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Between January 1970 and December 1981, a total of 21 reoperations for periprosthetic leak were performed on 20 patients out of 999 with previously implanted prosthetic mitral valves. In most of them reoperations were performed within the first year, since the initial procedure and the leading indications were intractable congestive heart failure or infection of the mitral prosthesis. The mortality rate was 30% and was related to the preoperative cardiac functional status. The preoperative variables significantly related to an increased incidence of dehiscence of the mitral prosthesis necessitating reoperation were a degenerative disease (P = 0.016) or an infective endocarditis (P = 0.0006) of the native valve, both causing mitral regurgitation. Rheumatic disease, type of prosthesis, supra- or subannular insertion, age of the patient, and operative year, were not significant, neither were calcifications that are probably neutralized by the routine use of special surgical techniques. It is suggested that the use of techniques specifically designed to eliminate periprosthetic leak in patients affected by mitral regurgitation due to degenerative or infective disease of the native valve, might lead to a further reduction of reoperations for this complication.

Background. Cardiogenic shock (CS) is the leading cause of in-hospital mortality in ST-segment elevation myocardial infarction (STEMI). Only limited data are available on the long-term outcome of STEMI patients with CS undergoing contemporary treatment. We aimed to investigate long-term mortality and its predictors in STEMI patients with CS and to develop a risk score for long-term mortality prediction. Methods and Results. We retrospectively included 465 patients with STEMI complicated by CS and treated with primary angioplasty and intra-aortic balloon pump between 2005 and 2018. Long-term mortality, including both in-hospital mortality and all-cause mortality following discharge from the index hospitalization, was the primary endpoint. The long-term mortality (median follow-up 4 (2.0–5.2) years) was 60%, including in-hospital mortality (34%). At multivariate analysis, independent predictors of long-term mortality were age (HR 1.41, each 10-year increase), admission left ventricular ejection fraction (HR 1.51, each 10%-unit decrease) and creatinine (HR 1.28, each mg/dl increase), and acute kidney injury (HR 1.81). When these predictors were pooled together, the area under the curve (AUC) for long-term mortality was 0.80 (95% CI 0.75–0.84). Using the four variables, we developed a risk score with a mean (cross-validation analysis) AUC of 0.79. When the score was applied to in-hospital mortality, its AUC was 0.79, and 0.76 when the score was applied to all-cause mortality following discharge. Conclusions. In STEMI patients with CS, the risk of death is still substantial in the years following the index event. A simple clinical score at the time of the index event accurately predicts long-term mortality risk.