Confused about stroke risk

I remember something written by Hans that was a compilation of studies where he concluded that stroke risk for a proximal afibbers was no greater than that of the general population. Then last time I was at my EPs office I saw one of the fellows who alluded to the fact that there were new guidelines that took into account the frequency of episodes. I have a CHADS of 0. I am female and have weekly episodes that can be as short as 5 hrs or as long as 24 hrs.

Another area where I have had conflicting info. is on how to address lengthy episodes. I used to have a cardiologist who said to go to the ER if I went more than 24 hrs. Now my EPs office says there is no need to go in after 24 or 48 hrs. unless you are uncomfortable. Seems like stroke risk should be a concern. Does anyone know what the guidelines are?

Lynn, under the new CHADS2-VASc scoring system for stroke risk, you would have one point for being female.

Jim

In addition, under these new guidelines you would get a point if you are between 65-74.

Although afib burden is not part of these guidelines some ep's will consider it when deciding on an anticoagulant strategy. My CHADS2-VASc is 0 and I was prescribed an anticoagulant because longest episode was 8 hours. I was in afib about 30% of the time.

Allan

Lynn,

The European Guidelines are here: <[www.escardio.org] You can start reading about anti-coaguation on p11 of the PDF. This goes through several scoring systems.

George

If your having episodes every week, then I think most all Cardio Dr.'s would recomend anti-coagulation.

When the Atria Fibrillates, the blood is stagnant in ther Atria, and thus the increased risk of stroke.
Even after you convert back to NSR, the Atria muscle is stunned, and does not contract for a period of time from several days, even up to 3 weeks. That is why the more freqent the episodes, the more advisable anti-coag is recommended.
In your case, your Atria may never me functioning properly, because the new episode may be starting before the Atria start contracting from the prior episode, and a clot could still be lodged in the Atria.

Sounds like you know precisely when your episode start and stop?

If you haven't been talked into that Ablation yet, consider that AFIB Ablations sucess rates for paroximimal AFIB, are misleading, because, during the process of during the Ablation, what is going on is that the nerve endings around the Heart are damaged (ablated), so the patient often merely does not feel the palpatations, and thinks that their still in NSR. The symptoms may be sucessfully treated, not the condition itself. That is why the EP Ablationists always want their patients on Anti-coag's just for added protection.

In your case an Ablation might make it harder to even know when your episode start/stop, which is a big negative.

The second question pertains to the 48hr rule (used to be 24hrs), after 48 hours of AFIB a clot may form in the Atria, so if you go for ECV, a TEE should be performed to scout the Atria for clots. If your case a clot may be pre-exsisting from an earlier episode, so a TEE should be performed regardless prior to ECV. The "unless you are uncomfortable" refers to the understated importance in AFIB literature about whether you are Symptomatic or Asymptomatic, or how bad the symtoms are. The worse the symtoms the more motivated pateints are to to do something about AFIB on a faster basis.

Also the more ECV you have vs. reverting back into NSR on your own, is more of a reason to be anticoagulated, as a ECV presents an increased risk of stroke, due to the jolt the Heart receives form the electric current.

I would talk to several doctors about your Anti-coag strategy, it's to compicated, to just relay on some formula or guidline.



Edited 1 time(s). Last edit at 08/19/2014 04:40PM by The Anti-Fib.

"it so the patient often merely does not feel the palpatations, and thinks that their still in NSR."

Anti Afib - I am very interested to know more about the basis for the above statement. Do you know this to be a fact? (Are you in a position of knowledge - ie a medical scientist or doctor)? I most definitely feel that I am in NSR continuously post ablation as I check my pulse at a number of locations and it is solid. I can feel my heart beat when I am quiet, and know it is steady. Are you saying there is something else going on I am not aware of, some un-detectable heart activity?

Also I was ablated in Bordeaux, and I know that North American protocol is different in a number of areas, but they are considered one of the top facilities worldwide. They wanted me off anticoagulation at the earliest reasonable time, which in my case was about 6 weeks, so your take on it somewhat confusing to me. Really appreciate any light you can shed on this.
Ron

PS, I dug this out of page 12 of the European Guidelines from George, which confirm the earlier report from Hans.

Patients aged ,60 years, with ‘lone AF’, i.e. no clinical history or
echocardiographic evidence of cardiovascular disease, carry a very
low cumulative stroke risk, estimated to be 1.3% over 15 years.
The probability of stroke in young patients with lone AF appears
to increase with advancing age or development of hypertension,
emphasizing the importance of re-assessment of risk factors for
stroke over time.

RonB

I said "patient often", doesn't mean all patients. You sound like you are most indeed in steady NSR. There obvouisly is a wide spectrum of how well or often patients accurately monitor thier Heart rythm status. Doctors in US assume most patients are niave about the details of their Heart rythm status. I've consistently heard the figure that the Doctors think that only 10% of patients know when their episodes start and stop.

How long since your Ablation? The decrease in sensivity in the nerve endings would subside over time. I would pay attention to see if you can feel your heartbeat any better as time goes on, especially if you have any episodes. Also as the lesions from the Ablation begin to heal over time the likelyhood of an increase in episodes goes up. This has been documented in the studies showing long-term effectiveness of ablations to decrease over time.

That's good they got you off after 6 weeks, maybe you convinced them that you were on top of monitoring your status. Most accounts of post-ablationers cite a much longer Anti-Coag timeframe.



Edited 1 time(s). Last edit at 08/23/2014 07:10AM by The Anti-Fib.

The Anti-Fib

Are you suggestion to get ablations? Or not to get ablations?

It sounds like you're suggesting that ablations may not be effective long-term, and that even if you are ablated, you may be in afib, but just not know it.

Or are you saying, even when ablated, it makes sense to be on anti-coags for a long period of time?

The Anti-Fib - what do you base the following statement on:
"Even after you convert back to NSR, the Atria muscle is stunned, and does not contract for a period of time from several days, even up to 3 weeks. That is why the more freqent the episodes, the more advisable anti-coag is recommended.
In your case, your Atria may never me functioning properly, because the new episode may be starting before the Atria start contracting from the prior episode, and a clot could still be lodged in the Atria"

I've never heard anything like that - when my afib stops I can feel my atria beat again - ta-dump, ta-dump (atria - ventricle). Can you cite something to support your statement?

, so the patient often merely does not feel the palpatations, and thinks that their still in NSR. The symptoms may be sucessfully treated, not the condition itself. That is why the EP Ablationists always want their patients on Anti-coag's just for added protection.

This seems wrong to me. EKGs, Holter harnesses and other devices can show NSR. After my ablation I was on Warfarin for 10 days and the EP told me to stop after that. I think NSR = NSR.

Ralph,

<[www.ncbi.nlm.nih.gov] "Atrial stunning is a function of the underlying arrhythmia becoming apparent at the restoration of sinus rhythm, not the function of the mode of conversion, and does not develop after the unsuccessful attempts of cardioversion or the delivery of electric current to the heart during rhythms other than atrial fibrillation or flutter. Tachycardia-induced atrial cardiomyopathy, cytosolic calcium accumulation, and atrial hibernation are the suggested mechanisms of atrial stunning. Atrial stunning is at maximum immediately after cardioversion and improves progressively with a complete resolution within a few minutes to 4-6 weeks depending on the duration of the preceding atrial fibrillation, atrial size, and structural heart disease. Atrial stunning causes postcardioversion thromboembolism despite restoration of sinus rhythm. Duration of anticoagulation therapy after successful cardioversion should depend on the duration of atrial stunning. "

I'm guessing what you are perceiving - ta-dump ta-dump is not atria - ventricle, but all in the ventricle. I don't think atrial beats can be detected without an ECG. Afib can be indicated with just heart rate vs. time because of the randomness of the beats.

George

George - I have an AliveCor - the atrial beats are there when I convert. Suggesting to me (someone who feels everything accutely) that the ta-dump is double ventricle beats is akin to doctors telling me that laying on my left side can't trigger my afib!
That article seems focused on CARDIOVERSION (although it says that it has been "reported" with spontaneous conversion - far from saying that it is the normal mechanism during spontaneous conversion). Doesn't surprise me that cardioversion would have a radical effect. And the low side for normal atrial activity in those events is several minutes, not several days!

Ralph,

I think the sounds are created by the valve closings <[en.wikipedia.org] The AV valve opens when atrial pressure is greater than ventricular pressure. <[www.biosbcc.net] However this happens even if the atria are fibrillating.

I know the heart sounds weird in afib as that is how I figured out I had a problem on my first afib episode.

If your atrial beats are there when you convert, that is excellent, however this may not be true for all, especially after electrocardioversion or ablation.

George



Edited 2 time(s). Last edit at 08/21/2014 11:38PM by GeorgeN.

George,
I am speaking my own experience, and agree that it may not be the same for others - how would I know? On the other hand, I wrote my response because I think The Anti-Fib misrepresented the situation in a way that would cause unnecessary fear for most people, perhaps leading them unnecessarily towards anti-coagulants.

George, thanks for the guidelines. I'd love to compare those to US guidelines. There seems to be no reference to using frequency of episodes as a guideline for making anti coag. decisions.

Anti afib, it would be helpful to know your background or source of your info. I too have an alivecor and my strips after conversion look identical to those I take when in NSR.

To me anti coag has it's own list of negatives. Not that having a stroke isn't a big negative. My mom had afib and lived to be 86. As I recall it started around age 50 and became permanent around age 60. She used asprin until switching cardios around age 75. Her new cardio put her on warfarin. After about 4 yrs on warfarin she was developing calcium deposits in the arteries in her brain. Vitamin K tells the body where to put the calcium so it is my assumption that the warfarin caused this issue which led to dementia type symptoms. So damned if we do and damned if we don't in regards to anticoagulants.

Ralph,

I also don't want to encourage unneeded anti-coagulation.

I got the pleasure of using my AliveCor this morning for the first time in afib. This was my first episode in 15 months (fortunately PIP flec converted in about an hour). I ran an ECG strip very quickly after conversion. I compared the P waves with those from several months ago in NSR and they visually appeared to be the same. So I appear not to have significant stunning either.

I've not found data on stunning on spontaneous conversion to NSR for episodes longer than 15 minutes. All the data I've found are for the aftermath of electro-cardioversion and the 3 months after an ablation. The standard is to anti-coagulate for ECV's for episodes longer than 48 hours.

If it were me, I'd like to have an Alive Cor or other ECG and be able to see P waves.

10 years ago, when I used PIP flec to convert a 2 1/2 month episode, they kept me on warfarin for a month.

I noticed that a Lead II presentation (left knee and right hand on the device) on the Alive Cor gives a more distinct P wave that is easier to see. For those with an AliveCor, an example of a Lead II P wave presentation is shown about 1/2 way down here: <[www.richardbogle.com]

George



Edited 1 time(s). Last edit at 08/22/2014 03:40PM by GeorgeN.

P-waves don't show if the Atria is contracting like you want it to:

There is Electrical Stunning of the Atria (no p-wave)
There is Mechanical stunning of the Atria (normal electrical activity (p-wave), but muscles still not contracting)
And there is mechanical stunning of the LAA (left atrial appendage) even while Atria is contracting.

LAA functioning usually takes longer than Atria to restart normal functioning.
TEE aka TOE is the only sure way to see if the LAA is functioning correctly.
90% of bloodclots (thrombus) form in the LAA in AFIB patients.
Duration of Atrial Stunning appears to be porportional to duration of Atrial fibrillation.

No I am not a Doctor
I relay info gathered from multple EP Doctors correlated with information garnered from medical articles, studies and official guidlines.



Edited 1 time(s). Last edit at 08/23/2014 08:39AM by The Anti-Fib.

Lynn how frequent are your episodes? You said weekly, does that literally 52 episodes a year?

As far as I know if your in known NSR for longer than 20 days, then you don't need to be Anti-Coagulated.
At least that is what I do, and I have LAF with a Chads score 0.

I have been told that even if there was a clot in the Atria, that after 20 days it is reabsobed into the Atria wall, and by that time there is assumed to be no more possibility of Atrial Stunning. Also the 20 day time period will come into play if you try to get cardioverted. I believe that Cardio Dr's will not cardiovert a patient unless they know that the patient has either been in NSR fo 3 weeks prior to the recent episode, or at least been on Anticoagulants. And in this scenario, then they will want to do the CV within 48 hours, or mandate that a TEE be performed.

Have you considered just takin aspirin 325mg a day? I have cosistently read it is about 1/2 as effective as the regular blood thinners.

To The Anti Afib: I get that you are well intentioned, but it sounds to me like you are at least somewhat mis-informed in combination with an air of certainty, which is - for me - a difficult situation to deal with. Are we supposed to believe a) your unsupported claims about days in stunning after a spontaneous conversion , or b) our alivecors, ears, awareness of our bodies (senses) and absence of any data suggesting that stunning is happening for any significant amount of time (if at all)?

That is what I meant to say, only way to know for sure that Atrial stunning is not occuring is via getting a TEE. I meant to imply that their was uncertainty or the possibility of stunning, I never meant to imply that Atrial Stunning would always occur for days.

Anticoagulation is given not just to deal with exsisting clots, but to prevent potential clots and their is always uncertainty whether or not a clot may form. Stunning occurs because of the Atria muscles have been fibrillating (contracting at 400-600 beats per minute), so they are "stunned" and don't contract properly, not because of a Electrocardioversion.

Why do you think a little Alivecor device, your ears, or your senses can tell you if your LAA is contracting properly?

The original question posed was about Anti-Coagulation and Guidlines that took into account the freqency of episodes, and in Lynn's case 52 episodes a year is very frequent. I tried to explain why the more frequent that the episodes are, that it would change the argument in favor of Anticoagulation.

Go ask your Doctor about 50+ episodes a year, and see what they say.

Hi Anti-AFIB, some of the info you shared above in this thread from other docs and journals that you have gathered above have some merit, but a number of these ideas are misinformed. One case in point is the case made above for anti-coagulation for low risk paroxysmal patients with a CHADS2 score of 0 which is overstated, though well intentioned no doubt, it's more a matter of over emphasis of the implication.

I know some if the drug companies, and those doctors that are deeply be holding to them, would love to paint a scenario where an NOAC could be theoretically justified for every man, woman and child, but there are real potential risks and downsides too to taking these drugs long term. The guidelines have stated for some time now that for paroxysmal AFIB of short to modest episodes for people in their mid 60s and lower and who have a CHADS2 of 1 or lower that use of full on anticoagulation is not recommended unless in specific cases and in those with other complicating factors at the doctors judgementsl discretion.

It's not that you might not minimize the odds for a few more iischemi stroke by say having everyone start an OAC the moment an Episode starts and not stop it until 20 days after conversion to NSR as it seems you are suggesting is your protocol with a CHADS2 score of 0. But that the risks of causing even more dangerous hemorrhage or bleeding is greater than the potetit tiny reduction in ischemic strokes for this class of low risk patients who make up a significant percentage of lone afibbers.

Also, a P wave is very much apparent on 12 lead EKG in people 'with atria pumping and contracting as we would want.' Its a common feature of a normal EKG.

The transient 'atrial stunning' you refer too that is derived solely from AFIB/Flutter episodes themselves is typically of a lessor degree and nature than is the temporary stunning due to electro-cardioversion, post ablation stunning and from more progressive structural remodeling and fibrosis of certain parts of the LA and LAA over time often from long term persistent AFIB.

You are right that any knowledgable EP will insist on a TEE prior to doing an ECV if there is any doubt that the arrhythmia the patient presents with at the ER of a hospital to get converted to NSR might have been ongoing for greater than 48 hours .. Many will hold the limit at 24 hours ... After which the TEE is necessary and most will add an NOAC these days if the person is not on one for a couple weeks post cardioversion out of an abundance of caution.

Aspirin is a definitely not recommended as a second tier anticoagulant for AFIB related index stroke prevention and this is clearly stated in both new European and US AFIB anticoagulation guidelines.

Aspirin in low dose is only recommended as a preventative for a second MI or ischemic stroke but not for busting LAA embolic clots to prevent such an LAA derived embolic stroke. The bleeding or hemorrhagic risks of low dose daily aspirin for AFibbers with low risk for embolic stroke such as yourself with a CHADS2 score of 0, and I assume no other significant cardiovascular or metabolic syndrome co-morbidities, are definitely higher than is the potential benefit of aspirin used for such an initial embolic stroke prophylactic. Making it a bad risk/benefit bargain all around for such patients. An up-to-date and knowledgable EP who prescribes aspirin to an afibber will typically be doing so to address primary cardiovascular risk factors the patient has in addition to their AFIB.

Those that are still hawking aspirin to their AFIB patients for primary embolic stroke reduction and touts that it has a good benefit vs risk equation is seriously out to lunch and far out of date with all the latest fin icings and official guidelines.

I've just now had a chance to skim through this thread and noticed too the implication that most afibbers are not aware of their episodes and that this is far more common after an ablation. This is simply incorrect. The figure quoted above of around only 10% who can tell when they are in AFIB symptomatically is almost the other way around.

Approximately 20% up to 30% tops, in most surveys, are asymptomatic afibbers and often have no idea they have aFIB until discovered with an encounter with a medical professional with a stethoscope or EKG. The large majority of the rest are quite aware of when they are in AFIB even if a good many can't pinpoint the exact seconds it started or stops. A big majority nevertheless can tell you with a good degree of accuracy when their 'flippies' are running and when the heart is quiet and solid.

This also remains true for the majority of post ablation patients as well. Its true there will be some who might become less symptomatic with breakthroughs for a period of time post ablation than they had been prior to the ablation due to overall voltage reduction of still active trigger sources from the ablation, not unlike what you were pointing toward in one of your posts above, buts it's not a solid argument at all against getting an ablation when the person needs one and qualifies for the procedure on all accounts.

Based on the theory you posit above I should not have been able to feel my HR at all after my very extensive index ablation for aggressive persistent AFIB with 117 minutes of actual burn time and yet I was every bit as sensitive to the what I felt in the only two episodes of flutter I had in the first 3years post ablation, both of which flutters were LAA sourced Left atrial flutter episodes in that period and could instantly feel the very second each one started and they could only be stopped by ECV. Until that last trigger was eliminated with my followup procedure isolating the LAA.

Its true that people can and do have silent breakthroughs both before and after ablation but extensive follow up protocol with real time monitoring in the the first 4 months and then 24/7 for a week once each six months over the first 18 months, has been shown to be a very robust to uncover the vast majority of ablation patients having any breakthroughs at all, symptomatic or silent.

And for those who already are asymptomatic but need an ablation to stop AFIB to reduce bradycardia or to try to get off blood thinner etc, the new Medtronic's LINQ small implantable 24/7 loop recorder can capture every best.

My dual chamber pacemaker has proven too how reliable my sense of being in or out of arrhythmia is even after my first ablation and after my second procedure to isolate my LAA and CS, I have had no mode switches at all in over two years and zero felt arrhythmia either.

And I'm very far from the exception here.

But the bottom line is that its not all that difficult to determine how generally accurate one's symptoms track with real episodes and thus adjust any anti-coagulation strategies accordingly.

Which ever EPs were trying to use that idea as a negative against getting an ablation when appropriate, may have been sincere in their mistaken impression, but they were conveying to you a skewed perspective when implying this concept was a major drawback to ablations.

My wife and I have to drive out of town tomorrow morning early for a couple of days, but when I've returned I'll have a bit of time to address some of the other points including a few other aspects from the posts above I agree with as well and that have some real merit too, along with a few others ideas from above that Id like to offer some further clarification regarding.

Best wishes,
Shannon
.



Edited 1 time(s). Last edit at 08/25/2014 09:24AM by Shannon.

Shannon;

I cannot take Coumadin, it causes internal bleeding, even at a low reading.. My doctor said that all of the blood thinners would react the same for me, so tell me what do I do? I do take some aspirin, I watch my fibrinogen, CRP and they are all good, when in AF, my events are shorter than 24 hours, we all do the best we can.

Liz

Yes Liz, there are limitations if you truly can't take blood thinners ... That's one if the big advantages of a successful ablation process if you have frequent episodes in that consistently continuous NSR is your number one protection from an AFIB related stroke. If you don't wan,t or need, an ablation then a Watcman or Lariat is also an option for those who truly can't tolerate blood thinners. Aspirin just won't buy you as much protection from an LAA related embolic stroke as they used to assume. Years of hard facts and one large trial after another have made that clear.

You could also follow Jonathan Wrights protocol combining Nattokinase along with big dose of Omega Three fish oil each day and use a complete Platelet aggregation profile test looking at up to 8 serum platelet aggregation markers and adjust your a Omega three doses upward until you hit around 40% above the upper end of the reference range on each platelet aggregation marker. Note; that these sophisticated platelet aggregation tests are typically found only at either university research labs or dedicated vascular/hemodynamic testing labs and are not found in every town by any means.

The properly titrated dose of Omega Three ( with a optimal ratio of DHA to EPA and combined with 300 to 400 mg a day in divided doses of a top quality Nattokinase has, according to Dr Wright, never resulted in a stroke or major bleed in well over 150 some odd patients followed for a good long while and all of those followed are (or were) at high risk for stroke or ischemia.

The quality and quantity of this evidence, though is only just a bit stronger than anecdotal, though it does make good common sense combining the fibrin lysing or breakdown effect of significant doses of Nattokinase along with the well know platelet aggregation inhibition of sufficient Omega 3.

Adding as well other supportive herbs and nutrients like pycnogenol, curcumin, ginger, grape seed extract, Astaxanthin, Vitamin C, a good B complex as well as healthy doses of Vitamin D3 and K2, could well go a long way toward helping to prevent a possible embolic stroke, or at least potentially greatly reducing or blunting the physical and brain effects of any embolic event that might happen.

That's about the full range of your choices Liz, you could look into taking a half dose of 2.5mg Eliquis if you are worried about no protection at all. That would be a lot better than aspirin alone and with even less bleeding risk than aspirin. Or, you could really investigate this natural protocol, although there is not the kind of large scale trials and studies behind it to give you the kind of reassurance you might wish for. It does have an excellent track record in a relatively limited number of patients followed by a smart MD and makes very good sense physiogically, but that is about as far as you can project with it.

It might work even better than warfarin and the NOACs when done properly and religiously, but no one can tell you that for sure, so it will require a little a fair dose of faith... Truth be told, so does the NOACs and warfarin require a good dose of faith too as none of them are close to absolute protection against both embolic stroke and hemorrhagic stroke, even under the best of circumstances.

A good LAA ligation or occlusion with confirmed on going closure, and combined preferably with, or even just as a substitute, confirmed permanent NSR resulting from a solid ablation process are about as close as we can get to a sure thing guarantee of no embolic stroke, and yet as we found in my Lariat experience, we still have to reaffirm the LAA ligation or occlusion remains closed long term for that real safety to be there.

Shannon



Edited 1 time(s). Last edit at 08/25/2014 08:03PM by Shannon.

Shannon:

Thank you, I will print your reply out for reference, I do take some of the vitamins you have recommended. I am seeing Dr. Brownstein next week and will go over some of what you have written, Dr. Brownstein and Dr. Wright are friends, I believe they were at the same college together.

Liz

Good Idea Liz,

I've met Dr Brownstein, though only briefly so doubt he'll recall, at one of the BHRT conferences I periodically work at and have followed his work for some time as well. He may well be familiar with Dr Wrights stroke prevention protocol, but if not, he can easily give him a call and get the scoop straight from him as they are long term friends and colleagues.

I'll be seeing Dr Wright again too in two weeks when he is a key speaker when I'll be helping Dr Thierry Hertoghe again with his training program for physicians at the large BHRT conference in Phoenix for 4 days. Its possible Dr Brownstein will be there too. In case I see him there Liz if you PM me your last name I'll tell him one of my pals is a patient of his and engage him some about this whole anticoagulation issue as well.

Take care,
Shannon



Edited 1 time(s). Last edit at 08/26/2014 10:50AM by Shannon.

The Anti-Fib Wrote:
-------------------------------------------------------
> That is what I meant to say, only way to know for
> sure that Atrial stunning is not occuring is via
> getting a TEE. I meant to imply that their was
> uncertainty or the possibility of stunning, I
> never meant to imply that Atrial Stunning would
> always occur for days.
>
> Anticoagulation is given not just to deal with
> exsisting clots, but to prevent potential clots
> and their is always uncertainty whether or not a
> clot may form. Stunning occurs because of the
> Atria muscles have been fibrillating (contracting
> at 400-600 beats per minute), so they are
> "stunned" and don't contract properly, not because
> of a Electrocardioversion.
>
> Why do you think a little Alivecor device, your
> ears, or your senses can tell you if your LAA is
> contracting properly?
>
> The original question posed was about
> Anti-Coagulation and Guidelines that took into
> account the frequency of episodes, and in Lynn's
> case 52 episodes a year is very frequent. I tried
> to explain why the more frequent that the episodes
> are, that it would change the argument in favor of
> Anticoagulation.
>
> Go ask your Doctor about 50+ episodes a year, and
> see what they say.

Anti-AFIB,

Its certainly true that the more frequent the episodes and the longer term the duration of those episodes the greater the logic and pressure to add anti-coagulation to the equation, all else being equal. Though for those with a low risk CHADS2 score and no other obvious risk factors beyond just the AFIB that threshold for adding in OAC is considerable higher than for those with even one extra risk factor, depending on what it is.

And you are very right too that OAC drugs are not just given to deal with existing clots as their main function is to prevent those clots from forming to begin with as you noted Anti-AFIB.

Your comment above about using one's ears, senses or an AliveCor to detect if the LAA is contracting properly ... I think you must have meant to say the left ventricle and to a degree the left atrium on EKG? The LAA mechanical function is really only detected with accuracy via TEE or angiography. Also Cardiac MRI or CT can detect some info about real time LAA mechanical function, but is not typically used for such due to cost and inconvenience.

I know of no clear way to define just what the LAA itself is reliably doing via a stethoscope, finger palpation or an Alivecor.

If you are looking at absolute risk/benefit statistic rather then the relative risk picture so often used to justify a give drug or therapy, it still is a bit of a stretch to recommend anticoagulation to a mild to moderate paroxysmal afibbers who has no other cardiovascular co-morbidities unless they have very frequent longer duration episodes.

More and more evidence points to the combination of the impact of a quivering atria during AFIB along with added risk factors for cardiovascular dysfunction that is what adds the real weight behind the anti-coagulation argument rather than just relatively short term paroxysmal episodes in a person with little to no added cardiovascular risk factors in play.

Its true that many docs will readily agree to put a patient on OACs a little earlier than the guidelines strictly spell out, and would rather err that way than risk their patient perhaps being an odd ball that had a stroke on their watch anyway even in spite of otherwise very good health and a CHADS2 of less than 1 and no other real risks factors that jump out. That doesn't make it necessary the better medical decision but you have litigious considerations and those other kinds of factors that weigh in on the decision too often times beyond the strict medical science as best we know it.

Nevertheless, I agree, as a person's AFIB burden begins to increase toward persistence and certainly when it has crossed that line, even if they were so called vagal lone afibbers up until the increase in burden, I would also strongly recommend adopting pharmaceutical coagulation at that point.

The exact timing of adopting OAC, as you noted, is not a black and white line, and should be the result of a collective decision between hopefully an informed patient and an even more informed physician (at least one would hope)

I would be far more likely to accept a recommendation for OAC if I were a paroxysmal patient with one or more additional CVD risk factors in addition to my AFIB, even with less frequent episodes and a bit total AFIB burden, than I would be for a purely paroxysmal afibber with no such added risks at all even with somewhat more frequent episodes and a bit more total AFIB burden.

Such are the nuances we face in making a wise decision while keeping in mind that these drugs are not a panacea, nor are they as risk free as they are sometimes painted. Especially when the more real world absolute risk/benefit equation is applied to the many studies looking at this question and not just the relative risk prism thorough which the risks of a stroke can look far worse and benefits of the drug significantly better than they really are for a given patient to truly benefit out of a large number of others who also need to take the drug who will derive no benefit and some added risks.

When looking at some of these large studies and adjusting warfarin to include a consistently maintained and verified INR to get a better comparison with Eliquis and Xeralto, those absolute risks are somewhere in the range of around 100 total people needing to be treated (NNT) for just a few who actually benefit from the treatment over time.

The relative risk analysis, for example, might imply a 30% to 50% effect window while the absolute risks in the form of NNT ( numbered needed to treat) with this class of drugs when looking at the very same data, can be in the 1% to 5% range for those who actually benefit from taking the drug out of the whole study cohort, depending on the nature of the study.

To my knowledge, Anti-Afib, there is no hard and fast rule that a clot in the LAA from an AFIB episode will automatically be broken down and lysed within the bloodstream in 20 days. Its much more variable than that and some can last a good deal longer and some break down in much shorter time frame. It depends on a large number of variables including how well the natural clot busing enzymes in a given body are working, the size and density of the clot, the velocity of blood flow at the point in the LAA or LA that the clot is located ... for example a large clot lodged deep within the nooks and cranny's of striated pectinate muscles that form a labyrinth-like cave in the back half of many LAA morphologies, can last a very long time before breakdown or before breaking loose and gaining access to the venous blood flow and causing a stroke or PE at any time even much later than the conversion point to NSR and well after a cardioversion as well at times ... and a number of other factors.

Typically, when a clot is found that is a serious threat, heparin is started and/or an OAC perhaps with an anti-platelet drug are used depending on the given case.

The earliest a clot has been seen to form during an AFIB episode is 5 hours after onset of the episode, though more commonly it is a good eal later than 24 to 48 hours. Hence the general 48 hour rule.

It obvious you have done a lot of investigation and inquiry on these issue and I applaud that and some of your points in this thread Anti-Afib are well taken and address some valid concerns, but the info you have received also seems to paint the risks, and thus need, for OAC as being more urgent than the guidelines and real world scenarios portray, especially for those paroxysmal afibbers with little to no cardiovascular co-morbidites.

Its all good and stimulates a good discussion we can all learn from and thanks sharing your thoughts on this important issue.

Shannon

Sorry, to try and summarize what I'm seeing in this thread.

For someone like me, who's 36, CHADS score of 0, only two episodes over 5 hours (most convert in 2-3 hours) and what I would call "spotty" afibs. 3-4 weeks ago, I had 4 episodes, these past two weeks, I've had none. Before those 4 weeks ago, I went 2.5 months without any, the 2 months before that I had one a week, the 3-4 months before that I had none (I only get them when waking up from sleep).

Someone with a profile like me probably shouldn't be using anti-coags, even if I had an afib > 48 hours. I ask because I had talked to my cardio about this exact issue, if I should have PIP or OACs on hand, in case i had a long episode. She said she didn't think so, and not only that, that I should be fine even with an episode > 48 hours.

It sounds like this advice jives with what everyone is saying here. Is that correct?

Shannon:

Alot of issues here maybe I will start a separate Anti-Ablation thread later on, as to keep the focus on the original post.
I appreciate the feedback of correcting me if I am wrong.

On the 12-lead EKG detecting normal Atrial pumping via the P-wave: While this an indication of full normalization, it still seems to me that this would not show if the LAA is functioning normally, and that studies do indeed show that the LAA lags behind the LA in returning to normal function after an AFIB episode.

You stated that you could feel your A-Flutter both pre/post Ablation. What is your Flutter rate? I am thinking that your Flutter rate is fairly high, to have that kind of sensitivity. My NSR is about 58-60, and my Flutter rate is typically about 80-84. I can sense ectopics within seconds if I am not to busy, but I really can't tell much of a difference from NSR to A-Flutter.

Changing topic slightly, although I don't have as precise awareness as you seem to have on the issue of AOC, I am aware of what you are saying regarding LAF Chads2 0 patients not needing Anti-Coagulation. I was trying to convey what Lynn or someone else reading the thread would hear in REAL-LIFE SCENARIOS, going into a Doctor's office, or ER room. Maybe there is somewhat of a difference based on Geographical location, but having been to 3 different practices, and seen multiple Doctors, and gotten multiple ECV's in many Hospitals, I can speak from experience, that the one thing Doctor's insist upon is following a strict Anti-Coagulation protocal especially if the patient is going for ECV. I agree this is driven by liability issues. If a patient strokes out, it's a relatively easy liability claim for an attorney to make that the patient should have been on OAC's before the stroke occured.

It is obvious to me also that unfortunately busy EP Doctor's may actually be thinking on a less precise and less complex level than the patient, especially if the patient is versed on LAF by sites such as this. The point I am making is that the patient may have to listen to the recommendation for strict OAC, and then assert to the Doctor why that OAC may not be necessary.

On the aspirin issue, only 2 years ago, I did actually have a well known EP Doctor who was on the original team that did AFIB Ablations at The Cleveland Clinic tell me that I should take a daily Aspirin in my spot, that the studies showed stroke risk was lowered.
I counterred that by telling the EP, that I knew damn well when I was in NSR, and was'nt going to take anything being in known NSR, and then he backed down from the argument.

BTW what are your medical credentials? as I eluded to earlier, I have none.



Edited 4 time(s). Last edit at 08/27/2014 06:32AM by The Anti-Fib.

You think you need an MD to know a lot about AF? Tell that to my (ex) cardiologist..

Hi Anti-AFIB,

Thanks for clarifying what you were intending to convey in a couple of your posts above. And certainly OAC status at the time of ECV is a paramount question and concern of every EP doc and rightly so. I've had 16 ECVs total before my periodic left atrial flutter was put to sleep with an LAA isolation ablation. Those ECVS were done at hospitals from Holland to Hawaii as well as in between in hospitals in Texas, Arizona and California, so I have had the dubious opportunity to see a real variety of nuances to the protocol and thus know the drill well. None of them would dare do an ECV unless quite confident that the patient knew their AFIB status and were sure that no longer than 48 hours had past when not fully anti-caogulated. And they usually tell you to make it to the ER no later than 24 hrs after a fresh episode starts, in order to give a day long fudge factor before the real 48 hr threshold is reached.

I'm a retired Mechanical engineer who had to retire at age 38 and sell my mechanical engineering design/build firm that I owned due to the onset of an aggressive case of post polio muscular atrophy that started in my late 20s and almost 20 years after contracting polio from the oral Sabin vaccine in 1962 when I was 10 years old, the year it was first released in the US.

After as few years of physical therapy I made an initial great recovery and resumed my very active sports filled life up until around 1982 to 84 when the late effects of polio started to manifest with a vengeance, it took 6 years and multiple cervical fusions before the underlying post polio source of my declining orthopedic, neurological and energy status was formally diagnosed, and in the meantime I learned well from the school of hard knocks and many misdiagnoses that I would have to become a very proactive consumer of medical knowledge in the fields relating to my issues to survive long term with such complex chronic issues to deal with.

When AFIB arrived in 1992 ( it runs in the family with my father and sister also having it) my first 10 years experience in treatment only underscored that valuable lesson of learning all that one can and finding the very best doctors in a given field. That is paramount in the AFIB world more so than in most fields due in large part to the relatively recent onset of ablation knowledge and development of AAR and even OAC drugs over the last 20 years, and the extreme challenge in becoming a highly skilled ablationist which weeds out a huge number of otherwise good and smart doctors who you would not want within a country mile of your heart with a catheter. Alas, a fair number of those docs who probably should not be doing AFIB ablations at all are still at it, when a more objective and honest assessment of their own skills and track record might inspire them to stick with pacemakers and perhaps straight forward right sided SVT ablation at the most adventurous going forward.

In any event, my understanding of these related medical issues I keep up with is strictly from intensive self study for almost three decades and the great good fortune of somehow finding the company and mentorship of some very elite world renowned physicians in several unrelated fields that have had a direct impact on my life. So the school of hard knocks has been my constant teacher. And Im very grateful for all the generous time offered to me and my insatiable curiosity by quite a few top tier physicians and EPs through the years.

There is nothing like a serious case of a given chronic condition to inspire one to better understand what is happening to our bodies. And my discovery of Han's site in 2003 after 11 years of well-meaning but largely misguided treatment under a locally highly respected cardiologist in Hawaii who nearly killed me on two occasions, proved a watershed in my own understanding and improvement in my AFIB status to the point when now I live with no arrhythmia at all after having had aggressive persistent AFIB and dealt with the beast for 16 years of AFIB and another 15 months of periodic flutter starting after 3 years of quiet following my index persistent AFIB ablation in 2008 by Dr Natale and the flutter quelled by that second and last ablation over two years ago to isolate my LAA.

I'm definitely not a doctor, just have been around this block for a long long while and thus only share from my own extensive experiences and in-depth research in these particular areas of medicine and from all the borrowed wisdom that has been so generously shared with me over the years by some very smart and accomplished men and women.

About your aspirin experience with the CC doc a couple years ago, that is not uncommon unfortunately. And even as recently as two years ago a lot of EPs were still prescribing aspirin as a fall back if a person could not take OAC drugs, even when the potential benefits were known to be very equivocal. But the weight of a number of large and very well done studies in recent years has finally put a nail in the coffin for use of aspirin as a primary AFIB stroke preventative or warfarin substitute.

I imagine you might get a different story now from your Cleveland Clinic EP than from two years ago (although many Cardios and EPs are still
reflexively recommending aspirin for stroke just out of an old and now thoroughly discredited habit that's hard for them to break).

Dr Natale and I have discussed this issue several times again just in the last six months, and in recent years he has only prescribed low dose aspirin as a prevention aid for cardiovascular disease or if he suspects the person is at real risk for CVD, and especially for preventing second MI's for which the evidence does support aspirin use, but he never now prescribes it just for AFIB stroke prevention.

Also, regarding the P wave issue, there is absolutely no way to measure or indicate LAA mechanical function at all via even a 12 lead EKG, much less a single lead AliveCor reading. You need a TEE scan for that.

Shannon



Edited 2 time(s). Last edit at 08/27/2014 03:11PM by Shannon.

Shannon;

I saw Dr Brownstein yesterday, I gave him the printed copy of the protocol that you said Dr. Wright has for clots. Brownstein took it and didn't have the time to read it at my appt., but he will be calling me when my bloodwork comes in, he did say that Natto was good to take, he asked how long am I In AF when I get an episode, I told him around 14 hours, he said that a clot doesn't form until 72 hours, that is longer than most of us have been told, Dr. B. is not a cardiologist. He also is not going to attend the BHRT conference in AZ, so you won't be seeing him.

liz

Ok. So they changed from CHADS to CHADS2. Now all women with frequent episodes (how is frequent defined) should be on OAC? I can't help but wonder who paid for the studies that set the new guidelines. Sounds like a sales motivated change. Not that stroke isn't a real concern, but as Shannon pointed out there is the risk of having a bleed too. Sure wish there were more studies on natural anti. coag.