Aortic Valve Endocarditis

Infective endocarditis (IE) is an endovascular infection of cardiovascular structures – usually valves – but also large intra-thoracic vessels and intra-cardiac foreign bodies. It is typically caused by bacteria or fungi. In contrast, sterile thrombotic lesions are termed non-bacterial thrombotic endocarditis (NBTE). IE is generally characterised by lesions of vegetations composed of platelets, fibrin, microorganisms, and inflammatory cells, as well as leaflet disruption to a various degree. Endocarditis may also produce a wide variety of systemic signs and symptoms due to sterile and infected emboli, as well as various immunological phenomena. IE is a fatal disease if left untreated (Horstkotte et al., 2004). Characterising aspects of IE were first described by Jean François Fernel in his book Medicini in 1554. Lazaire Riviere followed suit with gross autopsy findings of the disease in 1723 after which, in 1852, Kirkes described emboli arising from heart valves in cerebral, renal, splenic and other arteries. Although several reports of IE have been published since – some from well-known physicians like Morgagni and Virchow, it was not until 1885 that IE was comprehensively documented when Sir William Osler accumulated various works and presented them to the public in the form of the comprehensive analysis of this disease (Millar & Moore, 2004). Despite substantial improvements in diagnosis and treatment of native valve IE, disease incidence is on an increase currently averaging 3.3 new cases each year per 100,000 population in the United Kingdom, similar figures in the United States, and 1.4 to 4 new cases over the same population in European countries (Bashore et al., 2006). Native valve IE continues to be associated with high morbidity and mortality rate. Even though IE was previously associated with poor dentition and rheumatic heart disease, many factors have altered its epidemiology but have maintained its incidence: an aging population with degenerative valvular disease, injection drug use, increasing number of valve replacements, and medical interventions i.e. invasive vascular procedures (Wang & Bashore, 2009). Several variants to valve endocarditis have also been recognized: nosocomial IE, intravenous drug abuse IE, and prosthetic valve endocarditis (PVE). Nosocomial infective endocarditis is defined as acute IE, occurring 48 to 72 hours or more post-admission to hospital, or endocarditis directly related to a hospital-based procedure performed during a prior hospital visit within eight weeks of admission (Haddad et al., 2004). Intravenous drug abuse IE most commonly affects tricuspid valve and is associated with no previous structural damage of the valve. PVE accounts for 10-20% of cases. Incidence of PVE is reported to be most often between 0.2 and 0.8% for each year of life with an implanted valve (Dominik &