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BackgroundInfective endocarditis (IE) after transcatheter pulmonary valve implantation (TPVI) in dysfunctioning right ventricular outflow tract conduits has evoked growing concerns. We aimed to investigate the incidence and the natural history of IE after TPVI with the Melody valve through a systematic review of published data.Methods and ResultsPubMed, EMBASE, and Web of Science databases were systematically searched for articles published until March 2017, reporting on IE after TPVI with the Melody valve. Nine studies (including 851 patients and 2060 patient‐years of follow‐up) were included in the analysis of the incidence of IE. The cumulative incidence of IE ranged from 3.2% to 25.0%, whereas the annualized incidence rate ranged from 1.3% to 9.1% per patient‐year. The median (interquartile range) time from TPVI to the onset of IE was 18.0 (9.0–30.4) months (range, 1.0–72.0 months). The most common findings were positive blood culture (93%), fever (89%), and new, significant, and/or progressive right ventricular outflow tract obstruction (79%); vegetations were detectable on echocardiography in only 34% of cases. Of 69 patients with IE after TPVI, 6 (8.7%) died and 35 (52%) underwent surgical and/or transcatheter reintervention. Death or reintervention was more common in patients with new/significant right ventricular outflow tract obstruction (69% versus 33%; P=0.042) and in patients with non‐streptococcal IE (73% versus 30%; P=0.001).ConclusionsThe incidence of IE after implantation of a Melody valve is significant, at least over the first 3 years after TPVI, and varies considerably between the studies. Although surgical/percutaneous reintervention is a common consequence, some patients can be managed medically, especially those with streptococcal infection and no right ventricular outflow tract obstruction.

Human parechoviruses (HPeVs) are closely related to human enteroviruses and exhibit many similarities in disease spectrum and symptoms. HPeV1 is most commonly associated with mild disease, but rare associations with severe disease such as myocarditis have been reported. Currently, no treatment is available for severe HPeV infections. In this case report we describe an infant with a severe, dilated cardiomyopathy in whom HPeV1 was revealed to be the only identifiable cause. The infant was treated with intravenous immunoglobulins (IVIGs) and recovered completely. In vivo blood samples revealed a high HPeV1 antibody titer after treatment with IVIGs. In vitro IVIGs contained high titers of neutralizing antibodies against HPeV1. Our hypothesis is that patients with myocarditis caused by viruses with a high prevalence in the population and hence high antibody titers in IVIGs are likely to benefit from treatment with IVIGs. More research combining virological and clinical data is needed to see whether this hypothesis is true.