a quick question that I think the FDA might ask for anyone who...

a quick question that I think the FDA might ask for anyone who is interested in replying (@otherperspective, @col69, @ddwn, @ecoool2, @theyankee to name a few)

Regarding the 60% reduction in stroke risk, if we accept this is true and as a result of some form of anti inflammatory mechanism, then this suggests that the cells work via pathways independent of their site of delivery. So natural question is why the cells need to be delivered as an intramyocardial injection? Surely they would be just as effective if given into skeletal muscle which would be much less invasive.

I guess an alternative mechanisms could be a direct anti platelet effect or an improved embolic risk profile such as improved LVEF, a reduction in LV size, LVEDD or thrombus formation, or reduced rates of AF. Even so, I imagine each of these mechanisms might still be valid with a standard IM injection.

To suggest that the cells are risk free (a big selling point according to MSB) is probably invalid if they require cardiac catheterisation (which carries a probably ~1% morbidity).

I wanted to make a new thread to ask this but resisted the urge, the MSB forum is a bit crazy right now. I raised this issue years ago (I could probably find and reference the post if needed) bit that was before this reduction in stroke risk.