AF Association
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NOACs and Valves?

Is anyone out there prescribed a NOAC when their primary diagnosis is valvular caused AF? I understand US docs prescribe them but UK docs don't. My case is Afib, heart rate 120-140...for 18 months. Recommended ablation after 6 months and Pace and Ablate after 18 months. I didn't go for either...but did go for a second opinion. Second opinion in US diagnosed with need for Mitral Valve repair. I now have a titanium ring inserted into my valve...or around it, MAZE procedure also and Left Atrial Appendage tied off.

Cardiologist in states says come off Warfarin as the risk for internal bleeding is higher than with a NOAC (Rivaroxiban in this case). Cardiologist here in UK says if I stay on Rivaroxiban it will be against medical advice.

Any thoughts or advice out there? Thanks.

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This is a very specialist area and I don't think we're qualified to give advice. However I know there's been discussion about trials involving valvular AF and anti-coagulation. But as the risk of stroke is so high with valvular AF, it was considered unethical to have placebo-controlled trials. So the NOACs are only currently considered suitable for non-valvular AF.

Personally, in your position, if you follow the advice of your UK cardio, I would concentrate on getting warfarin treatment as optimal as possible - that means self-testing weekly as a minimum.


I have a tissue aortic valve and all the makers have confirmed to me when I asked them directly that NOACs are contra indicated for me. The patient information leaflets with NOAC's all say that.

Several God like cardiologists and EP's have told me that they can over rule that and it is 'Just that they have not been tested on tissue valve patients' I say 'Please Sir can I have a Watchman'


See this thread.‘valvular’-atrial-fibrillation-a-reappraisal-valvular-and-non-valvular-af

The reference is to: eurheartj.oxfordjournals.or...

One quote: Vitamin K antagonists are here likely to be more effective than dabigatran at suppressing coagulation activation because they inhibit the activation of both tissue factor-induced coagulation (by inhibiting the synthesis of coagulation factor VII) and contact pathway-induced coagulation (by inhibiting the synthesis of factor IX), as well as inhibiting the synthesis of factor X and thrombin in the common pathway,9 whereas dabigatran exclusively inhibits thrombin.40 If contact activation is intense, the resulting thrombin generation may overwhelm local levels of dabigatran, which can lead to thrombus formation on the surface of the valve and related embolic complications.

Simply put, you cover more bases with Warfarin. That alone is a very strong argument for choosing it. In other situations in the cost-benefit comparisons, it needs to be there.

There is also the fact that Warfarin is cheap, well known, easy to manage provided you allow wider tolerance bands, and it is known to be tolerated and effective in the long term.

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I liked that. It was my thread.

I was unlucky that my surgery put me into AF. If only he had removed my LAA at the same time as some do it would have partly compensated.


I think the question of, NOACs have not been tried on tissue valves is largely irrelevant, given the fact that Warfarin has more than one site/mechanism of protection. That to me is the killer argument -- I want that broadspectrum protection.

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