Collateral vessels and new vessels are 2 distinct processes that occur on the optic disc in retinal vascular disorders. Morphological differences between these 2 phenomena have been described previously using multiple imaging modalities.1-3 Studies using invasive methods have reported increased preretinal oxygen tension in eyes with new vessels.4 However, to our knowledge, noninvasive oximetry measurements of disc collateral vessels or new vessels have not been reported to-date. A noninvasive method of quantifying and differentiating these 2 processes will add value in understanding the mechanisms of the consequences of retinal vascular diseases. We hypothesized that blood in disc collateral vessels in venous occlusion should have a lower oxygen saturation compared with blood in disc new vessels given that collateral vessels develop to bypass an obstruction in the venous circulation unlike the development of new vessels, which is a proliferative process driven by hypoxia.5,6
To test this hypothesis, from January 1, 2016, to July 1, 2016, we retrospectively reviewed consecutive patients with a diagnosis of central retinal vein occlusion and proliferative diabetic retinopathy who had retinal oximetry measurements (Oxymap T1; Oxymap). Eyes with optic disc collateral vessels due to central retinal vein occlusion and eyes with disc new vessels due to proliferative diabetic retinopathy were identified. Collateral vessels and disc new vessels were confirmed by fluorescein angiography. Patients with poor-quality imaging were excluded. This study was approved by the Research Governance Committee of Moorfields Eye Hospital for the analysis of anonymized data, and written patient informed consent was obtained. The 35° disc-centered retinal oximetry measurements were used for analysis, and the minimum pixel tolerance was set at 6 pixels. The evaluated area was over the optic disc and excluded the central 50 μm. Oximetry measurements of disc collateral vessels and disc new vessels were recorded. Oximetry measurements were obtained by two of us (L.N. and C.S.), and the mean values were reported. An independent, unpaired, 2-tailed t test was used to compare means between the 2 groups. Intraclass correlation coefficient was used to assess intergrader agreement between the investigators. Statistical significance was set at 2-sided P = .05.
Three eyes with disc collateral vessels secondary to central retinal vein occlusion and 6 eyes with disc new vessels due to proliferative diabetic retinopathy were studied. Disc new vessels have a saturation of 83.14%, whereas disc collateral vessels have an average oxygen saturation of 66.92% (Figure). The difference between the 2 was 16.22% (95% CI, 4.14-28.30; P = .02). The intraclass correlation coefficient between the 2 graders was 0.899.
To our knowledge, this case series is the first report of noninvasive oximetry measurements of disc collateral vessels and new vessels in the literature. It is not surprising that the disc collateral vessels exhibit lower values because of their venous occlusion origin. However, disc new vessels appear to have significantly higher saturations. Diabetic microvascular changes predominantly occur on the venous end of capillaries, and earlier reports have highlighted that retinal neovascularization is nearly always of venous origin.6 The higher oxygen-saturation values of the new vessels in our study suggest that these new vessels either are of arterial origin or are venous but carry blood of higher oxygen saturation because of a direct shunt from the arteries. Limitations of this study include the small number of participants in our series and the comparison of new vessels in diabetic retinopathy with collateral vessels in retinal vein occlusion. This noninvasive clinical finding supports the notion that new vessels are rich in oxygen. This difference between collateral vessels and new vessels can be used to help differentiate the 2 in a clinical setting.
Corresponding Author: Sobha Sivaprasad, MD, FRCOphth, National Institute for Health Research Moorfields Biomedical Research Centre and University College London Institute of Ophthalmology, Moorfields Eye Hospital, 162 City Rd, London EC1V 2PD, England (email@example.com).
Accepted for Publication: June 5, 2017.
Published Online: August 3, 2017. doi:10.1001/jamaophthalmol.2017.2624
Author Contributions: Dr Nicholson had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Nicholson, Hykin, Bainbridge, Sivaprasad.
Acquisition, analysis, or interpretation of data: Nicholson, Sivapathasuntharam, Zola, Hykin, Sivaprasad.
Drafting of the manuscript: Nicholson, Zola, Hykin, Sivaprasad.
Critical revision of the manuscript for important intellectual content: Nicholson, Sivapathasuntharam, Bainbridge, Sivaprasad.
Statistical analysis: Nicholson, Sivapathasuntharam, Sivaprasad.
Obtained funding: Hykin.
Administrative, technical, or material support: Nicholson, Zola.
Study supervision: Hykin, Bainbridge, Sivaprasad.
Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Hykin reports receiving grants, personal fees, and nonfinancial support from Allergan, Bayer, and Novartis unrelated to this study. Dr Sivaprasad reports being a member of the advisory board and receiving grants and speaker fees from Allergan, Bayer, and Novartis unrelated to this study. No other disclosures were reported.
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