Abstract
The pathogenesis of infective endocarditis (IE) is a complex process which can include tissue damage to the valves during bacteraemia, pathogen adherence leading to the formation of non-bacterial thrombotic vegetations, platelet aggregation at sites of tissue damage, and a variety of biological interactions between pathogens and host matrix molecules (e.g. platelets).1,2 In the past few decades, the incidence of IE has increased significantly, which may be the result of an aging population, delayed diagnosis of valvular heart disease, and even new methods of valve implantation, including transcatheter therapies. The incidence of IE of the right heart has also increased due to the prevalence of intravenous drug use. Overall, the epidemiological profile of IE in China remains inadequately characterized, and the precise epidemiology differs between geographic location and study populations. For example, in Europe, the incidence of IE is reported to be 3–10 episodes/100 000 person-years and increases with age—the peak incidence being 14.5 episodes/100 000 person-years in patients between 70 and 80 years of age, with a male : female ratio of ≥2 : 1. Over the course of the 20th century, due to effective antibiotic treatment, the major cause of IE has changed from rheumatic valve disease, which mainly affects young adults, to a variety of other aetiologies. In many locations, the most common pathogen of IE has changed from Streptococcus to Staphylococcus . In the USA, staphylococcal infection has become the most prevalent, and, in China, case reports show that Streptococcus and Staphylococcus are the most common pathogens.3–6 Despite advances in its management, IE is still considered a severe disease with a high mortality rate and poor prognosis. This consensus is …
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