1 out of every 3 Afibbers will have a stroke??

When listening to a show on TV this morning, the tennis champion, Billie Jean King - who has Afib and was touting the website MyAfibRisk.com - made the statement that "One our of every three people with Afib will get a stroke". Where is she getting that information? That seems way out of sync with all that we've learned on this Board....

Comments?

Barb

Barb,

I will let someone else address the stroke risk for AF patients as several here have more knowledge than I . I want to state a caution about the website, Myafibrisk.com. That site is owned by Jannsen Pharmaceuticals and division of Johnson and Johnson. Janssen has been in the news a lot lately for all the wrong reasons. They have been accused of false and deceptive advertising both civilly and criminally by the US, several states and other jurisdictions concerning their anti-psychotic drug Risperdal. The company settled with the US Dept of Justice for $2.2 Billion, and have judgements from lawsuits against them for billions more. These cases comprise one of the most egregious corporate frauds in history.

Last week they were subject of a long article in Huffington Post by the journalist Steven Brill that can be perused here:
[highline.huffingtonpost.com]

The title "most admired" comes from J and J's handling of the Tylenol tampering case in the early 80s. The company has been working hard ever since to destroy the goodwill they earned at that time and is finally succeeding.

It is surprising that Jerry West and Billie Jean King, both admired former champion athletes with AF, would allow their names to be associated with this company.

Bill

One in three AFIBBERS having a real stroke (and not when including TIAs or SCIs ( silent cerebral ischemia) in that number is a big over-exaggeration ,, However, include the other two, especially SCIs and the numbers might easily hit that mark if not more ..... just saying. In a number of studies SCI have been seen in from 46 up to 80% of some AFIB cohorts studied.

The consequences of SCI as far as leading to real strokes are unknown and certainly dramatically less, However the contribution of unaddressed AFIB and the continual accumulation of SCI burden and it's potential association with early onset dementia and Alzheimer's is scary indeed. We still don't have in-depth larges scale meta analysis numbers on this but a rapidly increasing number of solid studies on AFIB related SCI and its association with these terrible diseases is definitely one of the main focal points now of ongoing AFIB research... No longer is ongoing modest AFIB even considered the relatively benign issue it once was when all they thought we had to worry about was stroke and heart failure due to uncontrolled rate.

Shannon\

I'm wondering why you capitalized the AFIBBERS like you did, Shannon...I also thought it had been said quite a few times on here that those of us with "lone" Afib did not have an increased stroke risk....or has that information changed? How does one safeguard themselves against a SCI - do blood thinners help with this too?


Just trying to understand it all....Barb

Yes blood thinners can help reduce SCI burden, likely cardiokinase too, but that is only speculative as I know of no data around that, just good common sense as SCI generally needs a lower level of OAC strength to lessen, as I understand it. As such, Cardiokinase, if it has any effect at all as Im sure it does to variably degrees, should help in reducing SCI accumulation.

However, the number one help in reducing SCI though is SOLID NSR!! Even sporadic AFIB/Flutter can allow the SCI burden to increase steadily over time from the bulk of evidence we have know.

Also Barb, I sometime capitalize a word or two here or there for emphasis though I realize it is probably annoying to some of you ( apologies if so ) ... but the AFIBBERS all caps was just an inadvertent extension of my common AFIB acronym and thus there was no intended purpose to using all caps there Barb.

Shannon

Well, good grief, having AF occasionally can give us a Stroke, Dementia, what else, not very encouraging for our future.

Liz

Not buying Billie's quoted stat till verified by a reliable source.

/L

Shannon,

Can you please expand on what is meant by sporadic AF? Is there anything known about the risk of stroke jointly with AF frequency and duration, as opposed to just AF burden (fraction of time in AF)? My EP believes that greater frequency and shorter duration for the same AF burden (especially durations exclusively on the order of minutes) entails far less risk of stroke. I asked if there was any statistical analysis but he did not know. I am also unclear about the nature of the stroke he was referring to. There is apparently some issue here, given the anticoagulation protocol prior to ECV for sufficiently long AF episodes - or is this no longer the case and/or was it never based on actual data?

Peter



Edited 1 time(s). Last edit at 10/10/2015 02:03PM by safib.

Quote

My EP believes that greater frequency and shorter duration for the same AF burden (especially durations exclusively on the order of minutes) entails far less risk of stroke. I asked if there was any statistical analysis but he did not know.

Your EP's assertion make sense from a fluid dynamics perspective.

It is commonly believed that most of the stroke risk associated with afib is due to the suboptimal fluid flow during afib. When the atria are in afib, blood in the LAA tends to pool/stagnate, rather than being moved through the heart along with the rest of the blood. It's that pool of not moving blood that tends to clot. If one has (say) 4 hours of afib, that's a 4 hour window for the clots to form. But if that 4 hrs is broken up into shorter windows (say multiple episodes of 5 minutes), then between each afib mini-episode the stagnant blood gets flushed out... thereby disrupting the clot formation process. Which is a good thing, and would (so the argument goes) reduce the risk of stroke from clots formed in the LAA.

Apache - that might be the case in instances where the blood viscosity, itself, was not conducive to clotting tendencies.
Check my recent response to Mike F about sticky, thick blood and the risk of stroke or MI.. and the other related links provided. [www.afibbers.org]

Also don't rule out age, itself. It's commented on frequently that age plays a significant role in stroke risk. Some say starting about age 60 the risk starts to increase; yet younger patients are known to form clots...which probably has to do with the hyperviscosity factor.

Additionally, the timing of the afib can help promote the tendency for clotting... ie, in the wee hours during sleep, clotting tendencies are greater due to PAI-1 levels of PAI-1 ...( Plasminogen Acitvator Inhibitor )

From CR 38 - page 12 [www.afibbers.org]

PLASMINOGEN ACTIVATOR INHIBITOR 1 (PAI-1)
Plasminogen activator inhibitor (PAI-1) is the primary inhibitor of tPA and other plasminogen activators in the blood.
During fibrinolysis, tissue plasminogen activator (tPA) converts the inactive protein, plasminogen, into plasmin.
Plasmin, in turn plays a critical role in fibrinolysis by degrading fibrin and also provides other localized protase
activities.

Increased PAI-1 levels are associated with a number of atherosclerotic risk factors. PAI-1 has been shown to act as a
prothrombic factor in both arterial and venous thromboembolic disorders. Increased levels are associated with an
increased incidence of acute coronary syndrome and acute and chronic artery disease in patients who suffer re-
stenosis after coronary angioplasty.

Of particular significance for this discussion is that increased PAI-1 levels may reduce the effectiveness of anti-
thrombolytic therapy.(9)

There is a correlation between the circadian variation in the time of onset of myocardial infarction, with the highest
incidence at about 8 a.m. and the circadian rhythm of plasma PAI-1 activity, which is also highest early in the morning
(10)

The inactivation of PAI-1 is directly related to the enhancement of fibrinolysis.(11) Studies have shown nattokinase
important in this mechanism.

The bottom line – there are elevated levels of PAI-1 at night and through the early morning. The most important dose
will be in the evening before bed to last until around 8 a.m.

TPA-1 is a most interesting research project all on its own because of its role in fibrosis. This piece only touches on
the one key issue for use when dosing with nattokinase.