ObjectiveTo assess the effects of Radix Salviae Miltiorrhizae (RSM) on patency and proliferation lesion of autologous vein to artery grafts in the earlymiddle stage.MethodsAutologous jugular vein was grafted into abdominal artery in the rats. The rats were divided into two groups: RSM group and control group. The rats in RSM group were fed with RSM ［24 g/(kg·d )］,which began 1 day before operation and continued until harvesting. Vein grafts were harvested at 1,3 days, 1, 2, 4 and 8 weeks after surgery for examining the patency, thickness of intimamedia and expression of proliferating cell nuclear antigen (PCNA). ResultsNo significant differences existed in patency of vein grafts between the two groups (Pgt;0.05). The intimamedia thickness of the vein grafts in RSM group decreased 1/3 compared with control group at 2, 4 and 8 weeks (P＜0.01). The PCNA positive cells in RSM group reduced significantly as compared to the control group (P＜0.01). ConclusionRSM can inhibit proliferation lesion of vein grafts but has no influence on patency of vein grafts in the earlymiddle stage.
Abstract: Coronary artery bypass grafting (CABG) is one of the conventional treatments of coronary artery disease. Though the artery grafts have its own superiority, autologous great saphenous vein is still commonly used. Ten years after operation, half of the vein grafts will be occluded and half of the remainder will often undergo severe pathological conditions. The poor long term patency of vein grafts has become the bottleneck of the efficiency of CABG. The restenosis of vein grafts resulting from neointima and atherosclerosis has become an urgent problem waiting to be resolved. As the study on the molecular mechanism and pathophysiology of the vein grafts disease develops, many therapeutic schedules have been made, including drug therapy, external stent, expanding solution and gene therapy. By contrast, gene therapy has a broader prospect. This article will have a review on the prevention of restenosis of the vein grafts after CABG.
In order to investigate the effect of vascular beds on the vascular wall of autogenously grafted vein, femoral veins were reversely placed in between the cut ends of collateral femoral arteries in 11 dogs with atraumatic technique. The grafted veins were covered with vivid muscle or skin respectively after being assured to be patent, and investigated by histomorphologic method and computerized image analysis technique at postoperative intervals of 1 week, 4 weeks and 16 weeks. The results showed that: 1. One graft developed pseudoaneurysm at 1 week, and two grafts were occulded in skin-covered group, whereas, no complications occurred in muscle-covered group. 2. Intimal thickening of grafts in skin-covered group was much more obvious than that in the muscle-covered group (P lt; 0.05). 3. The relative contents of microstructural components of the graft wall showed no significant difference quantitatively between the two groups. So, the conclusion was: 1. Subcutaneous transplantation appeared to be a potential causative factor in inducing short-term excessive dilatation and long-term intimal hyperplasia of vein graft. 2. Muscular covering is of priority in blood vessel graft.
ObjectiveTo summarize the experience of 4 patients with a great saphenous venous graft patency after 15 years of postoperitive great saphenous venous sequential aortic coronary artery bypass grafting. MethodWe retrospectively analyzed the clinical data of 4 patients accepted great saphenous vein aortic coronary artery bypass graft under moderate hypothermia cardiopulmonary bypass from November 1989 to December 1992 year. There were 3 males and 1 female with a mean age of 48.3 years ranging from 40-58 years. We harvested great saphenous vein under groin 45-50 cm. The proximal and distal anastomoses were performed with parachute technique under two clamps technique. Coronary artery bypass graft was performed by two sequential grafts routinely. Aspirin was given through nasal tube 6 hours after operation. The risk factors of arteriosclerosis were controlled by patients themselves after discharge. ResultFour patients received coronary angiography in 15, 16, 18, and 21 years after surgery and the grafts and both proximal and distal anastomoses were patent. The patients lived about 20 years without angina. Conclusioncarefully dealing with the vein graft, taking sequential bypass grafting to guarantee parabolic curve and meticulous anastomosis are preconditional and necessary for long-term patency.
Objective To investigate the expression of neutrophil gelatinase-associated lipocalin (NGAL) signaling pathways in the early stage of porcine vein graft restenosis, and to explore the possible role and mechanism in the early vein graftrestenosis after coronary artery bypass surgery. Methods We selected 18 ordinary healthy pigs weighing 25-30 kg and collected samples of the vein graft of pigs at the preoperation and postoperative days 7, 14 and 30. Hematoxylin-eosin (HE) staining and Masson staining, immunohistochemical method were used to observe the neointimal hyperplasia, the migration of smooth muscle cells and and vascular remodeling of the vein bypass graft. The expression changes of NGAL, matrix metalloprotenase (MMP)9, MMP2 and tissue inhibitor of metalloproteinase (TIMP)1 in different periods of the vein bypass graft was tested. Results By HE and Masson staining, with the passing of modeling time, degradation of collagen matrix in the vein graft, gradually thickening of muscle fibers and the migration to the inner membrance and vascular remodeling caused the vascular stenosis. By immunohistochemistry, NGAL, MMP9 and MMP2 of normal vein in the model were seldom expressed and even did not express. At 14 days after the modeling, NGAL expression in the membrane layer of blood vessels began to appear, peaked at postoperative 30 days, and began to appear in the inner membrance. MMP9, MMP2 expression began to appear at postoperative 7 days, peaked at postoperative 14 days, and tended to decline at postoperative 30 days. TIMP1 expression was less in normal vascular walls and at the 14 days after the modeling, expression peaked in the vein graft. Conclusion NGAL, MMP9, MMP2 and TIMP1 may be involved in the formation of early vascular graft restenosis. NGAL as initiator, results in the expression of MMP9 and MMP2, and participates in the degradation of collagen matrix and the migration of smooth muscle cells in vein grafts. TIMP1 as a negative factor, may play an important role in maintaining their own balance.
ObjectiveTo evaluate the changes of the flow parameters before and after the anastomotic port exploration and dredging during coronary artery bypass grafting by using the transit time flow measurement (TTFM).MethodsA total of 167 patients who underwent continuous coronary artery bypass grafting and anastomotic port exploration and dredging surgery in Beijing Anzhen Hospital from 2018 to 2019 were enrolled in this study. There were 136 male and 31 female patients aged 41-82 (58.35±17.26) years. If the probe entered and exited the anastomotic port smoothly, it was recorded as a non-resistance group; if the resistance existed but the probe could pass and exit, it was recorded as a resistance group; if the probe could not pass the anastomotic port for obvious resistance, it was recorded as the stenosis group. In the stenosis group, the grafts were re-anastomosed and the flow parameters were re-measured by TTFM.ResultsA total of 202 anastomotic ports were carried out by exploration and dredging. Among them, 87 anastomosis (43.1%) were in the non-resistance group, and there was no significant change in the blood flow volume (BFV) and pulsatility index (PI) before and after exploration and dredging (6.16±3.41 mL/min vs. 6.18±3.44 mL/min, P=0.90; 7.06±2.84 vs. 6.96±2.49, P=0.50). Sixty-four anastomosis (31.7%) were in the resistance group, the BFV was higher after exploration and dredging than that before exploration and dredging (17.11±7.52 mL/min vs. 4.96±3.32 mL/min, P<0.01), while the PI was significantly smaller (3.78±2.20 vs. 8.58±2.97, P<0.01). Fifty-one anastomosis (25.2%) were in the stenosis group, and there was no significant change in the BFV and PI before and after exploration and dredging (3.44±1.95 mL/min vs. 3.48±2.11 mL/min, P=0.84; 10.74±4.12 vs. 10.54±4.11, P=0.36). After re-anastomosis, the BFV was higher (16.48±7.67 mL/min, P<0.01) and the PI deceased (3.43±1.39, P<0.01) than that before exploration and dredging.ConclusionThe application of anastomotic exploration and dredging can reduce the occurrence of re-anastomosis, and promptly find and solve the stenosis of the distal coronary artery, improve the poor perfusion of distal coronary, and thus improves the prognosis of patients.
External support stent is a potential means for restricting the deformation and reducing wall stress of the vein graft, thereby improving the long-term patency of the graft in coronary artery bypass surgery. However, there still lacks a theoretical reference for choosing the size of stent based on the diameter of graft. Taking the VEST (venous external support) stent currently used in the clinical practice as the object of study, we constructed three models of VEST stents with different diameters and coupled them respectively to a model of the great saphenous vein graft, and numerically simulated the expansion-contraction process of the vein graft under the constraint of the stents to quantitatively evaluate the influence of stent size on the radial deformation and wall stress of the vein graft. The results showed that while the stent with a small diameter had a high restrictive effect in comparison with larger stents, it led to more severe concentration of wall stress and sharper changes in radial deformation along the axis of the graft, which may have adverse influence on the graft. In order to solve the aforementioned problems, we ameliorated the design of the stent by means of changing the cross-sectional shape of the thick and thin alloy wires from circle into rectangle and square, respectively, while keeping the cross-sectional areas of alloy wires and stent topology unchanged. Further numerical simulations demonstrated that the ameliorated stent evidently reduced the degrees of wall stress concentration and abrupt changes in radial deformation, which may help improve the biomechanical environment of the graft while maintaining the restrictive role of the stent.
ObjectiveTo investigate the role and potential mechanisms of neuropilin-1 (NRP1) in the pathogenesis of vein graft failure.MethodsThe rat vascular smooth muscle cells (VSMCs) were transfected with NRP1-shRNA adenovirus and negative control adenovirus respectively. Cell counting kit-8, flow cytometry, Transwell and Western blot were used to investigate the effects of inhibition of NRP1 on VSMCs proliferation viability, apoptosis, migration capacity and its downstream signaling pathway protein expression.ResultsThe proliferation and migration of rat VSMCs could be inhibited after down-regulation of NRP1, and the increase of apoptosis was also observed. Moreover, inhibition of NRP1 significantly reduced Akt and NF-κB phosphorylation in rat VSMCs, but had little effect on activation of ERK1/2.ConclusionNRP1 may promote vein graft hyperplastic remodeling by regulating the proliferation and migration of VSMCs through PI3K/Akt and NF-κB pathways, but further animal study is required.
In the American Heart Association’s Scientific Sessions 2021, the results of six clinical trials related to cardiovascular surgery were revealed. The PALACS trial demonstrated that posterior left pericardiotomy during open heart surgery was associated with a significant reduction in postoperative atrial fibrillation; the EPICCURE study found that injection of mRNA encoding vascular endothelial growth factor (VEGF-A mRNA) directly into the myocardium of patients undergoing elective coronary artery bypass grafting (CABG) improved patients’ heart function; the VEST trial once again proved the safety and potential value of external stent for vein graft. This article will interpret the above-mentioned three studies.
ObjectiveTo investigate the effect of simvastatin and mechanical pretreatment on intimal hyperplasia of venous graft and its mechanism.MethodsTwelve New Zealand rabbits were selected and randomly divided into 4 groups: a blank control group, a simvastatin topical treatment group, a mechanical precondition group and a combined group (n=3 in each group). Ultrasound was used to evaluate the changes of graft wall and blood flow velocity in the graft, and pathological section was used to evaluate the intimal hyperplasia. Human umbilical cord endodermal cells were cultured in vitro. A simvastatin group and a solvent control group were set to detect YAP phosphorylation, downstream target gene expression and cell proliferation.ResultsVascular ultrasound showed that except the simvastatin topical treatment group, the flow velocity in vein grafts in the other three groups significantly increased 21 days after surgery compared with 7 days after surgery (P<0.01). Pathological sections showed that the thickness of new intima in the simvastatin topical treatment group, mechanical precondition group, combined group and blank control group were 45.56±4.11 μm, 201.28±16.71 μm, 143.57±7.82 μm, 249.45±13.33 μm, respectively, and there were statistical differences compared with the blank control group (P<0.05). In vitro results showed that compared with the solvent control group, cell death was observed in high concentration simvastatin (5 mmol/L) group, cell proliferation was inhibited in low concentration simvastatin (2.5 mmol/L) group (P<0.05), the expression of YAP protein in the simvastatin group was unchanged, but the expression of phosphorylated YAP protein significantly increased (P<0.05), and the expression of downstream target gene ccn1 was down-regulated (P<0.001).ConclusionIntravascular local application of simvastatin and mechanical preconditioning alone or in combination can inhibit intimal hyperplasia of venous graft. High concentration of simvastatin has cytotoxicity, while low concentration of simvastatin has inhibitory effect on cell proliferation. Simvastatin can inhibit the formation of new intima by inhibiting the entry of YAP into the nucleus and reducing the transcription of cell proliferation-related target gene ccn1.