Found this 2019 article which contains this
January 10, 2020 Update that I don't quite understand. I didn't realize that there are patients whose heart valves cause afib.
"Patients with prosthetic heart valves should not take apixaban. Apixaban was not studied in patients with atrial fibrillation caused by a heart valve problem."
https://www.fda.gov/news-events/press-announcements/fda-approves-first-generics-eliquis
now, this is not medical advice as its well known that you should not even read forums on the internet, but I would incline to the view that there are two main streams of reasons for taking anticoagulants
- general stroke prophylaxis (especially when such is indicated by a series of TIA's or a non-transient Ischemic Stroke event or DVT event (or the like)
- prophylaxis in the case of a heart valve replacement
These two types have slightly different agendas: namely
what is the cause of thrombosis. For its in the causes and the distance these are from the brain that the risks vary and what is likely to trigger it (platelet aggregation or exposure to tissue factor).
Type 1 is pretty much going to be for life (even if you have had a tissue valve)
Type 2 is perhaps temporary for those who have a tissue prostheis
So lets wander off the farm here and get random internet dude on ya'll
Firstly lets look at Coagulation (a good
read to be had at Wikipedia), which says:
Platelets can be activated by the successive round trip
whack on the arse obtained as they pass through the gates of the mechanical valve (and are exposed to opening and closing pressure jets). Much is written on this (not least of which is Yoganathan 2004, and K. Dumont et al 2007) and platelet activation numbers of 35 dyne x s/cm2 {where Dyne-second per square centimeter is a dynamic viscosity measurement unit}). To my knowledge non of these fluid dynamic processes has been studied or had thresholds identified in tissue prosthesis valves.
However its important to re-mention tissue factor which is emitted by damaged endothelia (and that occurs in heart surgery when the endothelia of the aortic artery is cut with a knife to slice out the old valve and when the needle penetrates and stitches are used to attach the new valve. This will continue to be a problem until after re-endothelisation occurs. This is why you're on
blood thinners for 3 or so months after surgery no matter what.
So what can we make of this?
Well if your source of thrombosis is by platelet activation (virtually a certainty with a mech valve) you need something which will work on the areas above (factors II, VII, IX and X) to slow down this "Time for Thrombin to bunch up with fibrin.
If you have some other issue then simply stopping or slowing platelet activation will help (and that'd be aspirin or other antiplatelet stuff.
Where does this leave Apixaban? Well as that only works on X
I suspect that it leaves it in the "insufficient" category of anticoagulants for a higher demand situation like mech valves.
Lastly, where does AF fit into this? I'm not sure if it generates sufficient dynes to cause platelet aggregations however it may cause the release of some tissue factor due to the "gyrations" it causes in the Atria while its having its little spastic episode between beats.
All this is good material to look at and to ask your actual qualified medical professional, because as I previously mentioned I'm just some random internet dude who's shuffled through the data. As a reminder of that I'll leave you with the advice from Bon Scott:
But how was I to know
That she'd been shuffled before?
Said she'd never had a royal flush
But I should have known
That all the cards were comin'
From the bottom of the pack
And if I'd known what she was dealing out
I'd have dealt it back
She's got the jack, she's got the jack
She's got the jack, and who knows what else
