We read with interest the article by Mandecka et al. (1) describing reduced retinal vessel reactivity, as measured by the response to flicker light, in people with diabetes and diabetic retinopathy. Findings from this study provide further insights into the early retinal vessel diameter changes involved in the pathogenesis of diabetic microvascular complications.
Previous population-based studies have shown that individuals with diabetes have significantly wider retinal arterioles than individuals without diabetes (2,3). Data from these populations also demonstrated association of wider retinal arteriolar (4,5) and venular caliber (2,3) with diabetic retinopathy in individuals with both type 1 and type 2 diabetes. Thus, an important observation from these studies is that retinal arteriolar and venular caliber are structurally larger in people with diabetes and diabetic retinopathy.
This concept has direct relevance in studies that examine the functional parameters of retinal circulation, such as the study by Mandecka et al. (1). The reduced retinal vasodilation in response to flicker light observed in their study may indicate underlying pathological processes in diabetes, such as impaired autoregulation from endothelial dysfunction, retinal hypoxia, and inflammation (2–5). Alternatively, their findings could also reflect a reduced “vasodilatory reservoir,” or the inability of vessels to further dilate in already dilated retinal arterioles and venules, in people with diabetes and diabetic retinopathy (2–5). Possible analysis to determine whether this is the case includes adjustment for baseline retinal vessel diameter before exposure to flicker light or by stratifying patient subgroups according to larger and smaller retinal vessel diameter. If such data are not available, additional studies are clearly needed to verify the existence of reduced retinal vessel reactivity in individuals with diabetes and diabetic retinopathy.
