Maybe of interest to some

[Steve112]

youtu.be/StXu8NEHPJM(Not working as expected?)

[Hidden]

Thanks Steve.....as a Warfarin patient of 14+ years I found this very interesting. I'm in a bit of a quandary over whether I should ask to switch to a NOAC

[AnneTS in reply to Hidden]

Yatsura. As a fellow Warfarin user I am keeping a close eye on the NOACS. Unfortunately if your INR target is 3-4 then there isn't a NOAC available to cover this group of patients. Also, if you have a metal replacement mitral valve there doesn't seem to be a suitable NOAC. Let's hope these issues can be resolved soon!! Anne

[RobertELee in reply to AnneTS]

Annel, why would your target INR be 3-4? Not that there's anything necessarily wrong with 3-4 but in the balance between 'risk of stroke' and 'risk of bleed' a higher INR is weighted slightly towards the latter. But NOAC's don't correlate with INR in any way, so I don't really understand that particular point.

[AnneTS in reply to RobertELee]

Hi Robert. NOACS work with those patients who have a target rate lower than the target rate I have been given and so are not suitable for me. I understand these NOACS can bring clotting stability to this group of patients. People who have had repeated PE's normally are given an INR target of 3.5 and even though the NOACS do not work in the same way as Warfarin/Coumadin they do need to be able to reduce the clotting ability to that INR level. At the moment there is no NOAC that does this. In addition, if you have a faulty clotting gene (not a Factor V or Viii) as I have there is no NOAC that can compensate for this added problem. In addition, if you are borderline Antiphospholipid syndrome (Hughes syndrome) yet another layer of complication is added. One day I hope there will be a NOAC to cover us!! In the meantime NOACs seem to be very successful for the straightforward prevention of clots in patients with no other clotting or metal valvular contraindications.

[AnneTS]

Thanks Steve. This is very interesting. Annel

[jennydog]

Interesting. I have been taking dabigatran (Pradaxa) since my ablation in Aug 2014. It's so easy compared to warfarin. And there is an antidote called Praxbind.

I have often wondered why the EP who did my ablation chose Pradaxa for me, rather than any of the other NOACs. He justified the change from warfarin as " unstable INR." I'd tried a no-added sugar diet and it had caused a very stable INR of 2.5 to plummet to 1.3. The change to an NOAC has to be justified on cost grounds - Pradaxa costs £58/month. I suppose that the testing/time/travelling costs of warfarin are unquantifiable.

[MarkS]

This RE-CIRCUIT trial was funded by Boehringer Ingelheim, the makers of Dabigatran, so it's not surprising it has come up with these results.

Other independent trials have come up with similar rates of bleeding and thrombo-embolic events between warfarin and dabigatran, e.g.:

ncbi.nlm.nih.gov/pubmed/239...

Mark

[Beancounter Volunteer in reply to MarkS]

Hi Mark

That trial was for periprocedural comparison, in other words comparison during ablations themselves. As you probably know it took a while for some EPs to trust any of the NOACs during ablation, and they sometimes used to transfer you back to warfarin prior to the ablation. This report supports the use of Dabigitran during ablation.

I'd be interested to see the results of other trials for use outside of the periprocedural if you have any.

Be well

Ian

[MarkS in reply to Beancounter]

Hi Ian,

I'm not sure I get your point - I may be being a bit thick on a Sunday morning! Both trials were periprocedural - i.e. comparisons during the ablation itself, or am I missing something?

As I've mentioned before, the key requirement is for uninterrupted anti-coagulation during ablation for AF, and it doesn't matter of it's uninterrupted warfarin or NOAC, the results are pretty similar. The Re-circuit trial rather scratched the surface in my view. The real danger in ablation is the production of micro-emboli - i.e. small clots which are not big enough to cause a TIA or stroke but neverless damage the brain. This shows up in dementia later in life.

One trial involving uninterrupted warfarin and interrupted NOACs was:

jstage.jst.go.jp/article/ci...

This found that dabigatran was a risk factor for "silent cerebral ischemic

lesions" compared to warfarin, but this was probably because the dabigatran was interrupted.

Also in this trial comparing dabigatran, rivaroxoban and warfarin in peri-procedural ablation:

ncbi.nlm.nih.gov/pmc/articl...

The conclusion is "NOACs are comparable to warfarin in terms of bleeding complications. However, dabigatran therapy is potentially associated with a higher risk of silent cerebral lesions on MRI." It goes on to say that much more research is needed.

Mark

[Hidden in reply to MarkS]

Thanks Mark. More ' food for thought '.

Sandra

[Beancounter Volunteer in reply to MarkS]

Thanks Mark

Definitely me being thick on a Sunday morning, I misread the first trial as not being periprocedural

But the info gratefully received

Ian

[MarkS in reply to Beancounter]

Thanks, Ian!

[NooNoo14]

Thanks for your post Steve, this has come at a good time for me as I have a call booked with my GP for tomorrow to discuss changing to Dabigatran from Warfarin.

Netty