Objective To analyze the clinical effect of partial aortic root remodeling for root reconstruction on Stanford type A aortic dissection. Methods From January 2010 to December 2015, 30 patients (25 males, 5 females) underwent partial aortic root remodeling for root reconstruction on Stanford type A aortic dissection with involvement of aortic root. The range of age was from 27 to 72 years, and the mean age was 51.2±8.0 years. The proximal aortic dissection received partial aortic root remodeling, and the operation procedures included partial aortic root remodeling+ascending aortic replacement in 9 patients, partial aortic root remodeling+ascending aortic replacement+hemi-arch replacement in 6 patients, partial aortic root remodeling+ascending aortic replacement+Sun's procedure in 15 patients. The patients were followed up for 10 to 60 months with a mean of 37.9±3.2 months. Preoperative and postoperative degrees of aortic regurgitation were compared. Results All patients survived from the operation, and one patient died from severe pulmonary infection 15 days after operation. The overall survival rate was 96.7% (29/30). One patient died during the follow-up. Two patients underwent aortic valve replacement in the 12th and 15th postoperative month respectively because of severe aortic regurgitation (AI). Up to the last follow-up, trivial or no aortic regurgitation was demonstrated in 24 patients, but mild aortic regurgitation occurred in 2 patients. Conclusion The surgical treatment for aortic root pathology due to Stanford type A aortic dissection is challenging, and partial aortic root remodeling operations could restore valve durability and function, and obtains the early- and mid-term results.
Objective To investigate the change of vasa vasorum in vessel wall of varicose vein of the lower extre-mity. Methods Thirty-two patients with varicose vein of the lower extremity were collected， in which of 12 patients with simple varicose veins （varicose group）， 9 patients with recurrent varicose veins （recurrent group）， 11 patients withthrombophlebitis of varicose vein （thrombophlebitis group）， 9 patients with normal venous tissue as control group. HE staining was performed to observe the distribution of vasa vasorum and detect the vasa vasorum density. Results The increasing vasa vasorums were observed in the adventitia and media， but few was observed in the intima in the varicose， recurrent， and thrombophlebitis groups. The distribution of vasa vasorum was in the adventitia in the control group. The vasa vasorum densities （/mm2） in the varicose， recurrent， and thrombophlebitis groups （5.65±1.45，6.20±1.73， and 5.94±1.63， respectively） were greater than those in the control group （2.87±0.54）， the difference wasstatistically significant （P＜0.05）， but there was no significant difference of the vasa vasorum density among the varicosevein， recurrent， and thrombophlebitis groups （P＞0.05）. Conclusion Change of vasa vasorum is an important pathol-gical change with the nosogenis of varicose vein of the lower extremity.
ObjectiveTo investigate the expression of extracellular signalregulated kinase (ERK) and p38 mitogenactivated protein kinase （p38 MAPK） in autogenous vein grafts during vascular remodeling.MethodsAn autogenous vein graft model was established by transplanting the right jugular vein to infrarenal abdominal aorta in 80 Wistar rats. Vein graft samples were harvested 6 hours, 24 hours, 3 days, 7 days, 2 weeks, 4 weeks, 6 weeks and 8 weeks after surgery. Gene expression of ERK and p38 MAPK was measured by reverse transcriptionPCR. Western blot was used to detect the expression of protein products and phosphorylation protein products of ERK and p38 MAPK. Apoptosis of vascular smooth muscle cells (VSMCs) was determined by TUNEL. Proliferating cell nuclear antigen(PCNA) of VSMCs also was studied.ResultsThe expression of ERK1 mRNA and p38 MAPK mRNA increased considerably after surgery. ERK1 mRNA reached the peak on the 7th day 〔（33.2±14.2）%, P＜0.01〕, but p38 MAPK mRNA reached the peak on the second week after surgery 〔(58.8±26.2）%, P＜0.01〕. The expression of ERK1/2 detected by western blot reached the peak during 1 to 2 weeks and decreased gradually to normal level 6 weeks after surgery. The expression of p38 MAPK reached the peak during 2 to 4 weeks and decreased to 1/4 to 1/2fold 8 weeks after surgery. There was a positive relationship between ERK1 and PCNA(r=0.759 6，P＜0.01) and a positive relationship between p38 MAPK and apoptosis(r=0.892 2，P＜0.01). ConclusionActivation of MAPK system exists in autogenous vein grafts and it may become a new target for the therapy of stenosis after vein grafts.
Objective To evaluate the effect of smooth muscle cell transplantation on myocardial interstitial reconstruction shortly after myocardial infarction. Methods A total of 48 female Wister rats were randomly divided into two groups with the random number table, the control group (n=24) and the smooth muscle cell transplantation group (n=24). The left coronary artery was ligated to set up the myocardial infarction animal model. An amount of 05 ml phosphate buffered saline(PBS) containing 1×106 smooth muscle cells or 0.5 ml PBS without cells was injected into the injured myocardium immediately. By immunoblot and reverse transcriptionolymerase china reaction (RT-PCR), we observed the amount of protein and mRNA of matrix metalloproteinase2(MMP-2), matrix metalloproteinase-9(MMP-9) and tissue inhibitor of metalloprotease-3 (TIMP-3) in the myocardium of the rats. Results The transplanted smooth muscle cells survived well. Compared with the control group, myocardial TIMP3 mRNA (1.06±0.22 vs. 0.81±0.19, t=－2.358, P=0.033) and protein content (3.33±0.53 vs. 1.63±0.47, t=－6.802, Plt;0.001) were significantly increased in the transplantation group. Myocardial MMP-2, MMP-9 mRNA (0.49±0.12 vs. 1.16±0.18, t=8.453, Plt;0.001; 0.45±0.12 vs. 0.80±0.11, t=5.884, Plt;0.001) and protein content (3.98±1.08 vs. 6.05±0.91, t=4.139, P=0.001; 0.39±0.14 vs. 0.57±0.17, t=2.409, P=0.031) [CM(1585mm]were significantly reduced in the transplantation group compared with the control group. Conclusion transplanted smooth muscle cells can survive well in the infarction myocardium and can increase the amount of myocardial TIMP-3 mRNA and protein content and reduce myocardial MMP-2, MMP-9 mRNA and protein content, which is an effective way to prevent harmful cardiac remodeling.
ObjectiveTo explore the possibility that GREM1, a bone morphogenetic protein (BMP) antagonist, is a mechanical explanation for BMP signal suppression in congenital heart disease associated pulmonary arterial hypertension (CHD/PAH) patients.MethodsSystemic-to-pulmonary shunt induced PAH was surgically established in rats. At the postoperative 12th week, right heart catheterization and echocardiography evaluation were performed to evaluate hemodynamic indexes and morphology of right heart system. Right heart hypotrophy index and pulmonary vascular remodeling were evaluated. Changes of BMP signal pathway related proteins and GREM1 in lungs and plasma GREM1 concentration were detected. The effect of GREM1 on the proliferation and apoptosis of pulmonary arterial endothelial cells (PAECs) was also explored.ResultsThe hypertensive status was successfully reproduced in rats with systemic-to-pulmonary shunt model. BMP signal pathway was suppressed but GREM1 was up-regulated with no change in hypoxia inducible factor-1 in lungs exposed to systemic-to-pulmonary shunt, while this trend was reversed by systemic-to-pulmonary shunt correction (P<0.05). Immunohistochemical staining demonstrated enhanced staining of GREM1 in remodeled pulmonary arteries. In vitro experiments found that BMP signal was down-regulated but GREM1 expression and secretion were up-regulated in proliferative PAECs (P<0.05). Furthermore, BMP2 significantly inhibited PAECs proliferation and promoted PAECs apoptosis (P<0.05), which could be antagonized by GREM1. In addition, plasma level of GREM1 in rats with systemic-to-pulmonary shunt was also increased and positively correlated with pulmonary hemodynamic indexes.ConclusionSystemic-to-pulmonary shunt induces the up-regulation of GREM1 in lungs, which promotes pulmonary vascular remodeling via antagonizing BMP cascade. These results present a new mechanical explanation for BMP pathway suppression in lungs of CHD/PAH patients.
Atrial fibrillation(AF) is the most common disorder of cardiac rhythm. It has a high morbidity, mortality and disability, and serious impact on quality of life of patients. It is demonstrated that atrial remodeling which includes atrial electrical remodeling and structural remodeling,are the central contributors to the development and selfperpetuating of AF. However, The mechanisms that underlie the atrial remodeling process in AF have not yet been completely elucidated. New strategies for the prevention and termination of AF should build on our knowledge of the mechanisms of atrial remodeling. Medication for the reversal of atrial remodeling may be the new target for the treatment of AF. At present, drugs that target atrial remodeling have already obtained fruitful results in the experimental and clinical investigations. Now some recent advancements of this area is reviewed in this article.
In order to identify whether the regeneration of costal cartilage is the basis of post-surgical repair of pectus excavatum and thoracic cage remodeling, 151 cases were followed up for 0.25 to 14 years. The main procedures in treatment were 3 steps: To curve the mental strut as a bow, to repair the perichondrium as a tube, and to persist in post-operative therapy. The results showed that regeneration of the costal cartilages appeared 3 months postoperatively in the cases treated by this method. It was concluded that a satisfactory thoracic cage could be remodeled by improving the technique of repairing pectus excavatum and persisting in postoperative therapy according to the regeneration regularity.
ObjectiveTo summarize the research progress of pathological manifestations and mechanism of endochondral ossification in osteoarthritis (OA). MethodsThe literature about endochondral ossification, bone-cartilage remodeling in OA, and joints development was reviewed, analyzed, and summarized. ResultsChondrocyte hypertrophy and apoptosis, vascular invasion, replication of the tidemark, thickening calcified cartilage, and thinning superficial cartilage are the characteristics of cartilage degeneration in OA. Articular cartilage and growth plate are similar in structure, and cartilage degeneration in OA is similar to a process of endochondral ossification of the growth plate. ConclusionLoss of stability characterization from resting metabolic balance to a high conversion state of temporary cartilage in stimulation of abnormal mechanical stresses and cytokines would subsequently contributed to continual calcification and remodeling of articular cartilage, which may be the key link of the initiation and development of OA.
Craniofacial malformation caused by premature fusion of cranial suture of infants has a serious impact on their growth. The purpose of skull remodeling surgery for infants with craniosynostosis is to expand the skull and allow the brain to grow properly. There are no standardized treatments for skull remodeling surgery at the present, and the postoperative effect can be hardly assessed reasonably. Children with sagittal craniosynostosis were selected as the research objects. By analyzing the morphological characteristics of the patients, the point cloud registration of the skull distortion region with the ideal skull model was performed, and a plan of skull cutting and remodeling surgery was generated. A finite element model of the infant skull was used to predict the growth trend after remodeling surgery. Finally, an experimental study of surgery simulation was carried out with a child with a typical sagittal craniosynostosis. The evaluation results showed that the repositioning and stitching of bone plates effectively improved the morphology of the abnormal parts of the skull and had a normal growth trend. The child’s preoperative cephalic index was 65.31%, and became 71.50% after 9 months’ growth simulation. The simulation of the skull remodeling provides a reference for surgical plan design. The skull remodeling approach significantly improves postoperative effect, and it could be extended to the generation of cutting and remodeling plans and postoperative evaluations for treatment on other types of craniosynostosis.
Atrial fibrillation is a common arrhythmia associated with high mortality and morbidity, and the current treatment of atrial fibrillation is still limited. Histone deacetylase (HDAC) plays an important role in the pathophysiology of cardiovascular disease and promotes the occurrence of atrial fibrillation. Inhibition of HDAC may be a new therapeutic strategy through the regulation of atrial remodeling. Therefore, we reviewed the research progress of the HDAC and atrial fibrillation.