Mitral valve repair versus replacement in severe ischemic mitral regurgitation systematic review and meta-analysis.

BACKGROUND AND AIM: Ischemic mitral regurgitation (IMR) is a serious consequence of coronary artery disease. The choice of the optimal surgical strategy remains debatable. The aim of the present meta-analysis is to compare the outcomes of mitral valve repair (RPR) versus replacement (RPL) regarding perioperative mortality, overall mortality, reoperation, recurrence of MR, and reverse remodeling after surgery. METHODS: Electronic searches were performed using the searchable databases of Google Scholar, Pubmed, and Embase, and the search terms mitral valve, IMR, RPR, RPL, and coronary artery bypass grafting. The main outcomes of interest are perioperative mortality, overall mortality, reoperation, recurrence of MR, and reverse remodeling after surgery. Perioperative mortality was defined as death during the surgery or within 30 days after the operation. RESULTS: There was a trend towards better perioperative survival in the RPR arm. However, the difference fell short of statistical significance [odds ratio (OR) (95% confidence interval [CI]): 0.66 (0.41-1.07), p = 0.09]. Patients submitted to RPR experienced a significantly higher MR recurrence rate when compared with their counterparts submitted to RPL [OR (95% CI): 16.8 (5.07-55.7, p = 0.00001)]. CONCLUSION: There is a trend towards lower perioperative mortality in RPR in comparison to RPL. On the other hand, RPL was associated with significantly lower recurrence rates.

Testing alternatives: the use of adipose-derived mesenchymal stem cells to slow neurodegeneration in a rat model of Parkinson's disease.

Parkinson's disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson's disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P < 0.001) compared to levels in the rats with Parkinson's disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.