Preserving flow, saving lives: Successful treatment of aortic valve failure in acute myocardial infarction without flow down-regulation using ECMO - a case report and mini review.

Direct percutaneous coronary intervention (PPCI) has significantly reduced cardiac mortality in patients with acute myocardial infarction (AMI), but the mortality rate remains high for those who develop cardiogenic shock (CS), reaching 40% to 50%. Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) provides robust hemodynamic support and oxygen delivery for AMI patients with refractory CS, ensuring adequate organ perfusion and oxygen supply. However, there is currently no standardized optimal Mean Arterial Pressure (MAP) range during V-A ECMO support. Achieving the proper MAP is crucial for adequate myocardial perfusion, cardiac function recovery, successful weaning off of V-A ECMO, and improving long-term outcomes. In this case study, we successfully treated a 55-year-old man with AMI and refractory cardiogenic shock using V-A ECMO. By adjusting ECMO blood flow and employing hemodynamic strategies, including vasoactive drugs, we optimized the MAP, leading to improved cardiac function and successful weaning off of V-A ECMO. This presents a potential opportunity for MAP optimization under ECMO support in patients with acute myocardial infarction and cardiogenic shock.

Heparin-free adventitia pulmonary oxygenation in the treatment of trauma complicated with severe pulmonary infection: a case report.

The application of Venovenous (VV) extracorporeal membrane oxygenation (ECMO) in trauma and patients with severe bleeding tendency has been controversial. However, VV ECMO without anticoagulation contributes to reducing the risk of bleeding during ECMO maintenance. VV ECMO serves critical roles in therapy of patients with severe pulmonary infection and failure in conventional therapy. The common peripheral catheterization approach for VV ECMO is femoral vein-internal jugular vein catheterization, and bilateral femoral vein catheterization can also achieve the purpose of respiratory support for patients with limited cervical catheterization. In this case report, we described a patient with post-traumatic cervical spinal cord injury and severe pulmonary infection who was successfully treated with heparin-free intravenous ECMO.

Human umbilical cord mesenchymal stem cells pretreated with Angiotensin-II attenuate pancreas injury of rats with severe acute pancreatitis.

Mesenchymal stem cells (MSCs) pretreatment is an effective route for improving cell-based therapy of endothelial cell survival, vascular stabilization, and angiogenesis. We hypothesized that the application of human umbilical cord-MSCs (hUC-MSCs) pretreated with angiotensin-II (Ang-II) might be a potential therapeutic approach for severe acute pancreatitis (SAP). Therefore, the effect of Ang-II pretreated hUC-MSCs on SAP was investigated in vitro and in vivo. METHODS: In the present study, human umbilical cord-derived MSCs pretreated with or without Ang-II were delivered through the tail vein of rats 12 h after induction of SAP. Pancreatitis severity scores and serum lipase levels, as well as the levels of VEGF and VEGFR2 were evaluated. RESULTS: We found that the administration of Ang-II-MSCs significantly inhibited pancreatic injury, as reflected by reductions of pancreatitis severity scores, serum amylase and serum lipase levels. Furthermore, the reduced apoptotic rate and increased tube formation in human umbilical vein endothelial Cells (HUVEC) were found resulting from the administration of Ang-II-MSC-CM. Moreover, knockdown of VEGFR2 can block the effect of Ang-II-MSC-CM on preventing HUVEC from apoptosis, as well as the capacity of tube formation was also suppressed. In addition, the expression of increased Bcl-2 and alleviated caspase-3 were observed in HUVEC and HUVEC transfectants exposure to Ang-II-MSC-CM. CONCLUSION: Collectively, these results elucidated that the pretreatment of hUC-MSCs with Ang-II improved the outcome of MSC-based therapy for SAP via enhancing angiogenesis and ameliorating endothelial cell dysfunction in a VEGFR2 dependent manner.