Management of Ascending Aorta Calcification in Coronary Artery Bypass Grafting

Neurological complications are one of the most common complications after coronary artery bypass grafting. With the development of off-pump coronary artery bypass grafting (OPCABG), the incidence of postoperative neurological complications caused by aortic intubation decreased significantly; however, the continuous suture of the great saphenous vein-aortic anastomosis in the coronary artery bypass grafting requires the operation of surgical clamp and perforation on the ascending aorta, which may lead to potential plaque detachment. Calcification of ascending aorta is an independent risk factor for cerebrovascular events after OPCABG. Therefore, it is crucial to explore and operate on the ascending aorta. There are three main methods of proximal anastomosis in OPCABG: (1) partial blocking of ascending aorta with side wall clamp for anastomosis; (2) application of proximal anastomosis auxiliary device (Enclose, Heartstring, etc.) for proximal anastomosis; and (3) original auxiliary device (urethra catheter-water sac) or no-clamp surgical techniques for proximal anastomosis

Atherosclerosis T1-weighted characterization (CATCH): evaluation of the accuracy for identifying intraplaque hemorrhage with histological validation in carotid and coronary artery specimens

Background: Coronary high intensity plaques (CHIPs) detected using cardiovascular magnetic resonance (CMR) coronary atherosclerosis T1-weighted characterization with integrated anatomical reference (CATCH) have been shown to be positively associated with high-risk morphology observed on intracoronary optical coherence tomography (OCT). This study sought to validate whether CHIPs detected on CATCH indicate the presence of intraplaque hemorrhage (IPH) through ex vivo imaging of carotid and coronary plaque specimens, with histopathology as the standard reference. Methods: Ten patients scheduled to undergo carotid endarterectomy underwent CMR with the conventional T1-weighted (T1w) sequence. Eleven carotid atherosclerotic plaques removed at carotid endarterectomy and six coronary artery endarterectomy specimens removed from patients undergoing coronary artery bypass grafting (CABG) were scanned ex vivo using both the conventional T1w sequence and CATCH. Both in vivo and ex vivo images were examined for the presence of IPH. The sensitivity, specificity, and Cohen Kappa (k) value of each scan were calculated using matched histological sections as the reference. k value between each scan in the discrimination of IPH was also computed. Results: A total of 236 in vivo locations, 328 ex vivo and matching histology locations were included for the analysis. Sensitivity, specificity, and k value were 76.7%, 95.3%, and 0.75 for in vivo T1w imaging, 77.2%, 97.4%, and 0.78 for ex vivo T1w imaging, and 95.0%, 92.1%, and 0.84 for ex vivo CATCH, respectively. Moderate agreement was reached between in vivo T1w imaging, ex vivo T1w imaging, and ex vivo CATCH for the detection of IPH: between in vivo T1w imaging and ex vivo CATCH (k = 0.68), between ex vivo T1w imaging and ex vivo CATCH (k = 0.74), between in vivo T1w imaging and ex vivo T1w imaging (k = 0.83). None of the coronary artery plaque locations showed IPH. Conclusion: This study demonstrated that carotid CHIPs detected by CATCH can be used to assess for IPH, a high-risk plaque feature

Pulmonary artery perfusion with anti-tumor necrosis factor alpha antibody reduces cardiopulmonary bypass-induced inflammatory lung injury in a rabbit model.

Inflammatory lung injury is one of the main complications associated with cardiopulmonary bypass (CPB). Tumor necrosis factor-α (TNF-α) is one of the key factors mediating the CPB-induced inflammatory reactions. Our previous studies have shown that endotracheal administration of anti-tumor necrosis factor-α antibody (TNF-α Ab) produces some beneficial effects on lung in a rabbit CPB model. In this study, we further examined the effects of pulmonary artery perfusion with TNF-α Ab (27 ng/kg) on lung tissue integrity and pulmonary inflammation during CPB and investigated the mechanism underlying the TNF-α Ab-mediated effects in a rabbit model of CPB. Our results from transmission electron microscopy showed that the perfusion with TNF-α Ab alleviated CPB-induced histopathological changes in lung tissue. The perfusion with TNF-α Ab also prevented CPB-induced pulmonary edema and improved oxygenation index. Parameters indicating pulmonary inflammation, including neutrophil count and plasma TNF-α and malondialdehyde (MDA) levels, were significantly reduced during CPB by pulmonary artery perfusion with TNF-α Ab, suggesting that the perfusion with TNF-α Ab reduces CPB-induced pulmonary inflammation. We further investigated the molecular mechanism underlying the protective effects of TNF-α Ab on lung. Our quantitative RT-PCR analysis revealed that pulmonary artery perfusion with TNF-α Ab significantly decreased TNF-α expression in lung tissue during CPB. The apoptotic index in lung tissue and the expression of proteins that play stimulatory roles in apoptosis pathways including the fas ligand (FasL) and Bax were markedly reduced during CPB by the perfusion with TNF-α Ab. In contrast, the expression of Bcl-2, which plays an inhibitory role in apoptosis pathways, was significantly increased during CPB by the perfusion with TNF-α Ab, indicating that the perfusion with TNF-α Ab significantly reduces CPB-induced apoptosis in lung. Thus, our study suggests that pulmonary artery perfusion with TNF-α Ab might be a promising approach for attenuating CPB-induced inflammatory lung injury

Left Ventricular Aneurysm Repair: Off-pump Linear Plication versus On-pump Patch Plasty

Abstract Objective: The study aimed to compare the clinical outcomes of simplified linear plication and classic patch plasty in patients with left ventricular aneurysm (LVA). Methods: We retrospectively reviewed 282 patients undergoing LVA repair between 2006 and 2016. After propensity score matching, 45 pairs of patients receiving LVA surgery were divided into either a patch group (on-pump endoventricular patch plasty) or a plication group (off-pump linear plication). Then, their early surgical outcomes and long-term survival were compared in two matched groups. Results: The heart function improvement at discharge was similar in the two matched groups, while patients in the patch group more commonly suffered from low cardiac output syndrome (P=0.042) with higher proportion of intra-aortic balloon pumping assistance (P=0.034) than patients in the plication group. Compared with patients in the patch group, the patients in the plication group had shorter recovery times, regarding to mechanical ventilation, intensive care unit stay, and hospital stay (P<0.001, P<0.001, and P=0.001, respectively). No significant difference was found in the long-term survival (P=0.62). Conclusions: Off-pump linear plication presented acceptable results in terms of early outcomes and long-term survival. For high-risk patients, the simplified LVA repair technique may be an option

NIK-SIX1 signalling axis regulates high glucose-induced endothelial cell dysfunction and inflammation

Endothelial dysfunction and inflammation are the main manifestations of diabetes-associated atherosclerosis. This paper studied the roles of NF-κB-inducing kinase (NIK) and sine oculis homeobox homolog 1 (SIX1) in regulating high glucose-induced endothelial dysfunction and inflammation. The expression of NIK and SIX1 in human umbilical vein endothelial cells (HUVECs) was silenced by transfection with the specific shRNAs. HUVECs exposed to high glucose were considered as a cell model of endothelial dysfunction. Expression of NIK and SIX1 following transfection was measured by qRT-PCR and western blotting analysis. The proliferation, migration, and inflammation of HUVECs were evaluated by EdU staining, scratch test, ELISA, and western blotting. High glucose (30 mM) significantly decreased the proliferation and migration of HUVECs. High glucose-induced the expression of adhesion molecules VCAM-1 and ICAM-1. Moreover, high glucose increased the release of IL-1β, IL-6, TNF-α, and MCP-1. Transfection of cells with NIK shRNA significantly reversed the toxic effects of high glucose on HUVECs. Of contrast, SIX1 shRNA accelerated the effects of high glucose on HUVECs. NIK shRNA inhibited the accumulation of RelA, RelB, and p52. Meanwhile, NIK shRNA led to SIX1 downregulation which further induced the activation of the NF-κB pathway. NIK-SIX1 signalling axis was suggested to be critical in the regulation of high glucose-induced endothelial dysfunction and inflammation. SIX1 may function as an immunological gatekeeper to control the excessive inflammation mediated by NIK in diabetes-associated atherosclerosis

Comparison of the protein levels of Bcl-2 (%), Bax (%), and FasL (%), and the ratio of Bcl-2/Bax in alveolar epithelial cells in different experimental groups (mean ±SD, n = 10).

1<p>P<0.05, compared to group IV.</p>2<p>P<0.05, compared to group II.</p