Influence of Flickering Light on the Retinal Vessels in Diabetic Patients

  1. Aleksandra Mandecka, MD1,
  2. Jens Dawczynski, MD2,
  3. Marcus Blum, MD3,
  4. Nicolle Müller, DNUTR1,
  5. Christoph Kloos, MD1,
  6. Gunter Wolf, MD1,
  7. Walthard Vilser, MS4,
  8. Heike Hoyer, MS5 and
  9. Ulrich Alfons Müller, MD, MSC1
  1. 1Department of Internal Medicine III, Friedrich-Schiller University, Jena, Germany
  2. 2Department of Ophthalmology, Friedrich-Schiller University, Jena, Germany
  3. 3Department of Ophthalmology, Helios Klinikum, Erfurt, Germany
  4. 4IMEDOS, Jena, Germany
  5. 5Institute of Medical Statistics, Computer Sciences and Documentation, Friedrich-Schiller-University, Jena, Germany
  1. Address correspondence and reprint requests to Aleksandra Mandecka, Department of Internal Medicine III, Friedrich-Schiller University, Bachstrasse 18, 07743, Jena, Germany. E-mail: aleksandra.mandecka{at}med.uni-jena.de

Abstract

OBJECTIVE—Stimulation of the retina with flickering light increases retinal vessel diameters in humans. Nitric oxide is a mediator of the retinal vasodilation to flicker. The reduction of vasodilation is considered an endothelial dysfunction. We investigated the response of retinal vessels to flickering light in diabetic patients in different stages of diabetic retinopathy.

RESEARCH DESIGN AND METHODS—We studied 53 healthy volunteers, 68 type 1 diabetic patients, and 172 type 2 diabetic patients. The diameter of retinal vessels was measured continuously online with the Dynamic Vessel Analyzer (DVA). Diabetic retinopathy was classified using Early Treatment Diabetic Retinopathy Study criteria. Changes in vasodilation are expressed as percent change over baseline values.

RESULTS—After adjustments for age, sex, and antihypertensive treatment, the response of retinal arterioles to diffuse luminance flicker was significantly diminished in patients with type 1 diabetes compared with healthy volunteers. The vasodilation of retinal arterioles and venules decreased continuously with increasing stages of diabetic retinopathy. The retinal arterial diameter change was 3.6 ± 2.1% in the control group, 2.6 ± 2.5% in the no diabetic retinopathy group, 2.0 ± 2.7% in the mild nonproliferative diabetic retinopathy (NPDR) group, 1.6 ± 2.2% in the moderate NPDR group, 1.8 ± 1.9% in severe NPDR group, and 0.8 ± 1.6% in proliferative diabetic retinopathy group.

CONCLUSIONS—Flicker responses of retinal vessels are abnormally reduced in diabetic patients. This decreased response deteriorated with increasing stages of retinopathy. The response was already reduced before clinical appearance of retinopathy. The noninvasive testing of retinal autoregulation with DVA might prove to be of value in early detection of diabetic vessel pathological changes.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 28 August 2007. DOI: 10.2337/dc07-0927.

    A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact.

    • Accepted August 22, 2007.
    • Received May 15, 2007.
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  1. Published online before print August 29, 2007, doi: 10.2337/dc07-0927 Diabetes Care December 2007 vol. 30 no. 12 3048-3052
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