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Prosthetic valve endocarditis (PVE) is associated with significant mortality and morbidity.1 Despite medical advances in surgical techniques, PVE continues to complicate cardiac valve surgery. The incidence is highest within the first 12 months following surgery and affecting 1–3% of patients.2 PVE can arise early or late after surgery. According to the microbiological profile, the most appropriate cut-off time to distinguish between early and late-onset PVE is 1 year.2 The timing of the infection reflects different pathogenic mechanisms that, in turn, influence the epidemiology, microbiology, pathology and clinical manifestations of the infection. In early-onset PVE microorganisms can reach the valve prosthesis by direct contamination intraoperatively or via haematogenous spread during the initial days and weeks after surgery. As pointed out by Thuny et al in this issue (see page 743),3 different mechanisms, including iatrogenic causes and hospital-acquired infections, may contribute to the disease. In early PVE, pathogens have direct access to the prosthesis–annulus interface and to perivalvular tissue along suture pathways because the valve sewing ring, cardiac annulus and anchoring sutures are not endothelialised early after valve implantation. These structures are coated with host proteins that may favour the adherence of some microorganisms. …
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