AF and Strokes: Who is the real daddy

Atrial fibrillation is the most common heart rhythm disturbance in the world and can not only cause very unsettling symptoms but can also increase the patient’s risk of strokes. When you look at all the literature, we commonly read that AF increases the risk of strokes by 5 times.

The traditional thinking has been that when a person goes into AF, the atria stop contracting and therefore blood which would ordinarily be ejected from the atria into the ventricles is more likely to stagnate and therefore clot and this clot can sit within a beak shaped structure within the atria (otherwise known as the left atrial appendage) and someday this clot can get dislodged and travel out of the heart to either the brain to cause a stroke or to the somewhere else in the blood to cause a peripheral embolism. This hypothesis therefore has been the cornerstone of modern day management of AF where the detection of AF automatically triggers the consideration for eligibility for anticoagulant therapy; the idea being that if we could prevent clot forming when the blood is stagnant then we could reduce the risks of stroke. This strategy has been proven to be effective because studies suggest that by starting anticoagulant therapy, we can reduce the risk by about 60%. However anticoagulants aren’t without risk and it is therefore understandable when patients question why they should take anticoagulants for life even when they are not having frequent AF episodes. If AF causes stagnation of blood and this causes strokes (i.e if AF is the daddy of strokes), why should i take anticoagulants when i am not in AF or when the AF has been taken away by an ablation or a cardioversion?

There are indeed several studies over the last 20 years have questioned this traditional thinking..


As per this hypothesis, it would seem logical to assume that if AF causes stagnation of blood and that then leads to clots (i.e if AF is the daddy of strokes) then taking away the AF would stop the strokes happening because now the blood would not stagnate and therefore no further clots would form. However there were 2 big studies called RACE and AFFIRM which both showed that controlling the rhythm i.e taking away the AF did not appear to take away the strokes i.e patients continued to have strokes even when the AF had been taken away and this is the reason we recommend long term anticoagulation.

If we think about this hypothesis again it would again seem logical to think that if AF were the parent of strokes then surely there would be a temporal relationship between the AF and the stroke i.e you would expect the risk of strokes to be much greater within a certain time period of the appearance of AF. Again this has not been shown. There was a very interesting study called ASSERT. This study looked at 2580 patients with heart monitors/pacemakers which can detect even small episodes of AF and found that only 8% of patients who had strokes had any AF within 30 days of the stroke and 16% of patients actually had the first AF episode after the stroke. So again if AF were the daddy of stroke then surely it would have to precede the stroke which it doesn’t seem to on many occasions.

If AF were the cause of strokes then we would surely expect that the more the AF, the higher the risk yet again we fail to see a consistent relationship between the duration of AF, the permanence of AF, or even the rate of AF and strokes. In fact all the risk markers for stroke are to do with the patient’s age and comorbidities rather than with how much or how little AF they are getting.

Another interesting observation was that when you take young healthy people who have AF, they seem to tolerate it very badly but don't tend to have strokes whereas if you take older sicker patients, they may not even know they are in AF yet they seem to be at a much higher risk of strokes. Same AF but very different stroke risk - that again does not fit.

So based on all these observations we have to rethink this hypothesis. If we were sitting in a paternity lawsuit, it would be difficult to condemn AF as being guilty of being the father of strokes. They do seem to be in the same places but that’s about it. There does not appear be any convincing evidence that AF causes the strokes. So who is the real daddy?