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Longitudinal analysis of microvascular perfusion and neurodegenerative changes in early type 2 diabetic retinal disease
  1. Julia Aschauer1,
  2. Andreas Pollreisz1,
  3. Sonja Karst1,
  4. Martin Hülsmann2,
  5. Dorottya Hajdu1,
  6. Felix Datlinger1,
  7. Berit Egner1,
  8. Katharina Kriechbaum1,
  9. Eleonore Pablik3,
  10. Ursula Margarethe Schmidt-Erfurth1
  1. 1Department of Ophthalmology and Optometry, Medical University of Vienna, Wien, Wien, Austria
  2. 2Division of Cardiology, Department of Internal Medicine, Medical University of Vienna, Wien, Wien, Austria
  3. 3CeMSIIS, Medical University of Vienna, Wien, Wien, Austria
  1. Correspondence to Professor Ursula Margarethe Schmidt-Erfurth, Department of Ophthalmology and Optometry, Medical University of Vienna, Wien A-1090, Austria; ursula.schmidt-erfurth{at}meduniwien.ac.at

Abstract

Aim To prospectively monitor subclinical changes in capillary perfusion and retinal layer thickness in patients with type 2 diabetes and early diabetic retinal disease over 2 years.

Methods In this longitudinal study we performed biannual retinal vascular imaging using optical coherence tomography angiography (RTVue) to analyse the foveal avascular zone (FAZ) area, perimeter, acircularity index (AI) and parafoveal superficial/deep vessel density (VD). Spectral-domain optical coherence tomography (Spectralis) was used to measure the thickness of nine macular layers and the peripapillary nerve fibre layer.

Results Among 117 eyes (58 left) of 59 patients (21 female), 105 had no diabetic retinopathy (DR), 6 mild and 6 moderate non-proliferative DR at baseline. We found DR progression in 13 eyes at year 2. The FAZ area (+0.008±0.002 mm2/year, p<0.0001), perimeter (+0.036±0.010 mm/year, p=0.006) and AI (+0.005±0.002/year, p=0.0280) increased significantly. A pronounced decrease was found in the superficial (−1.425±0.290%/year, p<0.0001) but not the deep VD. Inner neuroretinal loss was confined to the ganglion cell (−0.539±0.150 µm/year, p=0.0004) and the inner plexiform layer (−0.361±0.127 µm/year, p=0.0045). In the outer retina, we observed a statistically significant decrease in thickness in the outer plexiform, photoreceptor layer and pigment epithelium of −0.921±0.161 µm/year, −0.325±0.139 µm/year and −0.385±0.084 µm/year, respectively.

Conclusion Subclinical signs of microangiopathy and neurodegeneration appear in parallel and are highly progressive even in the earliest stages of diabetic retinal disease.

Trial registration number EudraCT20156000239634.

  • retina

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Footnotes

  • Contributors JA: study design, study recruitment, study execution, manuscript preparation, manuscript review. AP, EP, KK, MH: manuscript review, statistical considerations. UMS-E, SK: study design, manuscript review. DH, FD, BE: manuscript review, study execution.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Obtained.

  • Ethics approval All study investigations were conducted in accordance with the tenets of the Declaration of Helsinki. The study was approved by the Ethics Committee of the Medical University of Vienna (EK1134/2015).

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement All data relevant to the study are included in the article or uploaded as supplementary information. Full data are available upon request to the Department of Ophthalmology, Medical University of Vienna, Austria.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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