Four-corners traction combined with continuous everting suture technique as a modification in bicaval anastomosis for orthotopic heart transplantation.

Background: Although standard bicaval techniques has become popular in orthotopic heart transplantation, distortion, bleeding, thrombosis and arrhythmia were still causes for concern. This study was designed to compare the standard bicaval techniques and modified bicaval techniques in our institution.

Materials And Methods: A total of 70 recipients underwent orthotopic heart transplantation at our center from June 2015 to April 2019 (standard group = 24 cases, modified group = 46 cases).

Application of prosthesis eversion method for ascending aorta replacement guarantees better clinical outcomes of type A acute aortic dissection surgery.

Background: The advantages of prosthesis eversion method in patients diagnosed with Stanford type A acute aortic dissection (AAD) undergoing ascending aorta replacement (AAR) is unknown. This research is designed to explore it.

Methods: We retrospectively analyzed the data of a total of 283 patients diagnosed with type A aortic dissection that underwent surgery in Renmin Hospital of Wuhan University from March, 2006 to April, 2020.

Two Cases Treated by Different Strategies for Common Carotid Artery Dissection with Thrombosis Due to a Type A Aortic Dissection.

Total arch replacement and stent trunk were performed for two patients. One of these underwent a total bilateral carotid artery replacement in anatomical position while the other underwent partial carotid artery dissection. The first patient demonstrated no neurological complication after surgery and a postoperative computed tomography angiography (CTA) showed bilateral common carotid artery patency.

Obesity is a risk factor for preoperative hypoxemia in Stanford A acute aortic dissection.

Obese individuals are apt to develop Stanford A acute aortic dissection (AAD) complicated with acute lung injury (ALI), but the mechanism is still not well defined. We aim to investigate whether oxidative stress and inflammatory are involved in the aortic dissection lung injury caused by obesity.Seventy-nine patients were categorized into AAD with obesity group (n = 17) and AAD without obesity group (n = 62) according to body mass index (BMI).

Corrigendum to "JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 on Aortic Dissection with Acute Lung Injury".

[This corrects the article DOI: 10.1155/2017/1917804.].

Bindarit reduces the incidence of acute aortic dissection complicated lung injury via modulating NF-κB pathway.

The pathogenesis of acute aortic dissection (AAD) complicated acute lung injury (ALI) is not currently well defined. At present, no effective animal model has been established for AAD complicated ALI, which hinders research and development of an appropriate treatment regimen for the concurrent conditions. The aim of the present study was to evaluate the therapeutic effects of bindarit (Bnd), an indazolic derivative, on the production of monocyte chemoattractant protein (MCP)-1 in angiotensin II (AngII)-induced complicated ALI in rats.

JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 On Aortic Dissection with Acute Lung Injury.

Patients with aortic dissection (AD) may present acute lung injury (ALI) that may affect the prognosis. In this study, we aim to investigate the roles and mechanism of IL-22 in the pathogenesis of AD complicated with ALI. Six hundred and twenty-one AD patients were included, and the incidence of ALI and pulmonary CT findings were analyzed.

Interleukin 22 attenuated angiotensin II induced acute lung injury through inhibiting the apoptosis of pulmonary microvascular endothelial cells.

Apoptosis of pulmonary microvascular endothelial cells (PMVECs) was considered to be closely related to the pathogenesis of acute lung injury (ALI). We aim to investigate whether IL-22 plays protective roles in lung injury through inhibiting the apoptosis of PMVECs. ALI model was induced through subcutaneous infusion of angiotensin II (Ang II).

Dephosphorylation of Y685-VE-Cadherin Involved in Pulmonary Microvascular Endothelial Barrier Injury Induced by Angiotensin II.

Angiotensin II (AngII) caused pulmonary microvascular endothelial barrier injury, which induced acute aortic dissection (AAD) combined with acute lung injury (ALI). However, the exact mechanism is unclear. We investigated the role of dephosphorylation of Y685-VE-cadherin in the AngII induced pulmonary microvascular endothelial barrier injury.

VE-cadherin involved in the pulmonary microvascular endothelial cell barrier injury induced by angiotensin II through modulating the cellular apoptosis and skeletal rearrangement.

Objective: Angiotensin II (AngII) involved in the pathogenesis of pulmonary injury through impairing the integrity of pulmonary microvascular endothelial barrier, but the mechanism is still not clear. We aim to determine the roles of VE-cadherin, playing crucial roles in the adhesion of the vascular endothelial barrier and the barrier function, in the pulmonary microvascular endothelial cell (PMVEC) barrier injury mediated by AngII.

Methods: Mice acute lung injury (ALI) model was induced through pumping of AngII.

Angiotensin II is related to the acute aortic dissection complicated with lung injury through mediating the release of MMP9 from macrophages.

Background: Acute aortic dissection (AAD) patients usually show concurrent lung injury mainly featured by hyoxemia. To date, no effective treatment method has been established for the AAD complicated with acute lung injury (ALI). Matrix metalloproteinases (MMPs), especially MMP2 and MMP9, have been considered to be closely related to the onset of aortic disease including AAD.

Angiotensin II induces apoptosis of human pulmonary microvascular endothelial cells in acute aortic dissection complicated with lung injury patients through modulating the expression of monocyte chemoattractant protein-1.

Patients with acute aortic dissection (AAD) usually showed acute lung injury (ALI). However, its pathogenesis is still not well defined. Apoptosis of pulmonary microvascular endothelial cells (PMVECs) is closely related to the alveolus-capillary barrier injury and the increased vascular permeability.