ObjectiveTo evaluate the mechanism of stromal vascular fraction (SVF) promoting angiogenesis and tissue regeneration in tissue engineering chamber. MethodsTwenty-four 6-month-old New Zealand white rabbits, male or female, weighing 2.5-2.8 kg, were selected. Thoracic dorsal arteriovenous bundle combined with collagen type I scaffold was transplanted to dorsal side, and wrapped by cylindrical hollow silicone chamber; all animals were randomly divided into the experimental group (n=12) and the control group (n=12). SVF was isolated from the back fat pads of rabbits in experimental group and labelled with DiI at 2 weeks after operation. The 1 mL cell suspension (1×106 cells/mL) and equal saline were injected into the chamber in experimental group and control group, respectively. The regenerative tissues were harvested for general observation and HE staining at 2 and 4 weeks after injection;and immunofluorescent staining was carried out in experimental group at 4 weeks. ResultsAt 2 weeks after injection, the regenerative tissue was cylindrical; obvious vessel network and incompletely degradable collagen scaffold could be seen on the surface of the new tissue in 2 groups. The volume of new tissue was (0.87±0.11) mL in experimental group, and (0.72±0.08) mL in control group at 2 weeks, showing significant difference (t=2.701, P=0.011). At 4 weeks, little collagen scaffold could be seen on the surface in control group, but no collagen scaffold in experimental group; the volume of new tissue was (0.74±0.14) mL in experimental group, and (0.64±0.10) mL in control group, showing no significant difference (t=1.424, P=0.093). HE staining showed new mature vessels at 4 weeks, but no adipose tissue or fat lobulus formed in both groups; the capillary density was significantly higher in experimental group than in control group at 2 weeks (t=6.291, P=0.000) and at 4 weeks (t=5.445, P=0.000). The immunofluorescent staining found that SVF survived and located at the edge area after 4 weeks; the expressions of CD31 and DiI were positive in some endothelial cells. ConclusionSVF can promote the angiogenesis and tissue regeneration in tissue engineering chamber, but it can not differentiate into adipocyte spontaneously without adipogenic microenvironment.
ObjectiveTo examine the cause of failure of mitral valve repair. MethodWe retrospectively anal-yzed the clinical data of 89 consecutive patients with non-rheumatic mitral valve diseases who underwent reoperation for failure of mitral valve repair in our hospital from January 2009 through January 2016. There were 54 males and 35 females at age of 36.2±17.4 years. ResultsThere were 16 patients with reoperation of mitral valve repairs and 73 patients of mitral valve replacements. The failure reasons of initial mitral valve repair were technique-related in 63 patients (70.8%) and valve-related in 18 patients (20.2%). Technique-related causes of repair failure included leaflet suture dehiscence (20 patients, 22.5%), edge-to-edge procedure (11 patients, 12.4%), leaflet thickening or retraction (11 patients, 12.4%), ring dehiscence (8 patients, 9.0%), inappropriate annuloplasty (6 patients, 6.7%), incomplete repair (4 patients, 4.5%), and chordal elongation or rupture (3 patients, 3.4%). Median interval since previous repair was 4.0 (0.04-18.0) years for the technique-related failure group, and 9.7 (0.21-35.6) years for valve-related failure group (P < 0.05). ConclusionTechnique-related factors are main causes of repair failure, which include leaflet suture dehiscence, edge-to-edge procedure, and leaflet thickening or retraction. Reoperation for technique-related failure needs to be adopted early.