Pooling Risk

It is well established that the stroke risk in AF comes from blood pooling in the left atrium appendage. Depending what, if any, comorbidities you may have there is a risk that a clot may form. What I'm wondering, is whether the type of AF you have affects this blood pooling and so are different types of AF more 'risky' than others? If one does not suffer giddiness, light headedness, etc, it seems to imply one's blood is still circulating okay. Does that lessen the impact of the blood pooling in the LAA. Just wondering because it could be yet another consideration when making a decision on anti coags.

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  • I don't have many symptoms with AF and can carry on much as normal. I didn't think I was in need of an anticoagulant because my circulation seemed OK. The medical world did not agree with me and nearly every one of the GPs at my surgery had a go at making me change my mind, as did a friend who is an anaesthetist. My family didn't see my viewpoint and I felt very out of step. The only person on my side was my other half. Scared of that stoke which was clearly right ahead, I gave in and then was even more scared of a haemorrhage which seemed equally imminent.

  • My understanding is .... AF is AF - particularly if your left atrium is damaged. If it is damaged then the risk is there ... end of ! I also think genetics comes into it and if either side of your family have a track record of strokes (be they AF in origin or from another cause) then going on anticoags is a no brainer.

    John

  • Google for articles like this as it seems that the shape of the LAA and how well it functions is the key to risk.

    medpagetoday.com/cardiology...

    medscape.com/viewarticle/82...

  • Very interesting x

  • Some of the stroke risk of AF comes from blood pooling in the left atrium during AF. However there are a lot of other factors as well. LAA shape has been mentioned. An association has been reported between inflammation of the heart surface and the stroke risk in AF patients and this is indicated by higher C-reactive protein levels in AF patients. AF patients also have higher levels of von Willebrand factor (vWF), also caused by inflammation. This also causes clotting.

    So this is why people need to continue with anti-coagulation after a successful ablation, at least until more trials are done. Some of the risk has reduced, but the interior heart surface is still inflamed - that caused the AF in the first place and that can still cause strokes.

    For more details see:

    j-stroke.org/journal/view.p...

    "The Mechanism of and Preventive Therapy for Stroke in Patients with Atrial Fibrillation"

  • Well, some cardios challenge this view. For example Sanjay Gupta has done a youtube video in which he presents his viewpoint and evidence that AF doesn't cause blood clotting and strokes - AF is a signpost to stroke risk, but not a direct cause of it. On another tack, I've read some studies which show that paroxysmal AF has half the stroke risk of permanent AF - e.g. in 2014 a European cardio organisation studied 6,000 AF cases and came to this conclusion. This could be interpreted as a weaker/stronger effect, either causative or signposting.

  • Very interesting replies. I found this paragraph from one of the links to be a little disturbing though:

    "These findings are important because patients deemed to have a low stroke risk based on the CHADS2 score could actually be at a higher risk if they have a non-Chicken Wing morphology, Natalie and colleagues concluded."

    How does one go about finding out what type of LAA one has?

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