Afib attack

Woke up this morning with palpitations and heart rate 70ish. Usually 50
Heart beat very irregular. Do I go to a &e or just sit it out. I’m not on any medication for it.
I get an attack once every 3 months or. So Lasting a couple of day each one
I’d like to see a specialist to be honest. Do I start with a gp appointment
Cheers

If you're not on any medication at all, then yes, go to A&E. If you're having episodes lasting a couple of days then you need to be on an anticoagulant (blood thinner). I'm not entirely sure how it works in the UK but if A&E can't refer you to a specialist then see a GP who can.

Make sure you are referred to an electrophysiologist not a cardiologist. AF is an electrical problem. Cardiologists are plumbers.

Gill

Quote
Carey
If you're not on any medication at all, then yes, go to A&E. If you're having episodes lasting a couple of days then you need to be on an anticoagulant (blood thinner). I'm not entirely sure how it works in the UK but if A&E can't refer you to a specialist then see a GP who can.

This is not the current recommendation of the American College of Cardiology/American Heart Association as newly issued in 2019 JACC. Those guidelines recommend anticoagulant therapy according to risk measured by CHA2DS2-VASc. The recommendation is adjusted according to relative risks of stroke and bleeding and patient's inclinations and preferences. The recommendation is not based on whether the AF is paroxysmal, persistent, or permanent, or any other temporal character of the episodes. There is some discussion of increased duration being associated with increased stroke risk, but this is in the context of device-detected AF, and the duration threshold for anticoagulants is unclear.



Edited 1 time(s). Last edit at 10/17/2019 10:12AM by safib.

I'm aware of that but we don't know Lenlec's details. The odds are pretty good he/she is more than a CHADS 1 so don't you think the best advice would be to see a doctor of some sort to get evaluated and get referred to an EP?

I wasn't objecting to Lenlec seeing a qualified doctor and getting evaluated, obviously he/she should. I was pointing out that the length of the episodes, including whether they last a couple of days, has no impact on the current recommendations for anticoagulants. I think it is an important point that the current evidence that frequency, duration, burden, etc., is somehow predictive of stroke risk does not rise to the level of setting thresholds for anticoagulation therapy. I have often read comments here suggesting that low cumulative AF burden is somehow a sign of success in dealing with the disease. In fact, it is only a measure of success in dealing with the symptoms, and not with the stroke risk, at least according to existing studies. It is really unknown what temporal measure (if any) is related to stroke risk, there is a lot of conflicting evidence. It may turn out to be something rather complicated, perhaps some feature extracted from mining time series of wearable devices as they become more common. And yes I understand that you are aware of these things, I was clarifying a certain viewpoint for others who are not as well informed.

Although that's what the guidelines say, in practice length of time in afib is still often considered. An easy example would be cardioversions. If you walk into an ER with afib and want a cardioversion, the first questions they're going to ask are how long you've been in afib and if you're on anticoagulants. If you say you've been in afib a couple of days and you're not on anticoagulants, I virtually guarantee they're either going to do a TEE first or just send you home and tell you they won't do it until you've been on anticoagulants for 3 weeks. In fact, the guidelines still say this:

Quote

For patients with AF or atrial flutter of 48 hours’ duration or longer, or when
the duration of AF is unknown, anticoagulation with warfarin (INR 2.0 to
3.0), a factor Xa inhibitor, or direct thrombin inhibitor is recommended
for at least 3 weeks before and at least 4 weeks after cardioversion,
regardless of the CHA2DS2-VASc score or the method (electrical or
pharmacological) used to restore sinus rhythm.

This seems odd because it contradicts their other guideline that goes solely by CHADS-Vasc. If I'm paroxysmal and I've been in afib 3-4 days, they won't cardiovert without anticoagulants. But if I convert on my own, that's okay, I don't need anticoagulants. Not sure how to rectify that.

And then there's the general "out" in the guidelines that many EPs are going to use to recommend anticoagulants even to their CHADS 0 patients:

Quote

In patients with AF, anticoagulant therapy should be individualized on the basis
of shared decision-making after discussion of the absolute risks and relative
risks of stroke and bleeding, as well as the patient’s values and preferences.

Anyway, I'm not trying to argue. You were right to point out that length of time in afib isn't considered in the general guideline. It's only considered in special cases and cardioversions.

Hi Carey,
you're right; "how do you rectify that"
Ideally, you need to take anti coag even if you revert yourself; the risk is the same (so I've been told by leading electrophysiologist) whether you have a successful cardioversion, or self-revert. Even injecting or taking an anti-coag at AF onset, if you've been slack (non-compliant) in taking the blood thinning drugs, will reduce your risk of stroke. (no RCTs done on that; that's only logical consideration from the Dr)

Quote
Carey
This seems odd because it contradicts their other guideline that goes solely by CHADS-Vasc. If I'm paroxysmal and I've been in afib 3-4 days, they won't cardiovert without anticoagulants. But if I convert on my own, that's okay, I don't need anticoagulants. Not sure how to rectify that.

This paper might be useful for this discussion.

One quote:

One important new finding in FibStroke study was that 21% of the patients who developed an ischemic stroke or TIA after cardiover- sion had a CHA2DS2-VASc score < 2. We have recently shown that a delay of cardioversion exceeding 12 h from the symptom onset caused a 3-fold increase in the risk of stroke when compared to later cardioversions of acute AF, and the risk of thromboembolism in the low risk patients with CHA2DS2VASc < 2 was as high as 0.9% if no anticoagulation was used [12]. In the light of these findings, it is possible that even low-risk patients might benefit from short term oral anticoagulation started at the time of cardioversion.

Hi,

Sorry to be tail-end Charlie on this thread.

And sorry, too, that my contribution has turned into a long one, but I hope it's a constructive maiden contribution to the forum.

I have been following the site for most of the decade since I got my LAF diagnosis and had just come back to it to check out a topic I'm interested in.

My search came up largely dry but flagged this topic because of the anticoagulation issue.

Lenlec's predicament is the classic one, which has certainly caused me some anxiety over time - what to do when you get stuck in AF for 48hrs plus and you're not on routine anticoagulation?

I note that (in my case anyway) medical opinion has changed in subtle ways on procedure following a protracted AF episode.

First, though, I have to say that, as has already been pointed out elsewhere, it sounds like the OP, Lenlec, needs to see a specialist electrophysiologist, probably via a GP referral.

The EP will do the relevant tests and assess stroke risk and any need for an anticoagulation regimen; stroke being the principal concern here, apart from QoL; no one dies of AF per se.

Fortunately, EPs are a little more conscious of quality of life issues now; rather than dumbly citing evidence that rhythm or rate maintenance are equivalent, which was only ever true for the most part if risk of death is the sole criterion.

One valuable innovation has been credit card sized, sub £100 ECG monitors that you hold between thumb and forefinger and can record a transitory episode with using your smartphone - a heck of an improvement on inconvenient, costly and frequently fruitless Holter monitoring (has anybody ever seen their EP spend much time looking at that hard-won Holter printout, anyway?).

The pity is that, in my experience, the people who know most about LAF often make their living doing ablations. And when you have a hammer everything is a nail.

So, apart from the threat of stroke itself, nothing was a better spur to ablation than the alternative threat of infinite Warfarinisation, fortnightly INRs and constant dietary vigilance.

Fortunately, things have changed with the advent of NOACs (and their antidotes) in recent years, but so has the thinking on stroke risk and cardioversion procedures.

Like a lot of us, I hate AF but I also hate taking any toxic and dangerous drugs. To start with the professional riposte to this position was 'it's better than death or stroke', which is as unanswerable as the tail-risk is imponderable.

But now we have better anticoagulants than Warfarin, perhaps inevitably, concerns have belatedly switched to the balance between risk of stroke and risk of iatrogenicly-induced bleeding.

So, while the default is still that if you have AF in any way shape or form you are at risk of stroke and need to be on an anticoagulant, bleed risk is a bigger, countervailing indication for many, and I am now told I shouldn't use AC.

I might add that medical advice across these options has sometimes been set by cost and proven efficacy issues, and hence subject to different interpretation between private and NHS practice - even by the same EP!

Time was that I was denied electrocardioversion because it required a month of Warfarisation first. In fact, I was left in permanent AF for almost a year after diagnosis before it seemingly occurred to my private EP to have a shot at EC (without Warfarinisation) - which worked on and off for the best part of five years (two subsequent ECs).

I had those ECs at the drop of a hat because a TOE was routinely performed first (it's actually hard to imagine that any professional would perform an electrocardioversion without a TOE).

Which raises the question whether (liability issues aside) it's in fact any safer to cardiovert yourself, spontaneously or chemically, without a TOE and outside a clinical setting...

Logically, if you've developed a silent clot in your LAA during AF and cardioversion of any kind shunts it into circulation, you're in trouble.

Nonetheless, for several years the advice to me was that if I had an AF episode of more than 48 hrs duration, which was refractory to the 300mg of Flecainide I used as a 'pill in the pocket' following my (partially successful) ablation, I should just jab myself with a daily Heparin shot until I could get to my private EP for an EC, to avoid the need for Warfarin.

This, not unnaturally, left me in constant fear of the onset of an AF episode of unknown persistence which might require me to find an EP pronto after two days were up! (Why did my episodes also often come on on Fridays?!).

I had on a couple of occasions to go to the ER, because initially I had no Heparin or NOAC and the NHS regime invariably indicated a month of Warfarin, which I hoped to avert with a private EC if I had extended my 48 hour grace period with AC cover.

Of course, if you go to the ER you had better have time on your hands because every intern knows that AF is a medical emergency. Consequently, they will see you pdq and want to do everything by the book; even if you assure them that you're otherwise perfectly fine, 220bpm is not an unusual rate for you in AF at a moderate walk, and you are really not about to go into heart failure.

Though, having been prescribed various mixtures of shots and NOACs to take after 48hrs of AF, to enable a prompt, private EC, I haven't actually needed an EC since my last ablation (in 2014).

My episodes have eventually succumbed to Flecainide doses or reverted on their own (even if it took three weeks of seeing almost every rhythm under the sun on my handheld ECG!).

Although my CHADS etc., has always been the same (zero, I'm glad to say), lately advice is not only that I shouldn't even be offered permanent AC 'just to be on the safe side' but that I shouldn't really be on AC at all, for the same reason.

And, having gone to my EP following another recent very protracted AF episode, I am informed that if I'm contemplating an ablation redo or EC, he'd really rather do an ablation while I'm in AF because that way he can be sure to zap the right pathways to stop it, which makes sense.

The trick is, though, that I've always wondered just why LAF has picked me out at all, and I'm guessing many of us are in the same boat.

The only things remarkable about my medical history (I'm pleased to say) are Gilbert's syndrome, former mercury fillings and pre-natal (pre-conception actually) radiation exposure (my mother worked in radiology in a hospital whose principal X-ray machine was miscalibrated for a long time).

There are just too many AF variables, and I've checked a lot of metabolic and lifestyle things out over the past decade - often with the help of this site. EPs as a rule are just not interested!

So, what brings me back to the site and this thread (maybe this ought to constitute a separate thread) is recent research suggesting that NOAC thrombin-blockade itself may inhibit both AF onset and subsequent development of the substrate which sustains it.

This is particularly interesting in the context of a discussion of appropriate anticoagulation, because it suggests that if you are using any AC at all there may well be a case for making it a Thrombin inhibitor - i.e. Dabigatran rather than any other (Xa blocking) NOAC.

And, arguably, even if you're not slated for AC, the risk of a bleed may recede in importance if Dabigatran actually demonstrates promise in short-circuiting the very vicious circle that predisposes us to AF in the first place. See for instance [academic.oup.com].

BTW, I rather suspect that my more frequent and protracted AF episodes may have been because I had become more blasé about taking my vitamins. Despite a great deal of stress and strenuous exercise (though mine is a vagal AF), a little more compliance has improved things a lot. I think zinc may be particularly important for me, and it's striking what a high proportion of the population is deficient in it.

It's probably also not accidental that I have Gilbert's Syndrome (and historic? Mercury overload) and that, while Gilbert's accentuates phosphorylation, bestowing some protection against CVD (https://www.nature.com/articles/srep3005), phosphorylation also drives hypercoagulability and thereby the AF substrate which Dabigatran may help combat (see first reference above).

I would be interested in any discussion I have missed here about the latter research, because it seems quite heartening (excuse the pun) - in contrast to other recent research at Oxford, which suggests that an AF predisposition persists despite ablation (https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.116.022931).

Wow, that's quite a huge wall of text and information, Bookworm. There are at least a half-dozen questions that warrant their own threads so I don't even know where to begin. Could you maybe cut it down to one question at a time?

Bookworm. most of my ER visits for AF were also on Friday evenings. At least 5 this year alone. Maybe once Friday evenings approaches I get anxiety and walk on egg shells and get AF.

Carey is 100% right. From my experience, I had been 100% denied a cardio conversion unless I had written proof from my personal ecg gadgets that I was in NSR within the prior 24 hours. I also get a ZIO patch twice a year and I knew when I was in AF because it would wake me up. Now, knock on wood, I have no problem getting cardio converted because I am on Eliquis and being zapped over 20 times, the same ER doctors know me and have no problem granting me a cardio conversion because I do well.

My cardio conversion on 11-18, I lost the battle. I flew in from Israel the day before and was in nsr for 18 hours. However, because I had an international flight (history of one time dvt) I had to get a test (TEE? TOE?) to search for clots before I was converted...even with ecg proof. Overnight hospital stay with them ordering me to be on Eliquis or they would not convert. So I went on it. It’s a breeze before my ablation getting cardio conversion. The past 4-5 visits, they recognized me and said loud “crash cart” and I was in and out within 2 hours of entering the ER. It was like in and out burger line.

I think it is poison because it’s a black label drug (actually this drug may have two black labels..or is it multaq...hmm, both have a black label, one of them has 2, but a stroke or death is worst. The only side effect for me is bruising because I get syncope and bang into walls and furniture.

Bookworm, I enjoyed reading your post. Thank you for sharing.

Flecainide also has a black label. (“Could cause death”)

If you have AF you should take the plunge and be safe.