Development of IE requires simultaneous existence of damage to endothelial lining of heart valve & presence of pathogen capable of causing IE in bloodstream Damage to endothelial lining occurs by two mechanisms: Mechanical - Trauma, turbulent blood flow, etc., cause damage to valvular endothelium
- Resulting damage exposes stromal cells & extracellular matrix proteins → triggers fibrin & platelet deposition (non-bacterial thrombotic endocarditis [NBTE])
- Bacteria in bloodstream adhere to the NBTE causing recruitment of monocytes & subsequent release of mediators of coagulation cascade & other factors encouraging growth of vegetation
- Further deposition of platelets, fibrin, bacteria, & other proteins & bacterial division lead to the maturation of vegetation & transition of NBTE to IE
Inflammatory - Valvular inflammation, in the absence of mechanical insult, results in the expression of proteins on the endothelial cell surface capable of binding & promoting adherence to the inflamed cells
- Some microorganisms, such as S. aureus, express surface fibronectin-binding proteins; allowing direct adhesion to inflamed cells, endothelial internalization of bacteria, & endothelial apoptosis
- Inflammatory events & apoptosis result in cascade of events similar to that seen in mechanical cases; ultimately results in formation of a mature vegetation
|
Infective Endocarditis: Native Valves (NVES) “Classically” seen in patients with congenital heart disease & chronic rheumatic heart disease >60yoa, degenerative valve & other cardiac lesions are primary cause of IE ↑ frequency of intracardic pacemakers & defibrillators has led to corresponding increase in IE. Most frequently caused by S. aureus (38%) & viridans group streptococci (21%) | Infective Endocarditis: Prosthetic Valves (PVES) Risk of PVE ranges from 0.3% to 6%/patient-year No significant differences in infection rates between mechanical vs bioprosthetic valves Early-onset PVE (≤2mo after surgery) dominated by S. aureus & S. epidermidis Late-onset PVE pathogen distribution similar to native valve disease Prosthetic valve often lengthens treatment duration & expands therapy required | Infective Endocarditis: Intravenous Drug Users (IVDUs) 1–5%/y of IVDUs ∼70% S. aureus >50% involve tricuspid valve; 60–80% have no preexisting valvular lesions Cure rates for right-sided (tricuspid valve) IE >90% | Nosocomial Infective Endocarditis (Int J Infect Dis 2004;8:210) Acute IE: ≥48h post-admission or directly relating to hospital-based procedure or admission ≤8wk prior native or prosthetic valves; left-sided valves most common >65% of patients elderly (>60yoa) Majority (45–55%) directly attributed to intravascular catheter or other intravascular device Staphylococci, predominantly S. aureus >75% |