BACKGROUND. Noninvasive detection of Alzheimer's disease (AD) with high specificity and sensitivity can greatly facilitate identification of at-risk populations for earlier, more effective intervention. AD patients exhibit a myriad of retinal pathologies, including hallmark amyloid β-protein (Aβ) deposits. METHODS.Burden, distribution, cellular layer, and structure of retinal Aβ plaques were analyzed in flat mounts and cross sections of definite AD patients and controls (n = 37). In a proof-of-concept retinal imaging trial (n = 16), amyloid probe curcumin formulation was determined and protocol was established for retinal amyloid imaging in live patients. RESULTS.Histological examination uncovered classical and neuritic-like Aβ deposits with increased retinal Aβ 42 plaques (4.7-fold; P = 0.0063) and neuronal loss (P = 0.0023) in AD patients versus matched controls. Retinal Aβ plaque mirrored brain pathology, especially in the primary visual cortex (P = 0.0097 to P = 0.0018; Pearson's r = 0.84-0.91). Retinal deposits often associated with blood vessels and occurred in hot spot peripheral regions of the superior quadrant and innermost retinal layers. Transmission electron microscopy revealed retinal Aβ assembled into protofibrils and fibrils. Moreover, the ability to image retinal amyloid deposits with solid-lipid curcumin and a modified scanning laser ophthalmoscope was demonstrated in live patients. A fully automated calculation of the retinal amyloid index (RAI), a quantitative measure of increased curcumin fluorescence, was constructed. Analysis of RAI scores showed a 2.1-fold increase in AD patients versus controls (P = 0.0031). CONCLUSION.The geometric distribution and increased burden of retinal amyloid pathology in AD, together with the feasibility to noninvasively detect discrete retinal amyloid deposits in living patients, may lead to a practical approach for large-scale AD diagnosis and monitoring.

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Although the true incidence of postoperative dysphagia after cardiac surgery is unknown, it has been reported to occur in 3 to 21.6 per cent of patients. Historically, dysphagia has been associated with increased surgical complications and prolonged hospital stay. This study aimed to evaluate the costs and outcomes associated with dysphagia after cardiac surgery. Patients undergoing nonemergent, nontransplant cardiac operations between June 2013 and June 2014 were eligible for inclusion. Independent predictors of cost were identified through a multivariate linear regression model. Of the 354 patients (35% female) included for analysis, 56 (16%) were diagnosed with postoperative dysphagia. On univariate analysis, patients with dysphagia had increased intensive care unit and total hospital lengths of stay (11.8 vs 5.2 days, P < 0.001 and 18.2 vs 9.7 days, P < 0.001, respectively), and a 57 ± 15 per cent increase in cost of care ( P < 0.001). Dysphagia was not associated with higher rates of in-hospital mortality (3.6% vs 3.0%, P = 0.83). On multivariate linear regression, the development of dysphagia was independently associated with a 45.1 per cent increase in total hospital costs [95% confidence interval (31% and 59%), P < 0.001]. Dysphagia is an independent and major contributor to health care costs after cardiac operations, suggesting that postoperative dysphagia represents a highly suitable target for quality improvement and cost containment efforts.

Our initial experience with CorMatrix in the repair of CAVSD in children has resulted in good initial and midterm outcomes. The CorMatrix patch remained stable through midterm follow-up, thus may be efficacious for use in CAVSD repair.

Despite changes in antibiotic prophylaxis duration and postoperative skin treatment, our data demonstrate a stable incidence and composition of surgical wound infections during the study period. doi: 10.1111/jocs.12756 (J Card Surg 2016;31:367-372).