CHF complicating IE is primarily the result of valve destruction or distortion or rupture of chordae tendinae. Intracardiac fistulas, myocarditis, or coronary artery embolization may occasionally contribute to the genesis of CHF.
Renal insufficiency as a result of immune complex-mediated glomerulonephritis occurs in less than 15 per cent of patients with IE. Azotemia as a result of this process may develop or progress during initial therapy. Renal dysfunction in patients with IE is most commonly a manifestation of impaired hemodynamics or toxicities associated with antimicrobial therapy (interstitial nephritis or aminoglycoside-induced injury).