Stroke risk in lone atrial fibrillation

Recent postings could create the impression that the risk of ischemic stroke is elevated in lone afibbers. There is no evidence to support this except in cases where the afib is accompanied by comorbid conditions that in themselves carry a significant risk, notably hypertension, heart disease and diabetes. During the 13 years this Bulletin Board has been in operation I can only recall hearing of 3 strokes - one was associated with stunning after an electrical cardioversion, one was a hemorhagic stroke probably due to warfarin overdosing and one was of unknown origin. The following excerpt from the March 2012 issue of The AFIB Report provides additional evidence that stroke risk for lone afibbers is indeed exceedingly low and that life span is not shortened at all.

Long-term prognosis for lone afibbers
BELGRADE, SERBIA. In June 2007 cardiologists at the Mayo Clinic reported the results of a study carried out to determine the long-term prognosis of 76 patients with lone atrial fibrillation (AF). After an average follow-up of 30 years, 29% of paroxysmal and persistent afibbers had progressed to permanent AF. In most cases the progression to permanent AF occurred within the first 15 years after diagnosis. Survival in the study group at 92% at 15 years and 68% at 30 years was similar to or even slightly better than expected for an age- and sex-matched group of Minnesotans (86% and 57% at 15 and 30 years respectively). The development of congestive heart failure (19% of the group at 30 years follow-up) was not significantly higher than expected (15%).

During the follow-up, 5 strokes (0.2%/person-year) and 12 transient ischemic attacks (0.5%/person-year) occurred in the group – mostly among permanent afibbers. All strokes and TIAs (transient ischemic attacks) occurred in participants who had developed one or more risk factors for stroke during follow-up (hypertension in 12 patients, heart failure in 4, and diabetes in 3). Not a single stroke or TIA occurred among lone afibbers with no risk factors for stroke. This prompted the remark from the researchers – Our long-term data suggest that the increased risk of stroke in atrial fibrillation is due to “the company it keeps”. In other words, lone AF as such is not a risk factor for ischemic stroke. The overall conclusion of the study is highly reassuring to lone afibbers – After >30 years of follow-up of our rigorously defined cohort, findings confirm that overall survival is not affected adversely by lone atrial fibrillation.[1]

A group of Serbian cardiologists now report on a larger long-term study involving 346 patients with newly diagnosed lone atrial fibrillation (LAF). Their definition of LAF was AF in patients 60 years old or younger with no hypertension, underlying heart disease or other comorbid conditions that could explain the presence of AF. The average age of the study participants at baseline was 43 years (range of 18 to 60 years), 76% were male, and 12% had asymptomatic AF. The majority (70%) had paroxysmal (intermittent) AF at baseline with 22% having persistent and the remaining 8% having permanent AF. Permanent afibbers were significantly more likely to have an enlarged left atrium and asymptomatic AF when compared to paroxysmal afibbers. During the average 12-year follow-up, 35% of the group developed heart disease, 25% hypertension, and 10% diabetes.

During follow-up, 27% of paroxysmal afibbers and 55% of originally persistent afibbers progressed to permanent AF. The average time to progression was 10 years and the average age at which progression was documented was 55 years (range of 24 to 74 years). Older age at diagnosis and development of congestive heart failure were predictors of progression. Somewhat surprisingly, the development of hypertension was associated with a 30% decrease in the risk of progression from paroxysmal to persistent or permanent AF. It is likely that this is due to the fact that therapy with angiotensin II converting enzyme inhibitors was much more common among patients with hypertension (77%) than among those who retained normal blood pressure (5%). NOTE: Hypertension was defined as a blood pressure reading above 140/85 mm on 3 separate occasions.

A newly developed risk score, the so-called HATCH score (1 point each for hypertension, age of 75 years or older, and chronic obstructive pulmonary disease and 2 points each for heart failure and prior stroke or TIA) was found to accurately predict the risk of progressing from paroxysmal to permanent AF. A score of 0 was associated with a 20% risk of progression, a score of 1 with a 36% risk, and a score of 2 with a 63% risk of progressing to permanent AF.

Thromboembolism was documented in 14 patients (4%) over the 12-year follow-up period. Nine of the 14 patients suffered an ischemic stroke corresponding to an annual stroke incidence of 0.2%. This rate is identical to the one observed in the Mayo Clinic study and, once again, confirms that the risk of stroke associated with lone AF is extremely low – actually lower than the rate observed in the general population. Furthermore, it should be noted that 6 of the 14 patients had developed one or more risk factors for thromboembolism (5 patients with hypertension, 1 with coronary artery disease, and 2 with diabetes) by the time they experienced their stroke or other thromboembolic event. It is also of interest to note, that of the 14 patients 8 were taking aspirin, while 6 had no antithrombotic therapy. In multivariate analysis only the development of hypertension and coronary artery disease was significantly associated with thromboembolism.

During follow-up, 14 patients (4%) developed congestive heart failure (CHF) at an average 10 years from diagnosis (range of 0 to 26 years). The only variable independently associated with an increased risk of CHF in multivariate analysis was progression from paroxysmal to permanent AF. The 10-year survival of study participants was 99.6%. It is not clear from the study whether permanent AF increases the risk of CHF, or CHF increases the risk of permanent AF. The former clearly makes more sense.

The Serbian researchers conclude that the prognosis of lone AF is favourable, but becomes less so with increasing age and the development of (new) underlying heart disease.
Potpara, TS, Lip, GYH, et al. A 12-year follow-up study of patients with newly diagnosed lone atrial fibrillation: Implications of arrhythmia progression on prognosis. Chest, Vol. 141, No. 2, 2012, pp. 339-47
Boriani, G, et al. Atrial fibrillation: It is better to be alone than in bad company! Chest, Vol. 141, No. 2, 2012, pp. 290-92

Editor’s comment: The Belgrade study clearly confirms the conclusions of the Mayo Clinic study that lone AF is a benign condition with excellent long-term prognosis. The risk of stroke is extremely low even without anticoagulation, and survival rate is excellent. There is a significant trend though for paroxysmal AF to progress to persistent or permanent AF. It is, however, likely that this trend would have been significantly less pronounced if 36% of paroxysmal and persistent afibbers had not been treated with digoxin. This “medicine from hell”, for lone afibbers at least, may not only prolong episode duration, but may actually convert paroxysmal AF to permanent.[2,3]
NOTE: I personally do not agree that chronological age should enter into the definition of lone AF. This conviction is supported by the following statement by Dr. Lars Frost of the Aarhus University Hospital in Denmark, Cardiologists with strong political influence have suggested that a diagnosis of lone atrial fibrillation should be restricted to patients <60 years of age, although there is no evidence of any threshold values by age regarding the risk of stroke in patients with atrial fibrillation – or in any other medical condition for that matter.[4]

References
1. Jahangir, A, et al. Long-term progression and outcomes with aging in patients with lone atrial fibrillation. Circulation, Vol. 115, June 19, 2007, pp. 3050-56
2. Sticherling, C, et al. Effects of digoxin on acute, atrial fibrillation: Induced changes in atrial refractoriness. Circulation, Vol. 102, November 14, 2000, pp. 2503-08
3. Falk, RH. Proarrhythmic responses to atrial antiarrhythmic therapy. In Atrial Fibrillation: Mechanism and Management, edited by Rodney H. Falk and Philip J. Podrid, Lippincott-Raven Publishers, Philadelphia, 2nd edition, 1997, p. 386
4. Frost, L. Lone atrial fibrillation: Good, bad or ugly? Circulation, Vol. 115, June 19, 2007, pp. 3040-41

Hans

If the lone afib stroke risk isn't any higher than the general population, why do all the doctors say otherwise? And why do they cite study after study showing otherwise?

Hans, the reason you don't hear of strokes on this list is that when members have them, they are likely too disabled to get back on the list (they'll just drop off and you'll never hear from them again).

Now the doctors are saying that even a successful ablation doesn't lower stroke risk, so a successful ablation may not prevent us from needing to take anticoagulant drugs as we get older.

Diane98683 Wrote:
-------------------------------------------------------
> >
> Now the doctors are saying that even a successful
> ablation doesn't lower stroke risk,


Huh?

I suppose if the stroke risk you refer to had nothing to do with AF that would be the case...but if the ablation was successful (no more AF), the stroke risk from AF would be eliminated.

I had a stroke exactly one year ago this labor day weekend and I was a CHADS 0.
Just 2 months earlier I had blood work done and my numbers were excellent. I check my blood pressure everyday too sometimes 3x a day. The only thing that was different last labor day weekend was I was in and out of afib for 4 days.
I've read some recent studies where many afibbers both paroxysmal and persistent have many TIAs, silent strokes and don't know it. I'll bet that most haven't' had a brain MRI and if they did they likely will show a TIA so now your CHADS score is automatically a 2. Natale told me that in affibers the shape of the LAA will probably or might be the most important factor in determining stroke risk along with the other CHADS scores as they reassess the CHADS scoring. At least that's what I understood he was telling me.Too bad I don't know my shape as I never had a CT scan, but he told me it doesn't matter unless afib comes back.
The problem I see with the Serbian study is no MRI was done to determine how many silent strokes affibers had. I had 2 other TIA's that were older on my MRI and I never knew it!!!!
I always wondered if the shape of my LAA mattered before I even saw anything about it and I wasn't surprised when I came across the first article about it.I suspect I have a cauliflower shape......Just some food for thought..............



Edited 3 time(s). Last edit at 08/30/2013 02:49PM by McHale.

Thank you, Hans, for reminding us that anecdotal reports, while helpful in many ways, are not necessarily indicative of statistical risk.

______________
Lone paroxysmal vagal atrial fibrillation. Age 62, female, no risk factors. Autonomic instability since severe Paxil withdrawal in 2004, including extreme sensitivity to neuro-active drugs, supplements, foods. Monthly tachycardia started 1/11, happened only at night, during sleep, or when waking, bouts of 5-15 hours. Changed to afib about a year ago, same pattern. Frequency increased over last 6 months, apparently with sensitivity to more triggers. Ablation 6/27/13 by Steven Hao.

McHale - did you have a result for your Lipoprotein (a) and if so was it out of line?
Ron

Most definitely for the vast majority of Afibbers in the Lone paroxysmal category the stroke risk is very low.. no doubt a good deal lower than Big Pharma would have us believe.

Also, I'm convinced that when it really is early to middle stage ( meaning roughly within the first 5 to 8 years of AFI the vast majority without other co-factors like CVD, Hypertension, Obstructive Sleep Apnea, prior TIA, Diabetes, Valve disease, CHF, etc etc., and just have lone AFIB are much less likely to have stroke as a major concern, even with AFIB happening periodically.

As AFIB progresses over the years and especially when it goes persistent, it is a possible contributor toward an increased likelihood of progressive fibrosis and possible decrease in LAA functional flow rates which, in turn, can predispose you to a greater stroke risk.

Hopefully, these days with better tools and protocols at our disposal, most people don't wait until they are persistent ( unless they never knew they had silent AFIB until it became persistent or are one of the unlucky few who start out persistent from the get go) before trying to get better control over the beast.

The new direction in trying to gain a better stratified stroke risk profile that McHale mentioned above from his conversation with Dr Natale, is in the developing art of categorizing LAA morphology as the prime independent risk factor for AFIB/LAA related embolic stroke.

This new angle of including LAA shape and morphology as the prime determinate, among several other factors also included in the anticoagulation decision such as CHADS-2 /CHADS2-VASc scores as the most common metric that most docs will use in addition to LAA morphology once this protocol is widely accepted, plus whether or not the person has any of the other risk factors above or is just an occasional lone paroxysmal Afibber, I feel has real promise for giving a far better and more effective guideline for who should consider anti-coagulation or even possibly LAA ligation/occulsion for the rarer few with more extreme stroke risk, from the vast majority of Afibbers who can likely get by with an aspirin (or nattokinase, preferentially, and other natural aids for reducing whole blood viscosity as well though few Cardios will take that leap as yet) and from those who might warrant Coumadin or one of the NOACs.

So, if you truly are a lone Afibber with none of the other risk factors, then you 'might' be perfectly safe with nothing at all or using nattokinase or an aspirin a day ( though I am not a fan of aspirin for every day use for the many reasons we've discussed before).

However, I say 'might' be safe because those of us that have a 'Cauliflower' in particular as the most dangerous morphology, or a 'Cactus' shape to our LAA need to be a little more careful in feeling like we have nothing to worry about stroke wise. Cactus is just behind 'Cauliflower' among dangerous LAA shapes, both of which seem to be associated with significantly enhanced risk for a TIA or stroke compared to those of us with the most favorable 'Chicken Wing' LAA shape and even the next least dangerous 'Windsock' morphology.

If you learn from a 3D CT scan or MRI scan of the LAA that you own a Chicken Wing and you are truly a Lone Afibber with a low CHADS-2 score to boot, you can likely take nothing at all, or at most an aspirin as prescribed by your Doc, or a high quality Nattokinase at 100mg 3x/day with one every 8 hours, and you should be well protected against embolic stroke.

Both of the most dangerous Cauliflower and Cactus shapes are, by definition, shorter than 4cm in length and the Cauliflower has no forked lobes at all and no secondary lobes greater than 1cm in length, while the Cactus has two or more secondary lobes of 1cm or greater in length and often those multiple lobes are 'forked' on both sides of these short LAA main lobes.

The Chicken Wing and Windsock LAA shapes both have a longer main lobe greater than 4cm with the Chicken wing having a folded or curved coronal angle of less than 100 degrees while the Windsock has a folded angle of greater than 100 degrees. The Windsock while less dangerous than the Cauliflower or Cactus, still brings about 4 times the stroke risk of the most favorable Chicken Wing shape.

In two significant studies, the first by Natale's group and a new one following up on that work from Japanese researchers highlight that using the usual CHADS-2 or CHA2DS2-VASc score for anti-coagulation determination was woefully inadequate!

in the Japanese study nearly one third of those Afibbers who had had an embolic stroke and were thus in the stroke group of this study had a CHA2DS2-VASc score of 0 at the time of the stroke and no difference was found between their stroke group and control group in terms of CHADS2..

In this study only the Cauliflower LAA Morphology was the sole independent predictive risk factor for a low CHADS2 score and it was very useful for determining stroke risk of these patients in this low CHADS2 score cohort study.

More such studies will have to confirm what these first two seminal studies strongly suggest, but with more investigation we may gain a far more valuable tool to more accurately determine who should pay attention to this stroke issue and who is more or less okay as it is and with a little effort to confirm you have low blood viscosity, should not have to worry about strokes.

For some of us though, with confirmed low LAA emptying velocity and an unfavorable LAA morphology, such as yours truly, then the embolic stroke issue is suddenly front and center and ignoring it would not be a wise step at all. But only those of us with super low LAA emptying velocity and a more dangerous LAA shape would need to consider steps like the Lariat or Watchman.

Although those devices and procedures could also be a good option for those whose combination of LAA shape plus a mid to high range CHADS2 score puts them in the recommended anti-coagulation category, but who either cant tolerate those drugs or really don't want to be shackled to them for life with the possible side effects and very real bleeding risks those drugs can bring themselves.

But as Hans noted in starting this thread, its highly likely that a large number of people are being overtreated with powerful anticoagulants who really don't need them and would be much safer with milder alternatives, if anything at all is needed. On the otherhand, there is just as likely a much smaller group of people who think they have no stroke risk from the far too broad and incomplete risk models we have now, and who really should consider protecting themselves more so than they suspect now.

That is, those of us with these more dangerous LAA shapes and also with either poorly controlled AFIB/Flutter or having a confirmed far too low LAA emptying velocity along with these unhandy LAA shapes .. especially if you have long standing persistent AFIB with a Cauliflower LAA for example, should pay much closer attention to this issue and take whatever steps you and a good EP determine will give you the most freedom from this infrequent and yet much too devastating consequence of our disease to ignore if you fall into one of these less fortunate categories.

Shannon

PS .. In evaluating where each of us fits, without yet knowing your LAA morphology, keep in mind that those with any of the other risk factors that knock you out of the 'Lone AFIB' category, such as CVD, hypertension and OSA (obstructive sleep apnea) need to consider that you don't really fall into the category of 'lone AFIB' as it is,, and as such Hans' definitions above may not apply fully to your case.

Its important to consider that OSA is a definite risk factor for CVD, hypertension, stroke, and AFIB as well and will knock you out of the strict Lone AFIB category so you need to evaluate your risk category accordingly. Nevertheless, learning your LAA shape would be a good thing if you still have AFIB activity or you wind up needing an LAA isolation ablation to stop said arrhythmia.



Edited 1 time(s). Last edit at 08/31/2013 11:33AM by Shannon.

Diane – Keep in mind that doctors must give out warnings as part of their protection against legal liability and litigation. My experience is that they always added a precautionary remark about stroke risk in most initial conversations with me at the onset of my Lone Afib. When I refused warfarin initially when my events were only a couple a year, I offered to sign a disclaimer to absolve the cardiologist. He declined my offer.

After my 2003 ablation, I attended Summit Conference here in Cleveland (2004) on Atrial Fibrillation. During lunch, I sat with several EPs and several EP nurses.. and I shared my AF story and recent ablation. I was asked whether or not I was using an anticoagulant to guard against "silent afib"... and I responded that I was not. They were alarmed and went into detail about the prevalence of post-ablation silent AF and my risk for stroke. I told them that I didn't do well on warfarin (which was the only anticoag available at the time) and that I relied on the fibrinolytic/proteolytic enzymes, magnesium and Omega 3 fish oils... just to annoy them.. because I knew what their reaction would be. I wasn’t disappointed.

During my 8 years of escalating events of AF that nearly became persistent, I relied on the data offered here …ie, that the risk of stroke was miniscule with LAF and also the fact that I had consistently met the “safe” parameters of all the other markers considered contributing factors that can lead to thick, sticky blood and therefore elevated blood viscosity…or hypercoagulability.

It has been my experience over the past 18 years of researching and discussing afib situations with those suffering from the ailment, that most are generally unaware of the contributing factors that set us up for risk of hyperviscosity and worse yet, so are their physicians....or so it would seem for lack of monitoring of all the risk factors. These tests are not new and have been discussed here with regularity. To ignore the total picture when it comes to this topic is just foolish. Once you know your numbers, you are in control to normalize and protect yourself. I am just dumbfounded that in many cases, patients have to argue about getting the tests ordered. It’s probably going to become worse now with the national healthcare act.

However, it makes no sense to walk around worrying about a cholesterol number – which isn’t part of the problem-- and not know the other significant indicators. Keep in mind that while inflammation is often a key player because of the body’s response to inflammation, it isn’t the only culprit… all those in the following list are contributory.

I didn’t then and don’t worry now about a stroke with LAF because I knew my numbers and I took action to make sure they stayed in safe range. I still do.

Iatrogenia recently posted the link to the Red Flags post on the important monitoring tests.

If anyone reading this post does not know their Lab numbers for……

PREDICTING YOUR RISK FOR HEART ATTACK OR STROKE –THE SILENT SYMPTOMS

High Sensitivity or Cardiac C-reactive Protein (CRP)
Fibrinogen
Ferritin
Homocysteine
Hemoglobin A1C
Lipoprotein (a)
Oxidized LDL

…it’s time to request the testing. Unless you test, you can’t possibly know where you stand with these markers.
[www.afibbers.org]

Arm yourself with knowledge and be safe.

Jackie

Hi Shannon,

A great post! Thank you for the detailed information.

One question, was your low emptying velocity due to ablation work or present before they ever started mucking around with your heart?

Thanks!

George

RonB Wrote:
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> McHale - did you have a result for your
> Lipoprotein (a) and if so was it out of line?
> Ron

Ron I don't know, they did blood work in the ER too, need to get back there and get my medical records before they shut down the hospital. It's slated to be chopped due to budget cuts.

IMO the size of the "reservoir" of the LAA would be a big factor in producing blood clots while in AFIB as the blood in a deeper appendage has more of a chance to pool and clot.

Shannon excellent post!



Edited 1 time(s). Last edit at 08/31/2013 01:04PM by McHale.

What annoys me are cardiologists (like the first one I consulted with) who say to 'just live with it' (PAF) if it doesn't bother you too much'. Well it did I told him and started using Flec PIP. Then I found this board (thank you Hans) and determined to get ablated. Nearly a year later I'm OK, in NSR..

Shannon,
Is a 3D CT or MRI the only way to learn the shape and size of your Left Atrial Appendage?
Can you get that information from TEE or ICE? Or do the TEE and ICE just give you the emptying velocity of the LAA?
Thanks,
Betty

Hi George,McHale, Betty,

I will try to answer the three questions/comments in order...

George, that's a good question.. Dr N said he noticed some delay already in my LAA, no doubt from the TEE I had just before that first ablation in 08 in Austin, and that there was some further progress in that slowing velocity noted during the LAA Isolation ablation last Aug 2012. As such, we both knew that my odds for maintaining a sufficient velocity after my LAA isolation enough to allow me to stop the Coumadin and be done with this business were not that good. Alas, that educated hunch was confirmed by my follow-up TEE last Feb, six months after the LAA isolation which, in turn, set the wheels in motion for my Lariat procedure due to the dangerously low remnant velocity left after that last ablation around my LAA.

That, and the fact that my LAA shape is a kind of hybrid Cactus-Cauliflower blend ... The worst shapes you can have, which pretty much clinched the decision to go for the Lariat. Knowing my fathers and sisters stroke history was the cherry on top of that decision tree.

The key point, though, is that a prolonged period in persistent AFIB, particularly after over 12 year paroxysmal history before it even turned persistent, can result in enough remodeling to show up as variable degrees of impairment to LAA mechanical function, even before an LAA isolation ablation is needed.

My hunch is that a fair number of the roughly 8% of longtime afibbers who are on Coumadin already and yet eventually still have a stroke/TIA are people that unknowingly fall in this category. In light of the new research on the major importance and role of LAA morphology variations in AFIB related stroke risk, it also would not surprise me to learn that this small (under 10%) but not insignificant group of people that wind up having strokes or TIAs while on Coumadin in a therapeutic range, have a combination of poor LAA shape, a bit too much remodeling from long time poorly controlled AFIB as well as the one or more other co-factors we all know of that predispose toward these kind of cerebrovascular events.

But George, it is true that an LAA isolation brings with it 50% to 60% odds that LAA velocity will slow enough to force the anti- coagulation/LAA ligation-occlusion question on the table front and center. All the more reason to not muck around too long trying to avoid a good ablation 'IF' the person is still getting a fair amount of breakthroughs.

And McHale, while intuitively it would seem that a deeper and longer LAA tube might favor clot formation over a shorter fatter tube, in reality its just the opposite ironically enough! The Cauliflower and Cactus shapes are both smaller with each less than 4cm long and often with more oval to rectangular mouths as well as more variegated and rougher endothelial lining within only certain parts of these stubbier LAA shapes. The safer Chicken wing is a longer smoother tube with a single coronal angle or curve of less than 100degrees.

What happens is the shorter wider and more variegated LAAs like Cauliflower/Cactus seem to provide wider open areas wherein the blood doesn't pick up as much shear velocity from the closer spaced and more tubular inner walls as found in a Chicken Wing, for example, and thus the blood tends to pool more in the middle and in little side chambers in the stubbier shapes, than in the longer more tubular Chicken wing and Windsock that seem to better facilitate smoother and faster flow in and out again from the LAA with each beat of the heart when the nearby mitral valve opens and closes and thus more easily flushes the blood in and out of these longer but narrower chicken wing or windsock shapes with their smoother more conical curved-tube shapes.

And Betty, yes the 3D CT Scan is, by far, the preferred method, followed by special MRI scans as a distant second preference, for most accurately determining your LAA morphology or shape. You can get an idea of what your shape is from the 3D Carto 3 images taken during an ablation, that are built around a pre-ablation 2D CT scan, but those are not all that reliable for judging LAA shape detail compared to a 3D CT scan which is best way to define what your LAA shape really is. I'm sure they will improve MRI scanning of the LAA to better define this issue as well before long.

Cheers, Shannon



Edited 1 time(s). Last edit at 08/31/2013 10:26PM by Shannon.

Shannon,

Thank you again!

I know that my 2 1/2 month episode forever puts me in the persistent category. That was 9 years ago and I've not given any of the subsequent episodes a chance to be paroxysmal as I've terminated all with PIP flec, usually in an hour or two. I'm sure if/when I go in for an ablation, more work will be required. My short list of ablation EP's is also limited to Natale and the Bordeaux team.

When my episode frequency increased in the last year, I thought it was time to get in line for an ablation. However since I subsequently and fortunately figured out the frequency increase was due to increased calcium intake from diet, I'm back to very infrequent episodes (don't know 'cause I'm only 4 months in to this revelation, but I seem to have the same control I did when my episode frequency was around 1/year). At this point, I just pay attention to keeping the electrolytes right. Typically my only triggers now are all day very hard exercise. I normally (but not always) have enough sense to avoid this. Even if I do participate in this kind of exercise, I can usually avoid afib by doubling down on the electrolytes and perhaps taking some flec (100 mg/day) prophylactically during the 2-3 day vagal aftermath that is my risk time.

George

Dianne,

I have never come across a study that concludes that LONE afibbers with no stroke risk factors (CHADS2 score of zero) have an elevated risk of ischemic stroke. If you or your doctor knows of any such studies I would sure like to know the references to them. For your information here is the abstract of the Mayo Clinic study [www.afibbers.com]

As you point out there are numerous studies concluding that atrial fibrillation (AF) is a significant risk factor for ischemic stroke. However, these studies involve patients with heart disease and usually, a plethora of co-morbid conditions which increase their risk of stroke. Such patients constitute 80% or more of the total AF population and are sure-fire candidates for lifelong anticoagulation. The studies however, do not specifically cover the risk associated with just having AF with no underlying heart disease i.e. LONE atrial fibrillation (LAF). NOTE: I am using the original definition of LAF here, which is atrial fibrillation in the absence of structural heart disease. The fact remains that stroke risk in lone afibbers with no stroke risk factors (hypertension, diabetes, coronary artery disease, heart failure or prior stroke/TIA) is extremely low. This is recognized in ACCF/AHA/ESC Guidelines for the Management of Patients with Atrial Fibrillation. These guidelines do not recommend anticoagulation for lone afibbers with a CHADS2 score of zero as the risks (major bleeding and hemorrhagic stroke) outweigh the benefits in this case. For a detailed explanation of the profound differences between “common” AF and lone AF please see Patrick Chambers article LAF vs. AF: Shape Matters [www.afibbers.org]

In considering the broader aspect of stroke risk it should be kept in mind that most ischemic strokes have nothing to do with atrial fibrillation. Only about 15% of ischemic strokes are what is known as cardio embolic (caused by a clot originating in the left atrium or left atrial appendage). The vast majority (85%) is caused by an obstruction, usually atherosclerotic plaque, getting stuck in a brain capillary. In the overall scheme of things hypertension, atherosclerosis, an elevated lipoprotein(a) level, diabetes, etc. are far more important risk factors for ischemic stroke than is LAF. For example, hypertension on its own doubles stroke risk while diabetes increases it by a factor of two to five.

Your final comment: “Now the doctors are saying that even a successful ablation doesn't lower stroke risk, so a successful ablation may not prevent us from needing to take anticoagulant drugs as we get older” would as Tom points out support the contention that AF is not a risk factor in itself because if it was, stroke risk and the need for lifelong anticoagulation would be eliminated by a successful ablation except in cases like Shannon’s where the blood flow in and out of the left atrial appendage was severely reduced during ablation in order to eliminate afib.

Hans

Shannon,

Thank you for for those most interesting postings on the importance of LAA morphology in determining stroke risk in atrial fibrillation patients. Unfortunately, at the moment I only have access to the abstracts of the Natale and Japanese studies so I have not been able to answer these questions myself:

What percentage of the population in the two studies had lone atrial fibrillation and a CHADS2 score of zero?

Was any attempt made to compare the effect of LAA morphology on stroke risk in "common" afibbers and lone afibbers?

Hans

Shannon,
Excellent post, I knew we kept you around here for a reason......
I guess I got it backwards or something like that....... So which one would be easier to strangle via Lariet?
My guess would be the Chicken Wing.

McHale



Edited 1 time(s). Last edit at 09/01/2013 06:35PM by McHale.

Hans,
Interesting new study.

[www.theheart.org]

McHale



Edited 2 time(s). Last edit at 09/01/2013 06:57PM by McHale.

McHale,

Yes, that looks like an interesting study. I am looking forward to learning the details when it gets published. At first glance it would appear that it, not surprisingly, makes no distinction between "common" afib and lone afib. By not listing coronary artery disease as a risk factor it sort of implies that all or at least most of the participants had underlying heart disease at baseline and therefore would not qualify for the "lone" designation. However, we'll have to wait for the details.

Hans

Thanks Shannon and Hans for answering our questions. Such good information!
Betty

Hi Hans

At the moment I only have the full Japanese study on hand called 'Anatomical Characteristics of the Left Atrial Appendage in Cardiogenic Stroke with low CHADS2 scores'

Also there is not a clear demarcation between Lone Afibbers and those will one or more of the co-morbitities that certainly complicate the stroke risk picture for sure. And I agree it is not age, per se, but more that fact that many of these co morbitities and added risk factors tend to pile on when one gets into the elderly category, unless they have paid good attention to sustaining their good health all along, perhaps also endowed with handy genetics and a fair dose of good luck as well during one's golden years.

But I agree with you in that I don't think they should judge a person at a higher CHADS or stroke risk solely by age number.

Anyway, back to the Japanese study, they chose a group of 80 patients who underwent AFIB ablation and examined them with contrast weighted CT ... The LAA characteristics were compared between 30 patients with histories of prior strikes with 50 age-matched controls with no stroke or TIA history.

The LAA morphology was discriminated between the four accepted types 'chicken wing', 'cactus', 'cauliflower' and 'windsock' .

Interestingly, the average CHADS2 score did not differ significantly between patients with stroke and the control group. Also, eight patients (26.7%) within the stroke group had a CHA2DS2-VASc score of '0' !

The LA size, LAA flow velocity, LVEF (left ventricular ejection fraction) and serum levels of BNP hormone were no more able than CHADS2 or CHA2dS2- VASc scores to predict stroke risk... Only cauliflower shape of LAA in this study consistently and independently showed up as the key real world stroke risk factor.

You would think that a fair number of those in the stroke group ought to have had some degree of risk factors like we all expect in non-lone Afibbers, that would have ferreted them out of the Lone AFIB category.But that wasnt clearly stated. These folks with stroke certainly were no longer in the Lone AFIB group after their strokes, although I'm not sure how much consolation we can take from that without knowing their full co-mobitities status prior to actually having what were deemed cardiogenic strokes?

It does indicate that the CHADS2 model is quite inadequate for stratifying real world stroke risk in the general AFIB population which we must assume, at this point, had some mix of Lone AFIB and sicker people making up the mix, perhaps a large majority of those 30 people in the stroke group would have been classified not as Lone-Afibbers prior to the stroke but there isnt enough info in the study to deterimine that for sure.

Regardless, when nearly 30% of your test group has a stroke even with a CHADS2 score of '0' that's a pretty compelling indicator of a not very trustworthy indicator for stroke risk for the overall AFIB population base, if you ask me.

But from all we know to date, those who are truly Lone Afibbers are not in a serious stroke risk category. These studies just highlight new tools for making a better discrimination of who really is at risk beyond, perhaps the overly broad definitions of Lone Afib or those with some degree of cardiovascular disease and AFIB. Knowing the LAA shape may some day soon become a step used when a patient progresses to the point where anti-coagulation would .. or should ... be considered to better define their real world risk and better allocate the kind of therapy that should be recommended.

For example, with a person even with a CHADS2 score of 2 and yet who has a favorable Chicken Wing shape, many more of those would likely do just fine with an aspirin ( as far as the EPs are concerned, or nattokinase for those more familiar with this agent) and not automatically stick them on Warfarin or an NOAC drug for life or until after a successful ablation process.

That would be a positive step. Also, though even those Lone Afibbers who are starting to have more issues and have symptomatic long standing AFIB episodes or persistent AFIB, and who have a Cauliflower LAA shape, it would likely be smarter advice to make sure they had confirmable anti-coagulation including very occasional TEE tests to verify no thrombus formation in their LAAs whether or not they are on Warfarin. This is especially true if they wind up also having a Cauliflower or Cactus shape combined with having low LAA emptying velocity either from the unablated AFIB continuing or from an LAA isolation procedure .. such people even if they were originally classified as 'Lone Afibbers' might well have considerably more risk than the more usual Lone Afibbers with occasional bouts of paroxysmal AFIB, but otherwise a more handy LAA shape and no other real risk factors.

Take care,
Shannon



Edited 2 time(s). Last edit at 09/03/2013 06:51PM by Shannon.

Hi Hans,

I did read through the much larger study by Natale's group with Luigi Di Biase as the lead investigator listed in the authors listing on the LAA Morphology and stroke issue in low CHADS2 score afibbers.

There was something like 932 patients evaluated by CT or MRI for LAA shape and size versus only 90-patients in the Japanese study.

In the Natale group study they used a bit different criteria for defining the various morphology's such as adding in the presence of an oval shaped mouth to the Cauliflower definition, in addition to the other criteria used for the Cauliflower in both studies. As a result, even though the Cauliflower had the worst outcome, by far, for stroke risk over the other two unfavorable shapes of Cactus and Windsock, relative to the one reasonably favorable Chicken Wing shape, the stricter definition of Cauliflower in the Natale group study results in only 3% of the 932 people prevalence of that shape, whereas by the looser definition of Cauliflower in the Japanese study they found 17.5 % of the 90 subjects with that most unhandy shape.

In the Natale groups much larger study they found that Cauliflower had 8 times the stroke risk over the reference Chicken Wing while Cactus and Windsock were 4.08% and 4.5% greater stroke risk than the most favorable Chicken Wing LAA shape.

As a result Natale's study says that all three shapes other than Chicken Wing were strong independent risk factors for stroke in AFIB patients coming for ablation, and more so than any of the usual stroke risk markers like CHADS2, age matching, etc etc. They also found these LAA morphologies to be particularly useful in predicting stroke risk in people with low CHADS2 CHA2DS2-VASc scores of 1 and 0.

The question is, were all 8% of the folks in the Natale group study that actually had strokes before their LAAs had been CT scanned and defined, truly non-Lone Afibbers are was there a mix of Lone Afibbers and people with other co-morbities,. for which the Di Biase- Natale paper said that compensated for age, co-morbities for stroke, CHADS2 score etc before determining that only those LAA shapes in the other three categories besides Chicken Wing are the only independent risk factors for actual stroke in this population of Afibbers.

Food for thought and it does seem that as this practice continues to evolve and get more refined, then typing people based on LAA shape, especially if and when they can do so most reliably with either MRI or even possibly the newer 3D TEE technology without having to use CT Xrays, might well offer a lot better guidance of who should consider anti-coagulation or a Lariat/Watchman type solution from the far greater number who can likely get by with little more than a nattokinase pill three times a day and a good diet.\ as well as making sure you maintain favorably blood viscosity readings.

Shannon