IE develops most commonly on the mitral valve, closely followed in descending order of frequency by the aortic valve, the combined mitral and aortic valve, the tricuspid valve, and, rarely, the pulmonic valve. Mechanical prosthetic and bioprosthetic valves exhibit equal rates of infection. All cases of IE develop from a commonly shared process, as follows: Bacteremia (nosocomial or spontaneous) that delivers the organisms to the surface of the valve, Adherence of the organisms. The common denominator for adherence and invasion is nonbacterial thrombotic endocarditis, a sterile fibrin-platelet vegetation.
The development of sub-acute IE depends on a bacterial inoculum sufficient to allow invasion of the preexistent thrombus. This critical mass is the result of bacterial clumping produced by agglutinating antibodies. In acute IE, the thrombus may be produced by the invading organism (i.e., S aureus) or by valvular trauma from intravenous catheters or pacing wires (ie, NIE/HCIE). S aureus can invade the endothelial cells (endotheliosis) and increase the expression of adhesion molecules and of procoagulant activity on the cellular surface. Nonbacterial thrombotic endocarditis may result from stress, renal failure, malnutrition, systemic lupus erythematosus, or neoplasia.
Treatment Antibiotic therapy Anticoagulation therapy Statistics Between 2000 and 2011, the incidence of infective endocarditis (IE) in the United States increased from 11 per 100,000 populations to 15 per 100,000 populations Major research Epidemiological Trends of Infective Endocarditis: A Population-Based Study in Olmsted County, Minnesota. Temporal relationship between infective endocarditis and stroke. Surgical management of tricuspid valve endocarditis in the current era: A review A systematic review of biomarkers in the diagnosis of infective endocarditis.