was unaware of any of the clinical diagnoses and were confirmed by a retinal specialist (P.M.).

Central RVO was characterized by widespread scattered superficial or deep retinal hemorrhages with or without optic disc hyperemia or edema, venous dilatation, retinal edema, or occluded or sheathed veins (Figure 1A). Old resolved central RVOs were diagnosed by the presence of anastomotic vessels at the disc. For hemispheric RVO, these signs were present in the upper or lower retinal half, corresponding to the branch of the central retinal vein in which the occlusion occurred. Branch RVO was characterized by retinal hemorrhages occurring within the retinal sector corresponding to the blood supply sector of the occluded venule (Figure 1B). Old branch RVO was characterized by the presence of collateral vessels or intraretinal microvascular abnormalities in a retinal sector.3032 Branch RVO occlusions were further subclassified into occlusions occurring in major venules (first order) or macular branches (second order). The affected branch RVO site (superotemporal, inferotemporal, or outside temporal field) and the arteriolar position (above or below the venule) at the crossing closest to the occlusion site were recorded.

Place holder to copy figure label and caption
Figure 1

Digitally processed images of 3 incident retinal vein occlusions (RVOs) showing the year of examination and the best-corrected visual acuity (VA). A, Incident central RVO at the 5-year follow-up examination in a 62-year-old man who died in 1999 (baseline examination in 1992 [left], 5-year examination in 1997 [right]). B, Incident branch RVO at the 5-year follow-up examination (1998 [center]) in a 57-year-old man that was resolved at the 10-year follow-up examination (2003 [right]). The arrow indicates arteriovenous nicking at baseline (1993 [left]) in both the figure and the inset, close to the site of the occlusion.

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Baseline retinal vessel wall signs were assessed using a standard set of retinal photographs, selected by 1 of us (P.M.) from standard photographic sets developed for the modified Airlie House diabetic retinopathy classification33 and the Wisconsin Age-Related Maculopathy Grading System.34 Focal arteriolar narrowing was graded as absent/questionable or present. Arteriovenous (arteriole to venule) nicking was considered present if the venular diameter decreased on both sides of the arteriole crossing it. It was graded as absent/questionable, mild, or severe. Opacification of the arteriolar wall was defined as an enhancement of the central reflex at the center of the arteriolar wall, associated with an increased width of the reflex. It was graded as absent/questionable or present. Retinal arteriolar narrowing and AV nicking were evaluated for arterioles at least 0.5 disc diameter from the optic disc. The intragrader reliability (κ statistic) for detecting focal arteriolar narrowing and AV nicking was 0.80 and 0.87, respectively.35 To measure retinal arteriolar and venular diameters, retinal photographs were digitized. All vessels passing through a circumferential zone between 0.5 and 1.0 disc diameter from the optic disc were measured using a retinal analysis software package (Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison). The Parr-Hubbard formula was used to standardize the arteriolar and venular calibers of each eye. These were summarized as central retinal arteriolar and central retinal venular equivalents.36

At baseline, blood pressure (BP) was measured after participants had been seated for 10 minutes. Systolic BP (SBP) and diastolic BP (DBP) were recorded from the first and fifth Korotkoff sounds. The mean arterial BP was calculated as the following: one third SBP+two thirds DBP. Severe hypertension was defined as a previous diagnosis of hypertension with current use of antihypertensive medication or as an SBP of at least 160 mm Hg or a DBP of at least 100 mm Hg at examination. Body mass index was calculated as weight in kilograms divided by the square of height in meters. Obesity was defined as a body mass index of at least 30. Participants were classified as smokers if they currently smoked or had stopped smoking less than 1 year before examination and were classified as heavy drinkers if they consumed at least 4 alcoholic drinks per day.

Of baseline participants, 88.1% reattended to provide fasting serum samples, which were analyzed for glucose, protein, creatinine, triglyceride, total cholesterol, and high-density lipoprotein cholesterol levels and for hematology profiles (platelet levels, hemoglobin level, hematocrit, fibrinogen level and white and red blood cell counts). Diabetes mellitus was diagnosed from the medical history or as a fasting serum glucose level of at least 126 mg/dL (≥7.0 mmol/L) at examination.

Goldmann applanation tonometry was used to record the intraocular pressure (IOP). Using the maximum IOP of the 2 eyes, the ocular perfusion pressure was calculated as the following: two thirds (DBP+[SBP−DBP]/3)−IOP.14

At baseline, the visual acuity of each eye was measured with current eyeglasses, if worn, and with pinhole using a logarithm of the minimum angle of resolution (logMAR) chart28 (VectorVision CSV-1000; VectorVision Inc, Greenville, Ohio). After obtaining the objective refraction using a Humphrey 530 automatic refractor (Allergan-Humphrey, San Leandro, Calif), subjective refraction was performed if the initial visual acuity was less than 54 letters read correctly (Snellen equivalent, 20/20 [6/6]) using a standard protocol. The spherical equivalent (in diopters [D]) was calculated using the spherical power plus one half of the cylindrical power.37 Myopia was defined as a spherical equivalent of –1.0 D or less, and hyperopia was defined as a spherical equivalent of 1.0 D or greater. Participants with unilateral or bilateral aphakia or pseudophakia were excluded from the analyses of associations between refractive error and RVO. The mean spherical equivalent of the 2 eyes represented the refractive status for each participant.

Analyses used SAS statistical software (SAS Institute Inc, Cary, NC). Because some participants who had not developed RVO by 5 years did not return for the 10-year examination, methods appropriate for censored observation were observed. The 10-year cumulative incidence was calculated using the Kaplan-Meier (product limit) method. We applied discrete linear logistic regression models38 to assess the associations between baseline factors and the long-term risk of RVO. Factors assessed for association with RVO included continuous variables (age, BP, IOP, obesity, body mass index, and fasting serum sample test results) and dichotomous variables (sex, obesity, presence of hypertension, and others). Of participants with incident RVO, 1 had diabetes at baseline, and 1 had open-angle glaucoma at baseline. Therefore, the association between diabetes or glaucoma at baseline and incident RVO could not be assessed. Tests for trend across age groups (at 10-year intervals) were performed using the Mantel-Haenszel χ2 tests. Odds ratios and 95% confidence intervals were calculated.

Of 3654 baseline participants, 2335 (75.1% of survivors) returned for the 5-year examination, and 1952 (75.6% of survivors) returned for the 10-year examination. Combining persons seen at either or both follow-up examinations, 2564 (70.2% of baseline participants) were followed up. Of these, 47 had RVO at baseline and 171 had no or ungradable photographs at either follow-up examination and were excluded, leaving 2346 participants who were at risk of developing RVO. Participants who were still alive 10 years after baseline but did not participate in the 10-year examination were older, less likely to own their homes, and more likely to be current smokers compared with nonparticipants (Table 1).

Table Graphic Jump LocationTable 1 Characteristics of Participants and Nonparticipants at the 10-Year Follow-up Examination

Incident RVO developed in 33 persons. The 10-year cumulative incidence of branch RVO was 1.2% (95% confidence interval, 0.8%-1.7%) and of central RVO was 0.4% (95% confidence interval, 0.1%-0.7%). Central RVO, including hemicentral RVO, developed in 6 participants (18.2%) after 5 years and in 2 additional participants (6.1%) after 10 years. Branch RVO developed in 15 participants (45.5%) after 5 years and in an additional 9 participants (27.3%) after 10 years. One participant (3.0%) developed central RVO in one eye at 5 years and branch RVO in the fellow eye at 10 years. Of 47 participants with RVO at baseline, 3 (6.4%) had a second RVO episode within 5 years: one developed hemicentral RVO, another developed branch RVO in the fellow eye, and the third developed branch RVO at another location in the same eye. Overall, 37 eyes had incident RVO, including 10 with incident central RVO and 27 with incident branch RVO.

Incident RVO was more frequent in the left eye (21 [63.6%] of 33 eyes) than in the right eye (12 [36.4%] of 33 eyes). Incident branch RVO occurred equally in the superotemporal and inferotemporal quadrants (11 [42.3%] of 26 eyes for both quadrants) but was infrequent outside the temporal quadrant (4 [15.4%] of 26 eyes). One participant with superotemporal branch RVO at baseline developed incident branch RVO in the inferotemporal quadrant of the same eye. In most eyes (85.2%) with incident branch RVO, the occlusion occurred in the macular (second order) branch, while only 14.8% occurred in a major (first order) branch. Macular edema was present in 5 eyes (18.5%) with incident branch RVO, including 3 eyes (11.1%) with superotemporal branch RVO and 2 eyes (7.4%) with inferotemporal branch RVO. A retinal arteriole crossing the venule near the occlusion site was found in 23 (85.2%) of 27 eyes with incident branch RVO.

Table 2 gives the age-specific 10-year cumulative incidence of RVO, which increased from 0.84% to 2.69% across the age ranges (P = .03 for trend). Figure 2 shows a similar trend for branch RVO (P = .34). Incident central RVO was not observed in any participant younger than 60 years, but among older participants a similar significant age-related increase in incident central RVO was noted (P = .04 for trend). Although incident RVO was more frequent in men (2.0%) than in women (1.3%), this was not significant after age adjustment (P = .24).

Table Graphic Jump LocationTable 2 Age Distribution of the Cumulative 10-Year Incidence of Retinal Vein Occlusion (RVO)*
Place holder to copy figure label and caption
Figure 2

Cumulative 10-year incidence of retinal vein occlusion (RVO), branch RVO, and central RVO by age group.

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Table 3 summarizes how, after age adjustment, increasing SBP, DBP, and mean arterial BP were significantly associated with increasing incidence of RVO. However, previously diagnosed hypertension was not significantly associated with incident RVO. The significant associations between ocular perfusion pressure, obesity, and incidence of RVO are given in Table 3. Table 4 summarizes how the association between obesity and incident RVO diminished after further adjustment for mean arterial BP.

Table Graphic Jump LocationTable 3 Association of Systemic and Ocular Risk Factors With the 10-Year Incidence of Branch and Central Retinal Vein Occlusion
Table Graphic Jump LocationTable 4 Multivariate Association of Risk Factors With the 10-Year Incidence of Branch and Central Retinal Vein Occlusion (RVO)*

Retinal vessel wall signs at baseline were strong predictors of incident RVO (Figure 1B and Table 4). Compared with persons without these signs at baseline, persons with these signs were more likely to develop RVO (focal arteriolar narrowing, 4.5% vs 1.2%; mild or severe AV nicking, 2.4% vs 0.6%; and severe arteriolar wall opacification, 6.0% vs 1.2%). After adjusting for age and mean arterial BP or for age and ocular perfusion pressure, all 3 retinal vessel wall signs detected at baseline remained significantly associated with incident RVO. No significant associations were found between baseline generalized arteriolar or venular calibers and incident RVO or branch RVO.

No significant associations were found between incident RVO and IOP, hematologic factors, or fasting serum glucose, creatinine, total cholesterol, or high-density lipoprotein cholesterol levels (Table 3), nor was there any association between incident RVO and smoking, baseline refraction, alcohol consumption, or history of cardiovascular disease or stroke. Separate analyses that were repeated for incident branch RVO showed associations that were similar to those for all incident (central and branch) RVO. A separate risk factor analysis for incident central RVO was prohibited by the small sample size.

Determining the long-term incidence of RVO and the risk factors associated with its development is important, as RVO is a potentially blinding eye disease. Although the 4-year and 5-year incidences of RVO have been reported in some studies,1,18,39 ours is the first population-based study (to our knowledge) with sufficient follow-up to provide 10-year incidence of RVO. The only other report of the 10-year incidence of RVO was a small Japanese study19 (with 20% follow-up) that assessed RVO from nonmydriatic fundus photographs only at the follow-up examinations. Among our older Australian cohort, we documented a 1.6% (95% confidence interval, 1.1%-2.2%) 10-year incidence of RVO. Although a slight underestimation of the incidence of RVO is likely because a small proportion of RVO cases may have resolved before the reexaminations, leaving no detectable abnormality, we believe that this underestimation is small.

For participants who had previously developed RVO, the probability of developing a second RVO in the same eye or in the fellow eye was 6.4% in our study, somewhat lower than the probabilities previously reported in a large clinic case series (0.9% during 2 years and 2.5% during 4 years for second episodes in the same eye and 7.7% during 2 years and 11.9% during 4 years for second episodes in the fellow eye).11 Compared with that study,11 our study is representative of a generalized older population, differing from a clinical case-series.

Findings from most studies,40,41 including a previous prevalence study,13 have suggested that branch RVO more frequently involves the superotemporal quadrant. This is supported by the incidence data from the Beaver Dam Eye Study,14 which reported involvement of the superotemporal quadrant in 45.5%, the inferotemporal quadrant in 36.4%, and the nasal quadrants in 18.2% of eyes that developed branch RVO. In our study, an equal proportion (42.3%) of eyes with incident branch RVO occurred in the superotemporal and inferotemporal quadrants, while 15.4% of incident cases occurred outside the temporal quadrants. However, it is possible that superotemporal vein occlusions may cause greater macular edema than RVOs elsewhere and be more symptomatic, leading to presentation bias. Macular edema was more frequent in superotemporal branch RVO than in inferotemporal branch RVO. Anatomical differences suggesting a more nasal distribution of the inferotemporal compared with the superotemporal venules40 have been considered a possible reason for the more frequent asymptomatic presentation of inferior RVO.42 This could, in part, explain the proportional differences in the 2 RVO locations observed between clinic-based and population-based samples.

Advancing age and elevated BP or ocular perfusion pressure were the principal baseline systemic variables predicting incident RVO, consistent with previous findings.5,14,15,20,21 Adequate control of elevated BP may be important in preventing RVO. The Beaver Dam Eye Study14 found a significant association of baseline ocular perfusion pressure with the prevalence of RVO but not with its 5-year incidence. However, we confirmed that ocular perfusion pressure is a modest predictor of long-term incident RVO.

Our finding that retinal arteriolar signs indicating established microvascular disease (focal narrowing, AV nicking, or wall opacification) were independent predictors of RVO risk is consistent with earlier data.14,15 Sclerotic arteriolar walls may compress underlying venules at AV crossings, leading to reduced blood flow, which in turn could facilitate the development of a thrombus and downstream venular occlusion. Based on this mechanism, sheathotomy at AV crossings has been proposed as a treatment option for branch RVO with macular edema.43

Some authors10 have noted hematologic abnormalities associated with RVO, but we did not. However, we did not collect baseline data for other thrombophilic factors (hyperhomocysteinemia, factor V Leiden mutation, protein C and S deficiency, and antithrombin or anticardiolipin antibodies) that are associated with RVO. We failed to find a significant association between incident RVO and elevated fasting glucose or cholesterol levels; the scarcity of incident RVO cases could have contributed to this negative finding.

Although the presence of acquired optociliary (anastomotic) shunt vessels generally indicates old central RVO,4446 this could indicate other conditions, including optic nerve sheath meningioma,45,47,48 papilledema,45,49 chronic glaucoma,45 or diabetes.50 In our sample, only 1 participant was diagnosed as having old central RVO based on the presence of optociliary shunt vessels in photographs from the 5-year examination; however, the optic disc was not pale, and the participant had neither diabetes nor symptoms or signs suggesting optic nerve compression. At 10 years, this participant had developed branch RVO in the fellow eye.

Our study has other limitations. Almost 30% of the baseline participants were not reexamined at the 5-year or the 10-year examinations. Most participants who were lost to follow-up had died; therefore, the incidence of RVO could have been underestimated. It is possible that there are unmeasured predictors of incident RVO that we did not adjust for. The association between cardiovascular risk factors and incident RVO3 may have been underestimated because of selective survival, a bias arising from the higher risk of dying during follow-up among persons with cardiovascular risk factors. Estimates of the incidence of RVO in our older white population can only be applied to other populations with similar age and characteristics. Nevertheless, our study has many strengths, including its representative population-based sample, the use of 6-field stereoscopic retinal photographs, and the detection of RVO from masked photographic grading, with confirmation by a senior clinician.

In summary, the 10-year incidence of RVO in this older Australian population was 1.6%. Elevated BP and retinal vessel wall changes reflecting chronic hypertension and arteriosclerosis were long-term predictors of incident RVO. Monitoring and adequate control of elevated BP in patients with these signs could be a useful strategy in preventing RVO.

Correspondence: Paul Mitchell, MD, PhD, Centre for Vision Research, Department of Ophthalmology, University of Sydney, Westmead Hospital, Hawkesbury Road, Westmead, New South Wales, Australia 2145 (paul_mitchell@wmi.usyd.edu.au).

Submitted for Publication: August 16, 2005; final revision received October 24, 2005; accepted November 29, 2005.

Financial Disclosure: None.

Funding/Support: This study was supported by grants 974159, 211069, 153948, and 302068 from the Australian National Health and Medical Research Council, Canberra.

David  RZangwill  LBadarna  MYassur  Y Epidemiology of retinal vein occlusion and its association with glaucoma and increased intraocular pressure. Ophthalmologica 1988;19769- 74
PubMed
Klein  RWang  QKlein  BEMoss  SEMeuer  SM The relationship of age-related maculopathy, cataract, and glaucoma to visual acuity. Invest Ophthalmol Vis Sci 1995;36182- 191
PubMed
Martin  SCButcher  AMartin  N  et al.  Cardiovascular risk assessment in patients with retinal vein occlusion. Br J Ophthalmol 2002;86774- 776
PubMed
Tsaloumas  MDKirwan  JVinall  H  et al.  Nine-year follow-up study of morbidity and mortality in retinal vein occlusion. Eye 2000;14821- 827
PubMed
Hayreh  SSZimmerman  BMcCarthy  MJPodhajsky  P Systemic diseases associated with various types of retinal vein occlusion. Am J Ophthalmol 2001;13161- 77
PubMed
Deramo  VACox  TASyed  ABLee  PPFekrat  S Vision-related quality of life in people with central retinal vein occlusion using the 25-item National Eye Institute Visual Function Questionnaire. Arch Ophthalmol 2003;1211297- 1302
PubMed
Rath  EZFrank  RNShin  DHKim  C Risk factors for retinal vein occlusions: a case-control study. Ophthalmology 1992;99509- 514
PubMed
McGrath  MAWechsler  FHunyor  ABPenny  R Systemic factors contributory to retinal vein occlusion. Arch Intern Med 1978;138216- 220
PubMed
Johnston  RLBrucker  AJSteinmann  WHoffman  MEHolmes  JH Risk factors of branch retinal vein occlusion. Arch Ophthalmol 1985;1031831- 1832
PubMed
Hayreh  SSZimmerman  MBPodhajsky  P Hematologic abnormalities associated with various types of retinal vein occlusion. Graefes Arch Clin Exp Ophthalmol 2002;240180- 196
PubMed
Hayreh  SSZimmerman  MBPodhajsky  P Incidence of various types of retinal vein occlusion and their recurrence and demographic characteristics. Am J Ophthalmol 1994;117429- 441
PubMed
Elman  MJBhatt  AKQuinlan  PMEnger  C The risk for systemic vascular diseases and mortality in patients with central retinal vein occlusion. Ophthalmology 1990;971543- 1548
PubMed
Mitchell  PSmith  WChang  A Prevalence and associations of retinal vein occlusion in Australia: the Blue Mountains Eye Study. Arch Ophthalmol 1996;1141243- 1247
PubMed
Klein  RKlein  BEMoss  SEMeuer  SM The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study. Trans Am Ophthalmol Soc 2000;98133- 141
PubMed
Wong  TYLarsen  EKKlein  R  et al.  Cardiovascular risk factors for retinal vein occlusion and arteriolar emboli: the Atherosclerosis Risk in Communities & Cardiovascular Health studies. Ophthalmology 2005;112540- 547
PubMed
Nwosu  SN Prevalence and pattern of retinal diseases at the Guinness Eye Hospital, Onitsha, Nigeria. Ophthalmic Epidemiol 2000;741- 48
PubMed
Hubbard  LDBrothers  RJKing  WN  et al.  Methods for evaluation of retinal microvascular abnormalities associated with hypertension/sclerosis in the Atherosclerosis Risk in Communities Study. Ophthalmology 1999;1062269- 2280
PubMed
Hirota  AMishima  HKKiuchi  Y Incidence of retinal vein occlusion at the glaucoma clinic of Hiroshima University. Ophthalmologica 1997;211288- 291
PubMed
Kashiwagi  KShibuya  TTsukahara  S De novo age-related retinal disease and intraocular-pressure changes during a 10-year period in a Japanese adult population. Jpn J Ophthalmol 2005;4936- 40
PubMed
Eye Disease Case-Control Study Group, Risk factors for central retinal vein occlusion. Arch Ophthalmol 1996;114545- 554
PubMed
Eye Disease Case-Control Study Group, Risk factors for branch retinal vein occlusion. Am J Ophthalmol 1993;116286- 296
PubMed
Beaumont  PEKang  HK Clinical characteristics of retinal venous occlusions occurring at different sites. Br J Ophthalmol 2002;86572- 580
PubMed
Hayreh  SSZimmerman  MBBeri  MPodhajsky  P Intraocular pressure abnormalities associated with central and hemicentral retinal vein occlusion. Ophthalmology 2004;111133- 141
PubMed
Cekic  OTotan  YAydin  EPehlivan  EHilmioglu  F The role of axial length in central and branch retinal vein occlusion. Ophthalmic Surg Lasers 1999;30523- 527
PubMed
Janssen  MCden Heijer  MCruysberg  JRWollersheim  HBredie  SJ Retinal vein occlusion: a form of venous thrombosis or a complication of atherosclerosis? a meta-analysis of thrombophilic factors. Thromb Haemost 2005;931021- 1026
PubMed
Glacet Bernard  AChabanel  ALelong  FSamama  MMCoscas  G Elevated erythrocyte aggregation in patients with central retinal vein occlusion and without conventional risk factors. Ophthalmology 1994;1011483- 1487
PubMed
Mitchell  PSmith  WAttebo  KWang  JJ Prevalence of age-related maculopathy in Australia: the Blue Mountains Eye Study. Ophthalmology 1995;1021450- 1460
PubMed
Attebo  KMitchell  PSmith  W Visual acuity and the causes of visual loss in Australia: the Blue Mountains Eye Study. Ophthalmology 1996;103357- 364
PubMed
Yu  TMitchell  PBerry  GLi  WWang  JJ Retinopathy in older persons without diabetes and its relationship to hypertension. Arch Ophthalmol 1998;11683- 89
PubMed
Pieris  SJHill  DW Collateral vessels in branch retinal vein occlusion. Trans Ophthalmol Soc U K 1982;102178- 181
PubMed
Patz  AYassur  YFine  SLFinkelstein  DOrth  DH Branch retinal venous occlusion. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol 1977;83 ((pt 1)) OP373- OP378
PubMed
Joffe  LGoldberg  REMagargal  LEAnnesley  WH Macular branch vein occlusion. Ophthalmology 1980;8791- 98
PubMed
Diabetic Retinopathy Study Research Group, Diabetic Retinopathy Study: report number 6: design, methods, and baseline results: report number 7: a modification of the Airlie House classification of diabetic retinopathy. Invest Ophthalmol Vis Sci 1981;21 ((pt 2)) 1- 226
PubMed
Klein  RDavis  MDMagli  YL  et al.  The Wisconsin Age-Related Maculopathy Grading System. Ophthalmology 1991;981128- 1134
PubMed
Wang  JJMitchell  PLeung  H  et al.  Hypertensive retinal vessel wall signs in a general older population: the Blue Mountains Eye Study. Hypertension 2003;42534- 541
PubMed
Leung  HWang  JJRochtchina  E  et al.  Relationships between age, blood pressure and retinal vessel diameters in an older population. Invest Ophthalmol Vis Sci 2003;442900- 2904
PubMed
Attebo  KIvers  RQMitchell  P Refractive errors in an older population: the Blue Mountains Eye Study. Ophthalmology 1999;1061066- 1072
PubMed
Hosmer  DWLemeshow  S Applied Logistic Regression.  New York, NY John Wiley & Sons Inc1989;
Sherry  LMWang  JJRochtchina  E  et al.  Reliability of computer-assisted retinal vessel measurement in a population. Clin Experiment Ophthalmol 2002;30179- 182
PubMed
Feist  RMTicho  BHShapiro  MJFarber  M Branch retinal vein occlusion and quadratic variation in arteriovenous crossings. Am J Ophthalmol 1992;113664- 668
PubMed
Zhao  JSastry  SMSperduto  RDChew  EYRemaley  NAEye Disease Case-Control Study Group, Arteriovenous crossing patterns in branch retinal vein occlusion. Ophthalmology 1993;100423- 428
PubMed
Battaglia Parodi  MIacono  PDi Crecchio  LSanguinetti  GRavalico  G Clinical and angiographic features in nasal branch retinal vein occlusion. Ophthalmologica 2004;218210- 213
PubMed
Yamaji  HShiraga  FTsuchida  YYamamoto  YOhtsuki  H Evaluation of arteriovenous crossing sheathotomy for branch retinal vein occlusion by fluorescein videoangiography and image analysis. Am J Ophthalmol 2004;137834- 841
PubMed
Priluck  IARobertson  DMHollenhorst  RW Long-term follow-up of occlusion of the central retinal vein in young adults. Am J Ophthalmol 1980;90190- 202
PubMed
Anderson  DPKhalil  MLorenzetti  DWSaheb  NE Abnormal blood vessels on the optic disc. Can J Ophthalmol 1983;18108- 114
PubMed
Giuffre  GPalumbo  CRandazzo Papa  G Optociliary veins and central retinal vein occlusion. Br J Ophthalmol 1993;77774- 777
PubMed
Dutton  JJ Optic nerve sheath meningiomas. Surv Ophthalmol 1992;37167- 183
PubMed
Wright  JEMcNab  AAMcDonald  WI Primary optic nerve sheath meningioma. Br J Ophthalmol 1989;73960- 966
PubMed
Eggers  HMSanders  MD Acquired optociliary shunt vessels in papilloedema. Br J Ophthalmol 1980;64267- 271
PubMed
Lee  JJYap  EY Optociliary shunt vessels in diabetes mellitus. Singapore Med J 2004;45166- 169
PubMed

Figures

Place holder to copy figure label and caption
Figure 1

Digitally processed images of 3 incident retinal vein occlusions (RVOs) showing the year of examination and the best-corrected visual acuity (VA). A, Incident central RVO at the 5-year follow-up examination in a 62-year-old man who died in 1999 (baseline examination in 1992 [left], 5-year examination in 1997 [right]). B, Incident branch RVO at the 5-year follow-up examination (1998 [center]) in a 57-year-old man that was resolved at the 10-year follow-up examination (2003 [right]). The arrow indicates arteriovenous nicking at baseline (1993 [left]) in both the figure and the inset, close to the site of the occlusion.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2

Cumulative 10-year incidence of retinal vein occlusion (RVO), branch RVO, and central RVO by age group.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable 1 Characteristics of Participants and Nonparticipants at the 10-Year Follow-up Examination
Table Graphic Jump LocationTable 2 Age Distribution of the Cumulative 10-Year Incidence of Retinal Vein Occlusion (RVO)*
Table Graphic Jump LocationTable 3 Association of Systemic and Ocular Risk Factors With the 10-Year Incidence of Branch and Central Retinal Vein Occlusion
Table Graphic Jump LocationTable 4 Multivariate Association of Risk Factors With the 10-Year Incidence of Branch and Central Retinal Vein Occlusion (RVO)*

References

David  RZangwill  LBadarna  MYassur  Y Epidemiology of retinal vein occlusion and its association with glaucoma and increased intraocular pressure. Ophthalmologica 1988;19769- 74
PubMed
Klein  RWang  QKlein  BEMoss  SEMeuer  SM The relationship of age-related maculopathy, cataract, and glaucoma to visual acuity. Invest Ophthalmol Vis Sci 1995;36182- 191
PubMed
Martin  SCButcher  AMartin  N  et al.  Cardiovascular risk assessment in patients with retinal vein occlusion. Br J Ophthalmol 2002;86774- 776
PubMed
Tsaloumas  MDKirwan  JVinall  H  et al.  Nine-year follow-up study of morbidity and mortality in retinal vein occlusion. Eye 2000;14821- 827
PubMed
Hayreh  SSZimmerman  BMcCarthy  MJPodhajsky  P Systemic diseases associated with various types of retinal vein occlusion. Am J Ophthalmol 2001;13161- 77
PubMed
Deramo  VACox  TASyed  ABLee  PPFekrat  S Vision-related quality of life in people with central retinal vein occlusion using the 25-item National Eye Institute Visual Function Questionnaire. Arch Ophthalmol 2003;1211297- 1302
PubMed
Rath  EZFrank  RNShin  DHKim  C Risk factors for retinal vein occlusions: a case-control study. Ophthalmology 1992;99509- 514
PubMed
McGrath  MAWechsler  FHunyor  ABPenny  R Systemic factors contributory to retinal vein occlusion. Arch Intern Med 1978;138216- 220
PubMed
Johnston  RLBrucker  AJSteinmann  WHoffman  MEHolmes  JH Risk factors of branch retinal vein occlusion. Arch Ophthalmol 1985;1031831- 1832
PubMed
Hayreh  SSZimmerman  MBPodhajsky  P Hematologic abnormalities associated with various types of retinal vein occlusion. Graefes Arch Clin Exp Ophthalmol 2002;240180- 196
PubMed
Hayreh  SSZimmerman  MBPodhajsky  P Incidence of various types of retinal vein occlusion and their recurrence and demographic characteristics. Am J Ophthalmol 1994;117429- 441
PubMed
Elman  MJBhatt  AKQuinlan  PMEnger  C The risk for systemic vascular diseases and mortality in patients with central retinal vein occlusion. Ophthalmology 1990;971543- 1548
PubMed
Mitchell  PSmith  WChang  A Prevalence and associations of retinal vein occlusion in Australia: the Blue Mountains Eye Study. Arch Ophthalmol 1996;1141243- 1247
PubMed
Klein  RKlein  BEMoss  SEMeuer  SM The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study. Trans Am Ophthalmol Soc 2000;98133- 141
PubMed
Wong  TYLarsen  EKKlein  R  et al.  Cardiovascular risk factors for retinal vein occlusion and arteriolar emboli: the Atherosclerosis Risk in Communities & Cardiovascular Health studies. Ophthalmology 2005;112540- 547
PubMed
Nwosu  SN Prevalence and pattern of retinal diseases at the Guinness Eye Hospital, Onitsha, Nigeria. Ophthalmic Epidemiol 2000;741- 48
PubMed
Hubbard  LDBrothers  RJKing  WN  et al.  Methods for evaluation of retinal microvascular abnormalities associated with hypertension/sclerosis in the Atherosclerosis Risk in Communities Study. Ophthalmology 1999;1062269- 2280
PubMed
Hirota  AMishima  HKKiuchi  Y Incidence of retinal vein occlusion at the glaucoma clinic of Hiroshima University. Ophthalmologica 1997;211288- 291
PubMed
Kashiwagi  KShibuya  TTsukahara  S De novo age-related retinal disease and intraocular-pressure changes during a 10-year period in a Japanese adult population. Jpn J Ophthalmol 2005;4936- 40
PubMed
Eye Disease Case-Control Study Group, Risk factors for central retinal vein occlusion. Arch Ophthalmol 1996;114545- 554
PubMed
Eye Disease Case-Control Study Group, Risk factors for branch retinal vein occlusion. Am J Ophthalmol 1993;116286- 296
PubMed
Beaumont  PEKang  HK Clinical characteristics of retinal venous occlusions occurring at different sites. Br J Ophthalmol 2002;86572- 580
PubMed
Hayreh  SSZimmerman  MBBeri  MPodhajsky  P Intraocular pressure abnormalities associated with central and hemicentral retinal vein occlusion. Ophthalmology 2004;111133- 141
PubMed
Cekic  OTotan  YAydin  EPehlivan  EHilmioglu  F The role of axial length in central and branch retinal vein occlusion. Ophthalmic Surg Lasers 1999;30523- 527
PubMed
Janssen  MCden Heijer  MCruysberg  JRWollersheim  HBredie  SJ Retinal vein occlusion: a form of venous thrombosis or a complication of atherosclerosis? a meta-analysis of thrombophilic factors. Thromb Haemost 2005;931021- 1026
PubMed
Glacet Bernard  AChabanel  ALelong  FSamama  MMCoscas  G Elevated erythrocyte aggregation in patients with central retinal vein occlusion and without conventional risk factors. Ophthalmology 1994;1011483- 1487
PubMed
Mitchell  PSmith  WAttebo  KWang  JJ Prevalence of age-related maculopathy in Australia: the Blue Mountains Eye Study. Ophthalmology 1995;1021450- 1460
PubMed
Attebo  KMitchell  PSmith  W Visual acuity and the causes of visual loss in Australia: the Blue Mountains Eye Study. Ophthalmology 1996;103357- 364
PubMed
Yu  TMitchell  PBerry  GLi  WWang  JJ Retinopathy in older persons without diabetes and its relationship to hypertension. Arch Ophthalmol 1998;11683- 89
PubMed
Pieris  SJHill  DW Collateral vessels in branch retinal vein occlusion. Trans Ophthalmol Soc U K 1982;102178- 181
PubMed
Patz  AYassur  YFine  SLFinkelstein  DOrth  DH Branch retinal venous occlusion. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol 1977;83 ((pt 1)) OP373- OP378
PubMed
Joffe  LGoldberg  REMagargal  LEAnnesley  WH Macular branch vein occlusion. Ophthalmology 1980;8791- 98
PubMed
Diabetic Retinopathy Study Research Group, Diabetic Retinopathy Study: report number 6: design, methods, and baseline results: report number 7: a modification of the Airlie House classification of diabetic retinopathy. Invest Ophthalmol Vis Sci 1981;21 ((pt 2)) 1- 226
PubMed
Klein  RDavis  MDMagli  YL  et al.  The Wisconsin Age-Related Maculopathy Grading System. Ophthalmology 1991;981128- 1134
PubMed
Wang  JJMitchell  PLeung  H  et al.  Hypertensive retinal vessel wall signs in a general older population: the Blue Mountains Eye Study. Hypertension 2003;42534- 541
PubMed
Leung  HWang  JJRochtchina  E  et al.  Relationships between age, blood pressure and retinal vessel diameters in an older population. Invest Ophthalmol Vis Sci 2003;442900- 2904
PubMed
Attebo  KIvers  RQMitchell  P Refractive errors in an older population: the Blue Mountains Eye Study. Ophthalmology 1999;1061066- 1072
PubMed
Hosmer  DWLemeshow  S Applied Logistic Regression.  New York, NY John Wiley & Sons Inc1989;
Sherry  LMWang  JJRochtchina  E  et al.  Reliability of computer-assisted retinal vessel measurement in a population. Clin Experiment Ophthalmol 2002;30179- 182
PubMed
Feist  RMTicho  BHShapiro  MJFarber  M Branch retinal vein occlusion and quadratic variation in arteriovenous crossings. Am J Ophthalmol 1992;113664- 668
PubMed
Zhao  JSastry  SMSperduto  RDChew  EYRemaley  NAEye Disease Case-Control Study Group, Arteriovenous crossing patterns in branch retinal vein occlusion. Ophthalmology 1993;100423- 428
PubMed
Battaglia Parodi  MIacono  PDi Crecchio  LSanguinetti  GRavalico  G Clinical and angiographic features in nasal branch retinal vein occlusion. Ophthalmologica 2004;218210- 213
PubMed
Yamaji  HShiraga  FTsuchida  YYamamoto  YOhtsuki  H Evaluation of arteriovenous crossing sheathotomy for branch retinal vein occlusion by fluorescein videoangiography and image analysis. Am J Ophthalmol 2004;137834- 841
PubMed
Priluck  IARobertson  DMHollenhorst  RW Long-term follow-up of occlusion of the central retinal vein in young adults. Am J Ophthalmol 1980;90190- 202
PubMed
Anderson  DPKhalil  MLorenzetti  DWSaheb  NE Abnormal blood vessels on the optic disc. Can J Ophthalmol 1983;18108- 114
PubMed
Giuffre  GPalumbo  CRandazzo Papa  G Optociliary veins and central retinal vein occlusion. Br J Ophthalmol 1993;77774- 777
PubMed
Dutton  JJ Optic nerve sheath meningiomas. Surv Ophthalmol 1992;37167- 183
PubMed
Wright  JEMcNab  AAMcDonald  WI Primary optic nerve sheath meningioma. Br J Ophthalmol 1989;73960- 966
PubMed
Eggers  HMSanders  MD Acquired optociliary shunt vessels in papilloedema. Br J Ophthalmol 1980;64267- 271
PubMed
Lee  JJYap  EY Optociliary shunt vessels in diabetes mellitus. Singapore Med J 2004;45166- 169
PubMed

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