BackgroundThe aim of this study was to evaluate the effect of uneventful phacoemulsification on the morphology and thickness of the macula, the submacular choroid, and the peripapillary choroid.MethodsIn 14 eyes from 14 patients, retinal macular thickness, choroidal submacular thickness, and choroidal peripapillary thickness were measured preoperatively and at one week and one month after phacoemulsification using enhanced depth imaging spectral domain optical coherence tomography. Changes in thickness of the different ocular tissues were evaluated.ResultsThere was a statistically significant increase in mean retinal macular thickness at one month. In horizontal scans, the mean increase was +8.67±6.75 μm (P<0.001), and in vertical scans, the mean increase was +8.80±7.07 μm (P=0.001). However, there were no significant changes in choroidal morphology in the submacular and peripapillary areas one month after surgery. In vertical scans, there was a nonsignificant increase in choroidal thickness (+4.21±20.2 μm; P=0.47) whilst in horizontal scans a nonsignificant decrease was recorded (−9.11±39.59 μm; P=0.41). In peripapillary scans, a nonsignificant increase in mean choroidal thickness was registered (+3.25±11.80 μm; P=0.36).ConclusionUncomplicated phacoemulsification induces nonpathologic increases in retinal macular thickness probably due to the inflammatory insult of the surgery; however these changes are not accompanied by significant changes in choroidal thickness. In the posterior segment, the morphologic response to the inflammatory insult of phacoemulsification is mainly observed at the retinal level, and seems to be independent of choroidal thickness changes.

Ghrelin is a recently described acylated peptide, which works as a somatosecretagogue and has described effects on the smooth, skeletal and cardiac muscle. We examined the production and effects of ghrelin on relaxation of the iris muscles. Contractile effects of 1e5 human ghrelin (frGhr, 10 À9 À6 Â 10 À5 M) and 1e5 human des-octanoyl-ghrelin (d-frGhr; 10 À9 À6 Â 10 À5 M) were tested on iris rabbit sphincter (n ¼ 11 frGhr; n ¼ 7 d-frGhr), dilator (n ¼ 6 frGhr; n ¼ 6 d-frGhr) and rat sphincter (n ¼ 6 frGhr; n ¼ 8 d-frGhr) precontracted muscles. On rabbit sphincter the effect of frGhr was also tested in presence of: i) L-NA (10GHRP6 (10 À4 M; n ¼ 6); and iv) apamin þ carybdotoxin (10 À6 M; n ¼ 6). Furthermore, on rabbit dilator the effect of frGhr was tested in presence of DLys 3 GHRP6 (10 À4 M; n ¼ 7). Finally, ghrelin mRNA production was assessed by ''in situ'' hybridization in Wistar rat eyes (n ¼ 8). In all muscles, frGhr promoted a concentration-dependent relaxation, maximal at 6 Â 10 À5 M, 1.5e3 min after its addition, decreasing tension by 34.1 AE 12.1%, 25.8 AE 4.8% and 52.1 AE 10.3% in the rabbit sphincter, dilator and rat sphincter, respectively. In the rabbit sphincter the relaxing effects of frGhr were: (i) enhanced in presence of DLys 3 GHRP6 (118.1 AE 21.1%); (ii) blunted by indomethacin; and (iii) not altered by apamin þ carybdotoxin (36.4 AE 14.4%) or L-NA (52.4 AE 11.4%). Relaxing effects of d-frGhr in rabbit (43.3 AE 5.2%) and rat (77.1 AE 15.3%) sphincter muscles were similar to those of frGhr. In rabbit dilator muscle, d-frGhr did not significantly alter active tension and the relaxing effect of frGhr was blunted by GHSR-1a blockage. Ghrelin mRNA was identified in iris posterior epithelium. In conclusion, ghrelin is a novel, locally produced, relaxing agent of iris dilator and sphincter muscles, an effect that is mediated by GHSR-1a in the former, but not in the latter. Furthermore, in the sphincter it seems to be mediated by prostaglandins, but not by NO or K Ca channels.

These results confirm the genetic contribution to PVR and the implication of SMAD7 and TNF locus in the development of PVR. This finding may have implications for understanding the mechanisms of PVR and could provide a potential new therapeutic target for PVR prophylaxis.

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Genetic profiling of patients with RRD can improve the predictability of PVR in addition to the well-known clinical biomarkers. This validated formula could be a new tool in our current clinical practice in order to identify those patients at high risk of developing PVR.

Proliferative vitreoretinopathy (PVR) is still the major cause of failure in retinal detachment (RD) surgery. It is believed that down-regulation in the p53 pathway could be an important key in PVR pathogenesis. The purpose was to evaluate the impact of T309G MDM2 polymorphism (rs2279744) in PVR. Distribution of T309G MDM2 genotypes among European subjects undergoing RD surgery was evaluated. Proportions of genotypes between subsamples from different countries were analyzed. Also, a genetic interaction between rs2279744 in MDM2 and rs1042522 in p53 gene was analyzed. Significant differences were observed comparing MDM2 genotype frequencies at position 309 of intron 1 between cases (GG: 21.6%, TG: 54.5%, TT: 23.8%) and controls (GG: 7.3%, TG: 43.9%, TT: 48.7%). The proportions of genotypes between sub-samples from different countries showed a significant difference. Distribution of GG genotype revealed differences in Spain (35.1–53.0)/(22.6–32.9), Portugal (39.0–74.4)/(21.4–38.9), Netherlands (40.6–66.3)/(25.3–38.8) and UK (37.5–62.4)/(23.3–34.2). The OR of G carriers in the global sample was 5.9 (95% CI: 3.2 to 11.2). The OR of G carriers from Spain and Portugal was 5.4 (95% CI: 2.2–12.7), whereas in the UK and the Netherlands was 7.3 (95% CI: 2.8–19.1). Results indicate that the G allele of rs2279744 is associated with a higher risk of developing PVR in patients undergoing a RD surgery. Further studies are necessary to understand the role of this SNP in the development of PVR.

João Barbosa Breda and Anca Croitor Sava contributed equally to the work and should therefore be regarded as equivalent first authors.

Cardiovascular (CV) disease (CVD) is the main cause of death around the world, and assessing a patient’s CV risk factors (CVRF) can play a major role in its prevention. Since it has been shown that retinal vascular alterations may reflect several systemic processes such as CVRF, we conducted a systematic review in order to summarize which ocular microvasculature changes can be found using Optical Coherence Tomography Angiography (OCTA) in patients without ocular diseases and with systemic pathologies/conditions that affect the CV system when compared to healthy subjects. We searched on online databases, namely PubMed, Scopus, Cochrane and Web of Science, and obtained additional studies through citation tracking. Case reports and review articles were excluded. A total of 47 articles were included in our review. We describe that patients with hypertension, diabetes mellitus, kidney disease, preeclampsia, coronary artery disease, carotid artery stenosis and obstructive sleep apnoea syndrome have, in general, lower retinal and choroidal Vessel Density (VD) and Length (VL), as well as an increased foveal avascular zone area and perimeter. Additionally, several characteristics and/or conditions in healthy subjects, such as smoking status, hyper or hypoxia conditions, race, among others, are also related to ocular vascular changes and should be accounted for. We concluded that OCTA could be a useful tool to assess a patient’s CV risk profile in a non‐invasive way, possibly integrating the diagnostic and prognostic algorithms of the most prevalent CV diseases in the future.