My question regarding endothelial dysfunction wasn't with regards to mechanisms of calming inflammation, which would be beneficial to increasing plaque stability, but more with regards to its mechanism via intracardiac injection.
Which vessels are you thinking are benefited? And why would it not be more beneficial to do a systemic infusion rather than intracardiac injection (this point again, I know).
The coronaries will be receiving the benefit from systemic, not local effects. And why wouldn't other vessels benefit further downstream?
If this is the mechanism then why aren't we looking at MSCs to treat peripheral vascular disease?
Also, heart failure is more nuanced than just looking at the LVEF, you're right. But LVEF is a great marker for progression or recovery, especially in those with HFrEF, which is the population we are observing.
I'll need to dig though the data again, as I did see them comment on the EF not being affected. Which really refutes the claim of affecting remodelling.
Cell Therapy News/Articles, page-13690
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