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Objective: We aimed to identify characteristics differentiating patients undergoing mitral valve replacement versus valve repair for mitral regurgitation (MR) and to investigate retrospectively mid-term clinical and functional outcomes., Methods: From January, 2004 to January, 2009 146 patients underwent mitral valve surgery (62 male / 84 female; age: 55.9+/-13.6 [18-80] years) by one surgical team. Mitral valve replacement was performed in 101 patients (69.2 %) and valve repair was performed in 45 patients (30.8%). Mean follow-up time was 586+/-413 days. Life tables were constructed for the analysis of 5-year complication free survival and comparisons were performed between the groups using Log-rank test within 95%CI., Results: The choice of surgical technique depended on the etiology of MR. Degenerative (p=0.001) and ischemic (p=0.014) MR were more common in patients undergoing repair whereas patients with complex rheumatic mitral valve disease (p=0.001) with subvalvular involvement commonly underwent replacement. Overall 30-day mortality was 3.2% (replacement, 3.96%vs repair, 2.22%, p=0.59). Although there was no significant difference between the groups regarding baseline left ventricular ejection fraction (EF) (ischemic p=0.61; non-ischemic p=0.34), improvement was more pronounced in the repair group for both etiologies (ischemic MR, p=0.001; non- ischemic MR p=0.002). Survival at 5-years was 91.7+/-4.7% after repair and 83.5+/-9.2% after replacement, respectively (p=0.83). Freedom from grade 2 or more mitral regurgitation, reoperation, endocarditis, and thromboembolism were 95+/-5% vs 97+/-3% (p=0.71); 95+/-4% vs 98+/-2% (p=0.98); 94+/-4% vs 100% (p=0.16); and 85+/-8% vs 100% (p=0.095) in replacement and repair groups, respectively., Conclusion: This study demonstrates that mitral valve repair is associated with an acceptable operative mortality, satisfactory mid-term survival and better preservation of left ventricular function. Significant differences in favor of repair are expected in long-term follow-up particularly regarding freedom from thromboembolism and endocarditis.

In the era of proton-antiproton collisions, stem cell field has emerged as the newly recognized protons of regenerative medicine. Great interest and enthusiasm were depending on their behavioral difference such as self-renewal, clonogenicity and differentiation into functional progeny that may become vehicles for regenerative medicine. Although progress has evolved dramatically strategies using stem-cell-driven cardiac regeneration involve extremely complex and dynamic molecular mechanisms. Cell death in transplanted heart continues to be a significant issue. Every step from stem cell homing, and migration to retention, engraftment, survival and differentiation in cardiac cytotherapy deserves intense research for optimum results. Furthermore, regeneration of contractile tissue remains controversial for human studies and careful interpretation is warranted for modest benefit in clinical trials. Currently, the only realistic approach to replace the damaged cardiomyocytes is cardiac transplantation for patients with end-stage heart failure. Ultimately, the giant footsteps in cell-based cardiac repair can only be achieved by an enthusiastic but also skeptical teams adhering to good manufacturing practices. Better understanding of cell-fate decisions and functional properties in cardiac cytotherapy may change the erosion of initial enthusiasm and may open new prospects for cardiovascular medicine.

The present review addresses the issues related to innovative contributions in biotechnology and their potential role in stem cell research at present and in the future. We can expect that future developments and applications in biotechnological sciences and industry will effect the direction of emerging cellular therapies. The use of these advances may offer a unique opportunity to investigate the mechanisms related to the journey from embryonic cells or bone-marrow derived stem/progenitor cells to cardiomyocytes or endothelial cells and the molecular regulators of cell differentiation.