title: Defective myogenic response to posture change in retinal vessels of well-controlled type 1 diabetic patients with no retinopathy.
abstract: OBJECTIVE
  The current approach to the prevention of diabetic retinopathy relies on intensive anti-diabetes treatment and is only partially successful. A marker of retinopathy risk would enable strategies of surveillance, screening of adjunct drugs, and targeted drug interventions. The authors sought to identify early abnormalities of retinal vessels that are not prevented by the current therapeutic approach.
  
  
  METHODS
  Retinal thickness (an informer of vascular permeability) and hemodynamic parameters at baseline and longitudinally were measured in 27 subjects (age, 32 ± 9 years [mean ± SD]) with well-controlled type 1 diabetes of 12.4 ± 6.4 years' duration and no retinopathy, and in 27 control subjects. In a subset of 17 patients and 11 controls, the hemodynamic response to reclining, a postural change that increases retinal perfusion pressure, was measured.
  
  
  RESULTS
  Baseline foveal thickness and hemodynamic parameters were similar in the diabetic and control subjects. Foveal thickness increased over 12 months in the diabetic subjects, from 217 ± 22 μm to 222 ± 20 μm (P = 0.0036), remaining however within the normal range. Reclining uncovered in 47% of diabetic subjects (P = 0.016 compared with controls) an absent myogenic response (i.e., unchanged or increased arterial diameter instead of the normal decrease). The patterns were repeatable. Only the diabetic group with defective vasoconstriction showed widening arterial diameter over 12 months, a change presaging vascular dilatation in diabetic retinopathy.
  
  
  CONCLUSIONS
  Defective myogenic response to pressure was the first detectable abnormality of retinal vessels in subjects with well-controlled type 1 diabetes. Because of its selective occurrence, interpretability in individual patients, and pathogenic potential, the abnormality deserves evaluation as a risk marker for retinopathy.
authors.affiliation: Schepens Eye Research Institute, Harvard Medical School, Boston, MA 02114, USA. mara.lorenzi@schepens.harvard.edu
authors.forename: Mara
authors.initials: M
authors.lastname: Lorenzi
authors.forename: Gilbert T
authors.initials: GT
authors.lastname: Feke
authors.forename: Linda
authors.initials: L
authors.lastname: Pitler
authors.forename: Fatmire
authors.initials: F
authors.lastname: Berisha
authors.forename: Julia
authors.initials: J
authors.lastname: Kolodjaschna
authors.forename: J Wallace
authors.initials: JW
authors.lastname: McMeel
mesh_terms: D000293:Adolescent; D000328:Adult; D001160:Arterioles / Q000503:physiopathology; D015415:Biomarkers; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006339:Heart Rate; D006801:Humans; D007231:Infant, Newborn; D017078:Laser-Doppler Flowmetry; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D011187:Posture / Q000502:physiology*; D012039:Regional Blood Flow; D012161:Retinal Artery / Q000503:physiopathology*; D012178:Retinopathy of Prematurity / Q000503:physiopathology*; D041623:Tomography, Optical Coherence; D014661:Vasoconstriction / Q000502:physiology; D055815:Young Adult
chemical_list: D015415:Biomarkers; D006442:Glycated Hemoglobin; C517652:hemoglobin A1c protein, human