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BackgroundThe choice of prosthesis for mitral valve replacement still remains controversial. This study assessed mortality, bleeding events and reoperation in patients who underwent mitral valve replacement surgery with biological or mechanical substitutes.MethodsA total of 352 patients who underwent mitral valve replacement surgery between 1990 and 2008 with 5 to 23 years of follow-up were retrospectively evaluated in a cohort study.ResultsThe 5, 10, 15 and 20 year survival rates after surgery using a mechanical substitute were 87.7%, 74.2%, 69.3% and 69.3%, respectively, while after surgery with a biological substitute, they were 87.6%, 71.0%, 64.2% and 56.6%, respectively. There was no significant difference between the two groups (p = 0.38). In the multivariate analysis, the factors associated with death were age, bleeding events and renal failure. The probabilities of remaining free of reoperation at 5, 10, 15 and 20 years after surgery using a mechanical substitute were 94.4%, 92.7%, 92.7% and 92.7%; after surgery with a bioprosthesis, they were 95.9%, 86.4%, 81.2% and 76.5%, respectively (p = 0.073). There was a significantly higher incidence of reoperation for the bioprosthetic valve replacement group (p = 0.008). The probabilities of remaining free of bleeding events at 5, 10, 15 and 20 years after surgery using a mechanical substitute were 95.0%, 91.0%, 89.6% and 89.6%, respectively, while after surgery with a bioprosthesis, they were 96.9%, 94.0%, 94.0% and 94.0%, (p = 0.267).ConclusionsThe authors concluded that: 1) mortality during follow-up was statistically similar for both groups; 2) there was a greater tendency to reoperation in the bioprosthesis group; 3) the probability of remaining free from reoperation remained unchanged after 10 years’ follow-up for patients with mechanical substitute valves; 4) the probability of remaining fee from bleeding events remained unchanged after 10 years’ follow-up for patients given bioprostheses; 5) the baseline characteristics of patients were the greatest determinants of later mortality after surgery; 6) the type of prosthesis was not an independent predictive factor of any of the outcomes tested in the multivariate analysis.

Purpose: To evaluate a model of chronic renal ischemia in rats and to characterize the effects on renal tissue. Methods: 168 Wistar rats were divided into two equal groups, control (GC) and ischemia (GI). The animals of the GI (n=84) were submitted to partial ligation of the left renal artery, and the animals of GC (n=84) stayed with the renal artery intact. In seven successive and identical periods of time, in weekly intervals, 12 animals of each group were submitted to nephrectomy, with morphometric determinations and histological and ultra-structural analysis. Results: The GI presented progressive reduction in renal weight, volume and cortical thickness observed from the 7 th day of the experiment, reaching maximum degree in the 49 th day (p < 0.05). The proximal tubular atrophy in the GI was observed in 75/84 analysis (89,2%), with highly significant difference among the groups starting from the 7 th day (p=0 .0009) and in the other periods of the experiment (p=0 .00001). The most prevalent interstitial alteration was the infiltrate, present in 98,8% of the GI, with highly significant difference among the groups in the whole experiment (p=0 .00001). Ultra-structural analysis didn't demonstrate glomerular lesions, evidencing that the glomerule preserves its intact architecture during chronic ischemia. Conclusion: The model showed that chronic renal ischemia in rats provokes progressive renal atrophy, with preservation of glomerular structure. Key words: Kidney. Ischemia. Models, Animal. Rats. RESUMOObjetivo: Avaliar um modelo de isquemia renal crônica em ratos e caracterizar os efeitos no tecido renal. Métodos: Utilizaramse 168 ratos Wistar divididos em dois grupos iguais, controle (GC) e isquemia (GI). Os animais do GI (n=84) foram submetidos à ligadura parcial da artéria renal esquerda, e os animais do GC (n=84) permaneceram com a artéria renal intacta. Em sete períodos de tempo sucessivos e iguais, em intervalos semanais, 12 animais de cada grupo foram submetidos à nefrectomia, com determinações morfométricas e análises histológica e ultra-estrutural. Resultados: O GI apresentou redução progressiva no peso, volume e espessura cortical renal a partir do 7º dia do experimento, atingindo grau máximo no 49º dia (p < 0.05). A atrofia tubular proximal no GI ocorreu em 75/84 análises (89,2%), com diferença altamente significativa entre os dois grupos a partir do 7º dia (p=0.0009) e nos demais períodos do experimento (p=0.00001). A alteração intersticial mais comum no GI foi o infiltrado, presente em 98,8%, com diferença altamente significativa entre os dois grupos (p=0.00001). A análise ultra-estrutural não demonstrou lesões glomerulares, evidenciando que os glomérulos preservam sua arquitetura intacta durante a isquemia crônica. Conclusão: O modelo mostrou que a isquemia renal crônica em ratos provoca atrofia renal progressiva, com preservação da estrutura glomerular.