Retinal Vascular Caliber in Persons with Type 2 Diabetes: The Wisconsin Epidemiological Study of Diabetic Retinopathy: XX
Received 14 October 2005; accepted 14 March 2006. published online 06 July 2006.
Purpose
To describe retinal vascular caliber and correlates in people with type 2 diabetes.
Design
Population-based study.
Participants
Thirteen hundred seventy persons diagnosed to have diabetes at or after 30 years of age in an 11-county area in south central Wisconsin from 1980 to 1982.
Methods
Retinal photographs of 7 standard fields were taken; light box grading was done to determine retinopathy severity. Computer-assisted grading was done from a digitized image of field 1 to determine the central retinal arteriolar equivalent (CRAE; arteriolar caliber) and central retinal venular equivalent (CRVE; venular caliber).
Main Outcome Measures
Retinal arteriolar and venular calibers.
Results
In multivariable analyses in persons with panretinal photocoagulation excluded, while controlling for refractive error, CRAE was associated independently with age (per 10 years, β = −2.0 μm), mean arterial blood pressure (BP) (per 10 mmHg, β = −2.2 μm), smoking status (current vs. never smoked, β = 5.6 μm), and intraocular pressure (IOP) (per 1 mmHg, β = 0.2 μm). The CRVE was associated independently with age (per 10 years, β = −2.5 μm), mean arterial BP (per 10 mmHg, β = −2.1 μm), smoking status (current vs. never smoked, β = 11.6 μm), pack-years smoked (per 10 pack-years, β = 1.0 μm), body mass index (per kg/m2, β = 0.3 mm), pulse rate (per 10 beats/minute, β = 1.5 μm), retinopathy severity (per 1 level, β = 1.05 μm), and IOP (per 10 mmHg, β = −0.5 μm). Smaller CRAEs and CRVEs were found in eyes with panretinal photocoagulation treatment than in eyes without such treatment.
Conclusions
In persons with type 2 diabetes, variations in retinal vascular caliber are related to various systemic and ocular factors. Understanding these relationships may provide further insights into early retinal vascular changes in diabetes.
1Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
2Department of Ophthalmology, University of Melbourne, East Melbourne, Australia.
3Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
Correspondence to Ronald Klein, MD, MPH, Department of Ophthalmology and Visual Sciences, University of Wisconsin–Madison, 610 North Walnut Street, 4th Floor, Madison, WI 53726-2336.
Manuscript no. 2005-993.
This work was supported by the National Institutes of Health, Bethesda, Maryland (grant no.: EY015117), and in part by Research to Prevent Blindness, New York, New York (Senior Scientific Investigator Award [RK]).
ABSTRACT