Impact of Conventional Cardiovascular Risk Factors on Left Internal Mammary Artery Graft Disease

Background:The development of atherosclerosis was considered as the common cause of the stenosis of coronary artery grafts. Left internal mammary artery (LIMA) was the best artery graft for further effectiveness of coronary artery bypass grafting (CABG). We sought to assess the impact of known conventional cardiovascular risk factors (RFs) on LIMA graft stenosis.Methods:A retrospective study including 618 participants, who had recurrence of chest pain after CABG, aged ≥18 years, hospitalized for coronary angiography in Beijing Anzhen hospital between 2010 and 2017 was performed. All the participants were confirmed to have LIMA graft. Multivariate analysis was conducted to determine the relationship between conventional RFs and LIMA graft stenosis.Results:Of the study, 220 (35.6%) participants continued to smoke, 504 (81.6%) were overweight or obese, and 411 (66.5%) and 242 (39.2%) reported concomitant hypertension and diabetes, respectively. LIMA graft stenosis occurred in 161 participants (26.1%). Postoperative smoking, a CABG duration of ≥10 years and hyperglycemia without diabetes had an increased risk of LIMA graft stenosis, the odds ratio (OR) was 1.86 [95% confidence interval (CI): 1.26–2.78], 2.24 (95%CI:1.33–3.478), and 2.44(95% CI:1.39–4.32), respectively. Statin use (OR, 0.28; 95% CI: 0.25–0.5) and low-density lipoprotein cholesterol (LDL-C) < 1.8 mmol/L (OR, 0.27; 95% CI: 0.14–0.53) had a significantly decreased risk of LIMA graft stenosis. While, only 15.4% (95/618) achieved the target LDL-C level.Conclusions:Postoperative smoking and hyperglycemia without diabetes had an increased risk of LIMA graft stenosis. Statin use and LDL-C <1.8 mmol/L decreased the risk.

In vivo performance of decellularized tracheal grafts in the reconstruction of long length tracheal defects: Experimental study

Background: The repair of long-segment tracheal lesions remains an important challenge. Nowdays no predictable and dependable substitute has been found. Decellularized tracheal scaffolds have shown to be a promising graft for tracheal transplantation, since it is non-immunogenic. Objective: Evaluate in vivo decellularized tracheal allografts performance to replace long tracheal segment. Methods: Forty-five swines underwent surgery as follows: Fifteen trachea donors and 30 receptors of decellularized trachea allografts. The receptors were randomly divided in five groups ( n = 6). In groups I and II, donor trachea segment was decellularized by 15 cycles with sodium deoxycholate and deoxyribonuclease, in group II, the allograft was reinforced with external surgical steel wire. Groups, III, IV, and V decellularization was reduced to seven cycles, supplemented with cryopreservation in group IV and with glutaraldehyde in group V. A 10 rings segment was excised from the receptor swine and the decellularized trachea graft was implanted to re-establish trachea continuity. Results: Both decellularization cycles caused decreased stiffness. All trachea receptors underwent euthanasia before the third post-implant week due to severe dyspnea and trachea graft stenosis, necrosis, edema, inflammation, hemorrhage, and granulation tissue formation in anastomotic sites. Histologically all showed total loss of epithelium, separation of collagen fibers, and alterations in staining. Conclusions: Both decellularization techniques severely damaged the structure of the trachea and the extracellular matrix of the cartilage, resulting in a no functional graft, in spite of the use of surgical wire, cryopreservation or glutaraldehyde treatment. An important drawback was the formation of fibrotic stenosis in both anastomosis.

Plain versus paclitaxel-coated balloon angioplasty in arteriovenous fistula and graft stenosis: An umbrella review

An umbrella review was performed to synthesize the evidence from systematic reviews/meta-analyses of clinical trials investigating the efficacy and safety of paclitaxel-coated balloons (PCB) vs. conventional balloon angioplasty in arteriovenous fistulas (AVFs) and grafts stenosis. Medline (via PubMed) and SCOPUS databases were searched up to July 15th 2020. All meta-analyses that enrolled randomized controlled trials (RCTs) comparing PCB with plain balloons in AVFs and grafts were included. Re-analysis of original data was performed assessing predictive intervals (PI). Quality of the included meta-analyses was assessed using AMSTAR score. Eight meta-analyses were included and four clinical outcomes [target lesion primary patency (TLPP), circuit primary patency, mortality, complication rate] derived from 14 RCTs, were analyzed. There were no significant differences in the TLPP in meta-analyses providing data purely from autologous AVFs. Significant benefits regarding TLPP and circuit primary patency at 3, 6, and 12-months in favor of PCB were reported in four meta-analyses mixing AVFs and grafts; however when PI were assessed, in all but one meta-analysis these included the null value, indicating no significant benefit. In only one meta-analysis significant difference of TLPP at 12-months in favor of PCB was noticed. (Odds Ratio 0.0009 PI: 0.28-0.85) No mortality difference was noticed in four meta-analyses providing data up to 24 months. In conclusion this overview revealed a modest benefit of using PCB angioplasty compared to plain angioplasty in AVFs and graft stenosis. No increased mortality was noticed in the PCB group.

Extracellular signal-regulated kinase inhibition prevents venous adaptive remodeling via regulation of Eph-B4

Objectives Vein graft adaptation (VGA) is a process that vein as a vascular graft conduits in arterial reconstructive surgery; VGA can lead to postoperative vein graft stenosis (VGS) and complications after coronary artery bypass graft and other peripheral artery bypass surgeries. VGA is characterized by vein graft loss the venous features without exhibiting arterial features; furthermore, the activation of ERK inhibited the maintenance of venous properties of the vein graft. We hypothesized that ERK inhibition can affect vein VGS through regulating the expression of EphB4. Methods Rat vein transplantation model was established using wild-type and EphB4+/− Sprague-Dawley rats. Hematoxylin-eosin, Masson, Verhoeff, actin staining, and immunohistochemistry were applied to observe the structure of the vein grafts. Vascular smooth muscle cells (VSMCs) were isolated from the vein and vein grafts. Western blotting was used to determine the expression of p-ERK1/2 and EphB4, and immunofluorescence was applied to detect the expression and location of EphB4. Cell wound scratch assay and CCK8 assay were used to determine the migration and proliferation of VSMCs. Real-time polymerase chain reaction was used to determine the mRNA expression of EphB4. Results Western blotting in vein sample and vein graft sample detected p-ERK1/2 and ERK1/2 expression in both EphB4+/+ and EphB4+/− rats. The expression of p-ERK was increased in vein graft compared to vein. Immunofluorescence in VSMCs form EphB4+/+ and EphB4+/− rats detected EphB4 expression in both cells, and the expression of EphB4 was increased in VSMCs form EphB4+/+ rats. SCH772984 reduces the proliferation and migration of VSMCs. Inhibition of ERK suppressed the increase of vein graft wall thickness, and the expression of collagen fibers, elastic fibers, and α-actin was decreased. Vein graft from EphB4+/− rats reduces the expression of EphB4, and SCH772984 suppressed the decrease of EphB4 in vivo. Vein graft from EphB4+/− rats increased the expression of EphB4, and SCH772984 suppressed the increase of EphB4 in vivo. Conclusions The inhibition of ERK1/2 suppressed the process of VGS by decreasing the proliferation of VSMCs. The ERK-inhibitor SCH772984 suppressed the level of VGS by extending the time of EphB4 expression during the process of VGA, thus maintaining the venousization of vein graft. The mechanism may be that the inhibitor SCH772984 suppresses the level of VGS by extending the time of EphB4 expression during the process of VGA. Therefore, our research provides a new target of VGS treatment by inhibiting the expression of ERK1/2 through the process of VGA.