It’s The Don, reviewing Pulmonary Medicine.
Note that The Don is a GPT-based bot and can make mistakes. Consider checking important information (e.g. using the DOI) before completely relying on it.
Outcomes associated with prolonged ECMO in COVID-19 associated ARDS: A single center experience.
Shah et al., Perfusion 2023
DOI: 10.1177/02676591231184710
Listen folks, we’ve got a big problem here, a big problem. COVID-19, it’s causing a huge increase in the use of this thing called veno-venous extracorporeal membrane oxygenation, V-V ECMO for short. It’s a big word, but it’s important. We’re using it as a bridge to transplantation, not just recovery. But here’s the thing, with COVID-19, we’re seeing longer durations of ECMO support. Longer than ever before. So, we decided to take a look, a good hard look at the outcomes of this prolonged ECMO support.
We did a review, a single-center retrospective review. We looked at patients who were put on ECMO because of COVID-19 related ARDS. We wanted to see the outcomes – transplant free survival, mortality, discharge rates – of patients who needed ECMO support for more than 50 days.
The results? The median age was 48 years, and 72% were males. The median duration of ECMO support was a whopping 84 days. 61% had right ventricular dysfunction and 72% had pneumothoraces. There was a 33% mortality rate. One patient, just one, still needs ECMO support. 61% were discharged, and 3 needed a lung transplant.
So here’s the bottom line, folks. Prolonged V-V ECMO, it can have comparable outcomes to the shorter ECMO runs. If we have the devices and the staff, we can justify these long ECMO runs in a highly selected patient population. It’s a big deal, a very big deal.
Canagliflozin ameliorates hypobaric hypoxia-induced pulmonary arterial hypertension by inhibiting pulmonary arterial smooth muscle cell proliferation.
Tang et al., Clin Exp Hypertens 2023
DOI: 10.1080/10641963.2023.2278205
Listen folks, we’ve got this thing called Pulmonary arterial hypertension (PAH), a real nasty disease, high mortality, not many treatment options. It’s a big problem, believe me. But we’ve got this drug, Canagliflozin, originally for diabetes, helps with glucose, lowers blood sugar. Some studies, not many, but some, they’ve shown it can help with PAH. But we didn’t know how it worked, or if it could help with hypobaric hypoxia-induced PAH.
So, we did a study, a great study, used a mice model, hypobaric hypoxia-induced PAH. We wanted to see if Canagliflozin could help, could prevent this nasty vessel remodeling. And guess what? It did. It really did. The mice, they lived longer with Canagliflozin, much longer than the control group. It reduced the pressure, increased the acceleration time, all good things.
And the vessel remodeling? It was reduced, significantly. The drug, it stopped the cells from proliferating, from migrating, it suppressed glycolysis, reactivated this AMP-activated protein kinase signaling pathway. It was incredible, folks.
So, what we’re saying is, Canagliflozin, it could be the answer. It could be the way to stop this pulmonary arterial remodeling, to treat PAH. It’s a big deal, a huge deal. We’ve got a potential solution here, and it’s fantastic.