Adverse association between diabetic retinopathy and cardiac structure and function
Received 6 August 2008; accepted 26 October 2008. published online 22 December 2008.
Background
Recent work has demonstrated a link between retinopathy, a marker of microvascular disease, and the development of heart failure, a finding particularly relevant in individuals with diabetes. Our objective was to assess the relationship between retinopathy and cardiac structure and function in a cohort of individuals with type 2 diabetes mellitus.
Methods
Stereoscopic fundus photography of 7 standard fields was obtained in 531 Mexican American adults with type 2 diabetes mellitus recruited as sibships from Starr County, Texas. Retinopathy was centrally scored and classified as no retinopathy, early nonproliferative diabetic retinopathy, moderate to severe nonproliferative diabetic retinopathy, or proliferative diabetic retinopathy. Echocardiography was used to assess cardiac structure and function. Multilevel mixed models were used to assess associations of clinical and echocardiographic variables with retinopathy while accounting for correlations among siblings.
Results
More severe diabetic retinopathy was associated with the presence of hypertension, previous cardiovascular disease, longer duration of diabetes, elevated glycosylated hemoglobin, and greater albuminuria. With worsening severity of diabetic retinopathy, left ventricular (LV) mass and left atrial dimension increased, and LV ejection fraction and LV fractional shortening decreased, independent of potential confounding variables.
Conclusions
More severe diabetic retinopathy was associated with worse cardiac structure and function by echocardiography independent of potential confounding variables. These data suggest a possible microvascular contribution to the development of diabetes-associated cardiac enlargement and dysfunction. Alternatively, common pathways may be leading to both disorders.
aWinters Center for Heart Failure Research and Section of Cardiology, Baylor College of Medicine, Houston, TX
bHuman Genetics Center, the University of Texas Health Science Center School of Public Health, Houston, TX
cUniversity of Wisconsin School of Medicine and Public Health, Madison, WI
Reprint requests: David Aguilar, MD, Cardiovascular Division; Baylor College of Medicine, 1709 Dryden Street, Suite 9.39, MS: BCM 620, Houston, TX 77030.
This study was supported in part by the National Heart, Lung, and Blood Institute Family Blood Pressure Program (HL54504), the National Eye Institute (EY12386), and an NIH Mentored Clinical Investigator Award (5K12RR017665-05) to Dr Aguilar.
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