Two recent trials have impacted the way many ep's are starting to look at anticoagulation, especially for those with short duration episodes and a low afib burden.
This is by no means a green light to stop taking anticoagulants on your own, but it suggests a conversation with your doctor might be in order for some of us.
Excerpts below on Dr. John Mandrola's commentary on these two studies.
"For an older patient with stroke risk factors and 3 hours of AF on a cardiac device, pre-2023 thinking would have us leaning toward anticoagulation. The results of the ARTESIA and NOAH-AFNET 6 trials strongly question that idea.
NOAH-AFNET randomly assigned about 2500 older patients with short-duration device-detected AF (median duration, 2.8 hours) to edoxaban vs placebo. The trial was stopped early at 21 months for perceived futility and excess bleeding in the edoxaban arm. Edoxaban reduced the primary endpoint of stroke, systemic embolism, and cardiovascular death by 19% (HR, 0.81; 95% CI, 0.60-1.08; P = .15) but increased bleeding by 31% (HR, 1.31; 95% CI, 1.02-1.67; P = .03).
ARTESIA randomly assigned about 4000 older patients with short-duration AF (median duration, 1.5 hours) to apixaban vs aspirin. More patients and longer follow-up of 3.5 years translated to more events. Apixaban reduced the primary endpoint of stroke or systemic embolism by 37% (HR, 0.63; 95% CI, 0.45- 0.88; P = .007). This was countered by an 80% increase in major bleeding (HR, 1.80; 95% CI, 1.26- 2.57; P = .001).
The results of both trials were consistent: Direct-acting oral anticoagulants reduce thrombotic events but increase bleeding rates. The biggest discovery — and reason for debate about net benefit — was the low stroke rates (< 1% per patient-year) in both trials. What clinicians need, and is probably forthcoming, is an analysis correlating duration of AF and net benefit. Right now, anticoagulation decisions with device-detected short-duration AF require high doses of judgement and patient preference."
Jim
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An interesting comment by Dr. Mandrola on these trials. Currently, the CHA2DS2-VASc score is deeply embedded in clinical guidelines for treating AF patients, making it particularly challenging to deviate from these guidelines. More research is definitely needed to guide doctor's better, so they can be more confident in their discussion with patients who have rare but verified AF episode duration and frequency.
My Cardiologist has me on Aspirin and not AC with my Chad score of 1. However if i slip into AF longer than an hour then i'm to start Apixiban for a month then back to aspirin. I have had 3 or 4 cardioversions after being in AF for a number days and each time he does a TOE with no signs of clots. My longest period in AF was 28 days when i was overseas and upon return he did the CV and TOE and again no sign of clots. It could be luck who knows but thats the protocol i was given.
And an hour is quite conservative as REACT-AF only requires wearing the watch 16 out of 24 hours, so in practice the one hour could be 9 or 10, which more closely aligns to the threshold that Passman and others believe may require anticoagulation. Using a longer threshold would also allow PIP conversion with an antiarrhythmic like Flecainide, further sparing anticoagulation usage. Maybe next trial!
Thanks for this Jim. It makes me feel more confident in my own protocol of varying my dose of Apixaban though I would never stop it altogether. I am not really worried about bleeding but the full dose undermines my QOL significantly.
may I ask in what way you feel Apixaban undermines your QOL? I have a hard time figuring out if it's the underlying (monthly) PAF or Apixaban that is exhausting and limiting etc.
For a few days I reduced my Apixaban dose but my cardiologist wasn't at all happy.
He said there's research that suggests reducing the dose of Rivaroxaban is ok while reducing Apixaban increases the risks. I'm no scientist or medic so it might be worth checking this out with your medics.
Thanks for sharing this Jim. It explains why my cardiologist was talking about taking me off my Rivaroxaban in a routine follow-up phone appt yesterday .
However I had a knee replacement a few weeks ago, and there was a query as to whether I might have had a DVT afterwards. The orthopods were pleased I was taking an anticoagulant, just in case, and told me to carry on.
Being brainwashed into thinking I'm at high risk of a stroke if I don't take it, I was a bit alarmed by my cardiologist's suggestion I could stop taking it! But I shall definitely discuss it at my next 6 month follow up, if I'm still in normal rhythm by then. Thank you.
Though having just found Dr. John Mandrola's article, I see it's talking about brief episodes of AF picked up by a device, while I had 2 periods of persistent AF reversed by cardioversion, which were picked up by symptoms not a device, but with long periods of normal rhythm (as far as I know) between and since the AF. So I shall have to ask more questions about the rationale for stopping anticoagulants in my situation.
Thanks Ozziebob. As an alternative protective without the risk of excessive bleeding, I've often wondered whether fish oil instead of an anticoagulant would help prevent stroke . I used to take fish oil before getting AF, but found that cuts and grazes bled a bit more if I took it once on Rivaroxaban. But I imagine no-one will do any trials on that - no profits to be made from patents.
We widely accept guideline recommendations and quality measures regarding risk-based oral anticoagulation. In doing so, CHA2DS2-VASc has morphed into something akin to mathematical truth. Little promoted, however, was that the seminal paperestablishing the score included just 1000 patients and 25 stroke events.
First, quality measures with strict thresholds for anticoagulation based on integer scores look even more silly. Guidelines need an immediate update.
Though if I had a reserve supply of Rivaroxaban, I could take one as soon as I became aware of the AF. Both attacks started around 5am and were very noticeable.
I wonder which doctor put you on them. Something I am learning is that you can have three doctors like I do my GP, Cardiologist and EP and have three different opinions
normally I go by my EP because he’s been in there. He’s the one that was working on me the most, and put me on my heart meds. If nothing the cardiologist should speak with them. I just had change my statin he said he was doubling the dose not only did he double it but he put me on it twice a day. I need to find out if that’s right because my GP changed my statin and when the cardiologist said he seemed displeased. I told him the other one causes me severe joint pain and has for years. I was told this one was better for women and I wanted to try it. What really angered me was he did not address why I went to him. I am meeting with a new EP the middle of April and hopefully find out who he works with I want someone on the same page with the other. I’ve never had a situation seems to think he’s better than the PE but this one does. When I mention going to this new PE because my other one has moved away he told me that the new one was going come here to his office. I don’t know how it goes where you are but here the PE is the top of the ladder not because they are stuck on themselves but because they are pretty amazing for the most part. So have my been until now. He did not address having trouble breathing or chest pain since I had a bad virus I was I didn’t have Covid or flu. He plans on waiting until my device check in April the end of April as I say to people on here if you feel uncomfortable about someone, maybe you should change and find a new one that’s what I am doing. I haven’t needed a PE lucky for me because six months later they still have not replaced my amazing. It’s a shame that we have the stress of a fib or whatever else and then we have to deal with garbage like this since I first with a fib. I have been blessed with incredible doctors except for one might need to retire, even though he’s not that old.
That sounds really difficult, that your doctors have conflicting views. Did the EP tell you why he was changing your statin and doubling it?
I've been on Rivaroxaban for nearly 6 years, and it's been standard practice for anyone of my age and AF history to stay on an anticoagulant for evermore up until now. At my hospital, the EP seems to have quite a small role - I think I've only seen one once or twice, when I was about to have a cardioversion. I'm quite happy with my current cardiologist - he didn't know about my recent knee surgery until I told him., and seems quite happy for me to stay on an anticoagulant. I can discuss it with him again next time and hopefully find out what his new thinking is.
I hope your new EP will be one that listens and adjusts their advice accordingly - and explains their reasoning
Thanks for that timely Dr Mandrola article. I've previously written here about how I work and roam the San Bernardino mountains (presently digging out of a foot of fresh snow and waiting for the next two storms this coming week.)
In the confusion surrounding the Line Fire evacuations last summer, I ran out of meds, but felt good, low BP (116/66), no AFib, so I stayed off till my next cardio visit.
He said he has few Px who stop needing meds, but he has a few and was supportive of watching how I'm doing. Zio patch during 3,500 ft, 8 hr 10 mile hike showed only slightly more ectopic than previously (under max stress) with no AFib and ultrasound continues to show good EF (55%) and *reduced* scar tissue. So, we're going to have another Zio in a couple of months and see how things are going.
While Eliquis is a walk in the park compared to Plavix which I was on after my MI, I hadn't really thought about my hemorrhagic bleed risk. But, even on Eliquis, I regularly bled like a stuck pig given how physically demanding my work. Off Eliquis, no bleeding issues.
I'm already paying renewed attention to eating Esselstyn's six-a-day greens & vinegar advice and I think that's the best habit to adopt to support endothelial health in addition to a vegan, no oil diet if one is taking a powerful anticoägulant.
Thanks for helping me to give my situation some more thought!
I would only argue with using percentages which without numbers are meaningless and can be frightening.
Also, there is, so far as I know, solid evidence that most clots occur in the LAA, with one particular kind of that giving the highest risk by far. It seems that this is ignored in these and other recent studies and this surprises me.
Steve, have you found any actual evidence, other than amateur AND professional opinions, about how long it takes for a clot to form in these different LAA shapes re AF patients? Or how long clots take to form in AF patients due to comorbidities other than AF? Both with and without anticoagulation? Surely some research must have been done. Every one on the Forum, as well as every EP and cardiologist offers different opinions, so I'm genuinely getting rather frustrated that this vital information is still surrounded by contradictions. Or am I missing something? Perhaps the REACT-AF trial will produce helpful results in this regard.
I feel similarly. I shall have another online search and if I find more will get back with a reply but at present, no - I don't have more than what I have read.
You would think, if the LAA of a "cauliflower shape" was, as studies have shown, genuinely the one that produced the "micro-thrombi" that can then lead to clots and strokes that it would be earnestly investigated.
I don't think it does. That article relates to "patients with severe aortic valve stenosis" and AF. Not an average AF patient really. And not me.
I was trying to find some clarity among the different opinions on the Forum about how long it takes for a clot to form during or after an AF event. Today someone said 30 mins, others have said 30 days, and others various times in between. It's crucial for the current REACT-AF trial to know how quickly to start and when it is safe to stop anticoagulation. I think their protocol will be allowing for the safest possible estimates, but it would be useful for AF patients like me to have a better knowledge of this now, and not just the confusing estimates currently available.
I have no issues being on anticoags. I haven’t had AF for almost 2 years now but my cardiologist was keen for me to stay on apixiban in case it was happening in the background and we weren’t aware. I have a complex conduction issue. I haven’t had any issues being on the medication so I’m happy to accept taking it still.
Thanks for your informative post Jim amd very timely for me . Briefly, had my 3rd ablation early May last year , not fully successful as the EP couldnt completely ablate the superior vena cava as it was too close to phrenic nerve and sinoatrial node, so advised to remain on dronedarone and 2.5 mg bisoprolol long term . After 3 months I liaised with my AF nurse re: trialling coming off the betablocker which I did . Had a great few months with more energy and improved exercise tolerance but gradually heart rate was raising at rest and then on gentle activity and felt like I could slip easily back into AF . Discussion with AF nurse re: going back on the bisoprolol but before then , zap, a 16 hour episode of high HR AF . I was so happy that it self converted and i was then back on the betablocker . On asking about anticoags i was informed by a different AF nurse ( mine was away ) that i absolutely did not need them , as the new scoring system does not add a point for being female and i am 59 , so scored 0 . He said even if i was in AF all of the time I would not need them ! I was very shocked as in my mind i am surely more at risk of a stroke with my atria fibrillating away for 16 hours than a person not in AF . What are your thoughts on this Jim ? Amanda
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