A Case of Endocarditis Following Endophthalmitis After XEN45 Gel Stent Implantation

Introduction: We report a case of endophthalmitis and endocarditis that developed after stent perforation following a XEN45 Gel Stent implantation 10 months ago. Case Report: A 79-year-old man was referred to our hospital because of endophthalmitis of the right eye. The patient had undergone XEN45 Gel Stent implantation in the same eye 10 months ago. On examination, the conjunctiva was perforated by the stent, and it was no longer covered by the conjunctiva. A 27-G pars plana vitrectomy with intravitreal antibiotic injection was performed. Moreover, the patient received intravenous antibiotic treatment and local anti-inflammatory and anti-infectious therapy. Streptococcus gordonii was identified as a bacterial cause of the endophthalmitis. Therefore, transesophageal echocardiography was performed, which revealed aortic valve endocarditis. Discussion: Although not proven, it is possible that the exposed XEN45 Gel Stent served as an entry point for S. gordonii, which caused the exogenous endophthalmitis and subsequent endocarditis. S. gordonii belongs to the viridans group streptococci, which is the etiological agent for endocarditis which is a severe and potentially life-threatening infection. Ophthalmologists should therefore consider the risk of systemic infections as endocarditis after endophthalmitis, particularly caused by the viridans group streptococci, which are known etiological agents of endocarditis

Nanomechanics of the endothelial glycocalyx contribute to Na+-induced vascular inflammation

High dietary salt (NaCl) is a known risk factor for cardiovascular pathologies and inflammation. High plasma Na+ concentrations (high Na+) have been shown to stiffen the endothelial cortex and decrease nitric oxide (NO) release, a hallmark of endothelial dysfunction. Here we report that chronic high Na+ damages the endothelial glycocalyx (eGC), induces release of inflammatory cytokines from the endothelium and promotes monocyte adhesion. Single cell force spectroscopy reveals that high Na+ enhances vascular adhesion protein-1 (VCAM-1)-dependent adhesion forces between monocytes and endothelial surface, giving rise to increased numbers of adherent monocytes on the endothelial surface. Mineralocorticoid receptor antagonism with spironolactone prevents high Na+-induced eGC deterioration, decreases monocyte-endothelium interactions, and restores endothelial function, indicated by increased release of NO. Whereas high Na+ decreases NO release, it induces endothelial release of the pro-inflammatory cytokines IL-1ß and TNFα. However, in contrast to chronic salt load (hours), in vivo and in vitro, an acute salt challenge (minutes) does not impair eGC function. This study identifies the eGC as important mediator of inflammatory processes and might further explain how dietary salt contributes to endothelialitis and cardiovascular pathologies by linking endothelial nanomechanics with vascular inflammation