In native-valve IE, acute CHF occurs more frequently in aortic-valve infections (29 per cent) than with mitral (20 per cent) or tricuspid disease (8 per cent). CHF may develop acutely from:
• Perforation of a native-or bioprosthetic-valve leaflet,
• Rupture of infected mitral chordae,
• Valve obstruction from bulky vegetations,
• Sudden intracardiac shunts from fistulous tracts or prosthetic dehiscence. CHF may also develop more insidiously, despite appropriate antibiotics, as a result of a progressive worsening of valvular insufficiency and ventricular dysfunction.
• CHF in IE, irrespective of the course or mechanism, signifies a grave prognosis with medical therapy alone and is also the most powerful predictor of poor outcome with surgical therapy.
• The decision to operate on the patient with IE is driven primarily by the severity of CHF.
Medical and surgical management decisions can be guided by echocardiographic detection of abscesses, fistulae, prosthetic dehiscence, obstructive vegetations, or flail leaflets, none of which will resolve with medical therapy alone. Delaying surgery to the point of frank ventricular decompensation dramatically increases operative mortality, from 6 per cent to 11 per cent for patients without CHF and 17 per cent to 33 per cent for patients with CHF.
Poor surgical outcome is predicted by preoperative New York Heart Association class III or IV CHF, renal insufficiency, and advanced age. In any patient, a decision to delay surgery to extend pre-operative antibiotic treatment carries with it the risk of permanent ventricular dysfunction.
The incidence of reinfection of newly implanted valves in patients with active IE has been estimated to be 2 per cent to 3 per cent, far less than the mortality rate for uncontrolled CHF.