Replacement valve endocarditis occurred in 3.7% of 2443 patients who underwent primary or redo aortic valve replacements at The Prince Charles Hospital between December 31, 1969, and January 1, 1992, based on a cross-sectional follow-up in 1992 which was 98.8% complete. Because some patients had re-replacements during the study period, a total of 2686 operations were considered for analysis. A variety of replacement devices were used, including 571 allografts (21%), 1152 xenografts (43%), and 880 mechanical valves (36%). Insertion of an allograft valve resulted in a constant risk of endocarditis which, by multivariable hazard function analysis, negated the effect of any early-phase risk factors ( p < 0.0001). With other replacement devices, the risk of infection peaked early after operation (9 weeks) and then gave way to a constant risk. Compared with the risk associated with allograft valves, constant risk was higher when the replacement device was a Carpentier-Edwards xenograft ( n = 1021, p = 0.02) and lower when a St. Jude Medical mechanical valve was used ( n = 505, p = 0.05). In nonallograft recipients, the presence of active preoperative endocarditis ( p < 0.0001) or a concomitant synthetic aortic root replacement ( p = 0.0006) increased the magnitude of the early peaking risk. Regardless of replacement device, constant risk was increased in patients with renal dysfunction ( p = 0.01), in younger patients ( p < 0.0001), and in those with active or healed preoperative endocarditis ( p = 0.04). When preoperative endocarditis was caused by Staphylococcus aureus, risk was higher than when it was caused by other organisms ( p = 0.04). A culture-positive postoperative wound infection was associated with increased risk of replacement valve infection ( p < 0.001) and when it occurred, the same organism was usually responsible (86%). Identification of patients at increased risk for replacement valve infection may lead to reduced morbidity through strategies such as selective use of replacement devices and antimicrobial prophylaxis. (J T HORAC C ARDIOVASC S URG 1995;110:1708-24)