Circulation, Vol 69, 223-232, Copyright © 1984 by American Heart Association
TS Ivert, WE Dismukes, CG Cobbs, EH Blackstone, JW Kirklin and LA Bergdahl
Fifty-three (3.6%; actuarially 4.1% at 48 months) of 1465 consecutive
in-hospital survivors of valve replacement from 1975 to July 1979 (aortic,
mitral, or aortic and mitral, only one untraced) developed prosthetic valve
endocarditis (PVE). Incremental risk factors for developing PVE were native
valve endocarditis (p less than .0001), black race (p = .0001), mechanical
prosthesis (vs bioprosthesis) (p = .005), male sex (p = .04), and longer
cardiopulmonary bypass time (p = .09). In general, the hazard function for
developing PVE was greatest at 3 weeks after valve replacement. Patients
with native valve endocarditis had a tendency to develop PVE early after
valve replacement, as did patients in whom mechanical prostheses were used.
PVE associated with Staphylococcus epidermidis tended to appear within 6
months of valve replacement, whereas streptococcal PVE tended to appear
later after valve replacement. PVE took an atypical form in some patients,
but patients with possible PVE (n = 6) had the same findings as those with
certain PVE (n = 47). In 11 patients bacteriologic confirmation of PVE was
not obtained. The typical prosthetic and periprosthetic characteristics of
PVE were present in 30 of the 40 cases in which observations were possible.
PVE is a serious condition; 34 (64%) of our 53 patients died. Most deaths
occurred within 3 months of the first evidence of PVE. Recovery of some
patients is possible with appropriate medical and surgical treatment, but
more intense preventive measures are indicated.
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Prosthetic valve endocarditis
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