Uncorrected Refractive Error in the African American Eye Disease Study.

Importance: Refractive error remains the largest cause of correctable visual impairment in the US. Correction of refractive error will reduce visual impairment and its associated morbidity but also improve quality of life and productivity. Objective: To determine the burden of and risk factors (RFs) associated with any uncorrected refractive error (UCRE) and unmet refractive need (URN) in a population-based sample of African American adults. Design, Setting, and Participants: This cross-sectional study, conducted from April 2014 to April 2018, included a population-based sample of self-identified African American participants 40 years and older from 30 contiguous census tracts in Inglewood, California. Participants underwent a complete ophthalmic examination and an in-home-administered questionnaire to assess sociodemographic, lifestyle, biological, medical, and health care and eye care usage RFs associated with UCRE and URN. Measurements of visual acuity (VA) were performed using a standard Early Treatment Diabetic Retinopathy Study protocol. Noncycloplegic automated refraction with supplemental subjective refraction was performed. UCRE was defined as an improvement of 2 or more lines with refraction in the better-seeing eye. URN was defined as an improvement of 2 or more lines with refraction in the better-seeing eye in those persons who were visually impaired. Sex- and age-specific burden of UCRE and URN were calculated, and multiple regression analyses were used to identify independent RFs. Study data were analyzed from May 2018 to December 2023. Exposures: Presence or absence of correctable refractive error. Main Outcomes and Measures: Self-reported sex- and age-specific prevalence of and risk indicators of UCRE and URN. Results: Of the 7957 eligible participants in the African American Eye Disease Study (AFEDS), 6347 (80%) completed both the in-home interview and the clinical examination. Of these, 6337 participants (mean [SD] age, 61 [11] years; 3997 female [63%]) with complete refractive error data were included in the analysis. Refractive error-related correctable visual impairment was present in over two-thirds of participants with visual impairment (68.7%). The overall prevalence of any UCRE was 14.6% (925 of 6337), and the overall prevalence of any URN was 5.4% (URN1 [those with presenting VA of worse than 20/40 in the better-seeing eye but who could achieve 20/40 or better with correction], 157 of 2893; URN2 [those with presenting VA of worse than 20/40 in the better-seeing eye but who could achieve an improvement of 2 or more lines with refractive correction], 155 of 2891). Conclusions and Relevance: Results of this cross-sectional study suggest a high burden of refractive error-associated correctable refractive error in African American adults, making it the leading cause of visual impairment in this population. Providing universal coverage for vision care and prescription glasses is an affordable and achievable health care intervention that could reduce the burden of visual impairment in African American adults by over two-thirds and likely raise the quality of life and work productivity, especially in this vulnerable minority population.

Anatomically specific reactive oxygen species production participates in Marfan syndrome aneurysm formation.

Marfan syndrome (MFS) is a connective tissue disorder that results in aortic root aneurysm formation. Reactive oxygen species (ROS) seem to play a role in aortic wall remodelling in MFS, although the mechanism remains unknown. MFS Fbn1C1039G/+ mouse root/ascending (AS) and descending (DES) aortic samples were examined using DHE staining, lucigenin-enhanced chemiluminescence (LGCL), Verhoeff's elastin-Van Gieson staining (elastin breakdown) and in situ zymography for protease activity. Fbn1C1039G/+ AS- or DES-derived smooth muscle cells (SMC) were treated with anti-TGF-ß antibody, angiotensin II (AngII), anti-TGF-ß antibody + AngII, or isotype control. ROS were detected during early aneurysm formation in the Fbn1C1039G/+ AS aorta, but absent in normal-sized DES aorta. Fbn1C1039G/+ mice treated with the unspecific NADPH oxidase inhibitor, apocynin reduced AS aneurysm formation, with attenuated elastin fragmentation. In situ zymography revealed apocynin treatment decreased protease activity. In vitro SMC studies showed Fbn1C1039G/+ -derived AS SMC had increased NADPH activity compared to DES-derived SMC. AS SMC NADPH activity increased with AngII treatment and appeared TGF-ß dependent. In conclusion, ROS play a role in MFS aneurysm development and correspond anatomically with aneurysmal aortic segments. ROS inhibition via apocynin treatment attenuates MFS aneurysm progression. AngII enhances ROS production in MFS AS SMCs and is likely TGF-ß dependent.