[Physiopathology of infectious endocarditis]

Infectious endocarditis (IE) develops following bacteremic episodes during which bacteria may attach to sterile thrombotic vegetations. Such thrombotic vegetations result from the deposition of platelets and fibrin on lesioned endothelium. These sterile vegetations are the most susceptible to infection in the left side of the heart, since this localization is found in as much as 80% of the patients with IE. Any circulating bacterial or mycotic organism may induce endocarditis, but streptococci are most often responsible, possibly because of their high capacity to adhere to thrombotic vegetations. The host cell defenses apparently cannot penetrate the dense network of platelet and fibrin in the vegetation, and humoral immunity (antibodies and complement) are of no help against gram-positive cocci. Thus, the infected vegetation has been compared to a localized agranulocytic focus, permitting the survival of infection and allowing bacteria to be released freely and continuously into the circulation (hence the constant bacteremia, a hallmark of IE). In the subacute and chronic evolution of IE, the clinical findings are mainly due to immunization of the host against the infecting microbe, resulting in antigen-antibody-complex-mediated vasculitis, and in nonspecific symptoms. Only positive blood cultures at this stage will confirm the clinical suspicion of endocarditis. Embolism may occur in any organ and falsify the diagnosis because of focal signs. Local complications of IE are the major cause of mortality in this disease, and are due to valve perforation, paravalvular abscesses, cardiac metastatic abscesses etc. If these complications occur early in the course of IE, the course may be acute.(ABSTRACT TRUNCATED AT 250 WORDS)