The port-access check details group had better preoperative New York Heart Association functional class (P = .007) and a higher rate of elective cases (97% vs 87%, P = .037). Other preoperative characteristics were similar between the groups, including mitral valve pathology and

repair techniques.

Results: Operative, bypass, and clamp times were significantly longer in the port-access group. Mean hospital stay was 5.3 +/- 2.5 days in the port-access group versus 5.7 +/- 2.5 days in the median sternotomy group (P = .4). Early postoperative echocardiographic analysis showed that most patients in both groups had none or trivial mitral regurgitation and none of the patients had greater than grade 2 mitral regurgitation. Follow-up extended for up to 100 months (mean, 34 +/- 24 months). New York Heart Association class improved in both groups (P = .394). Freedom from reoperation was 97% and 95% in the port-access and median sternotomy groups, respectively. Late echocardiographic analysis revealed that 82% (49/60) in the port-access group and 91% (73/80) in the median sternotomy group were free from moderate or severe mitral regurgitation (P =

.11).

Conclusions: In isolated posterior mitral valve pathology, quality of mitral valve Dinaciclib cell line repair with the port-access approach can compare with that with the conventional median sternotomy approach. (J Thorac Cardiovasc Surg 2010;140:86-90)”
“Bone marrow stem cells (BMSCs) express C188-9 mw cardiac markers in vitro and in vivo upon induction. Cardiomyogenic differentiation of embryonic stem cells induced by oxytocin (OT) involves the nitric oxide (NO)soluble guanylyl cyclase (sGC) pathway. Also, OT improved cardiomyogenic differentiation of porcine BMSCs (pBMSCs). Here, we document the role of NO pathway in

OT-mediated cardiomyogenic differentiation of pBMSCs obtained from bone marrow aspirates of juvenile pigs. Cells were exposed (OT cells) or not (control cells) to OT, in presence or absence of a NO synthase inhibitor (L-NAME) and a sGC inhibitor (ODQ). Gene (RT-PCR) and protein expression (immunocytochemistry) of NOS was up-regulated after OT induction. Exposure of OT cells to L-NAME, ODQ, or both, leaded to a significant reduction in cardiac troponin I transcripts, and protein (Western Blot) expression. For the latter, ODQ looked more performing in inhibition than L-NAME. Expression of cardiac troponin T and myosin heavy chain (immunocytochemistry) was less abundant in OT cells exposed to inhibitors without apparent synergic effect between L-NAME and ODQ. In control cells, protein expression remained low. Moreover, OT-induced cell proliferation, and this effect was counteracted by NOS/sGC inhibitors.