How does a stroke episode occur in an AF patient?
The heart rate needs to be racing to start the sequences of pooling and stagant blood to form the clot first?
Anyone knows where can i find such scientific information?
The percieved wisdom is that when a patient has atrial fibrillation, becasue the atrium is not contracting in a regular fashion blood can eddy and pool. especially in the left atrial appendage. This allows clots to form. At any time it feel like it, that clot may then be ejected and because it has formed in the heart it will be larger than say a thrombosis in a leg vein. This means that when it hits the brain it will kill off a much larger area which is why AF related strokes are so devastating and why anticoagulation in people with AF is so important. .
This sequence has no relationship to heart rate or any other goings on and can happen at any time although of course raised BP can increase likelyhood. So to answer your question no the heart does not neeed to be racing. Remember that many unfortunate people do not know that they have AF until that devastating stroke. which is why detection and protection are so important.
As Bob says the heart doesn’t need to be racing. When I went in for an ablation in August, I was all drugged up and didn’t notice any tachycardia or AFib in the days leading up to the procedure. I took my last anticoagulant 48 hours before the procedure as instructed. They couldn’t go ahead with the ablation because they found a clot in my left atrial appendage when they did the transoesophageal echocardiogram. My EP was very surprised and said it’s very rare that they see clots in anticoagulated patients that but I had/have aggressive arrhythmias. My story could have had a very different ending had that clot travelled to my brain.
What is an aggressive arrhythmia?
I have 3 different arrhythmias - atrial flutter, atrial fibrillation and atrial tachycardia and so my heart sometimes goes crazy. So in the 48 hours after taking my last anticoagulants and before my procedure, the blood obviously wasn’t flowing properly, hence the formation of the blood clot.
Is there any systematic way to classify the severity of an AF that will lead to life threathening event based on e.g. unmedicated heart rate, blood pressure etc.?
Any detail study on if clot can form, but may or may not break off? What conditions increase or decrease the likelihood of the danger of a clot other than using a blood thinner (e.g. bmi, regular exercise, stressful event, blood pressure etc.)
What about how frequent is stagnant blood pool in an AF patient? Once there is pooling, does the heart clear them usually in the next few strokes? Does anti oxidants from food play a role in preventing clot formation?
No because we are all different.
It could be there is no studies done in this area. Usually in a disease state there will be detailed pathological steps. My dad has been off apixaban ordered by the doc for a month due to anemia. Surprisingly, he seems better mentally and energy wise without it. Could apixaban be the same case as statin, with most studies showing its superiority over asprin funded by organisations with financial interest?
It is important to understand that aspirin is not an anticoagulant it is an anti-platelet and whilst it has some uses in cardiac care it does not in stroke prevention especially in AF. NICE who are an independent government body charged with making sure that any treatments or drugs used are fit for purpose, removed aspirin from this purpose in 2014. Regardless of which anticoagulation you choose to use it will be superior to aspirin in every way. This has nothing to do with finacial interest and is what we at AF Association (a registered charity) have been saying for many years. Personally having taken Warfarin for fifteen years with zero problems I see no point in changing but some people have difficulties in mainatining a steady INR and for those peoeple the DOACs such as apixaban are literally a life saver.
I just come across a 2017 study done in usa that concluded that both anti coagulant and anti platelets medicine do not help in reducing stroke risk in mild AF patients.
With regards to asprin do not reduce risk of stroke in AF patients. That big study funded by maker of apixaban actually shows that asprin do has significant benefit, just that their result indicate that apixaban is more superior. Maybe we wont be seeing another study not funded by the maker to double confirm on these findings siding apixaban.
Redshock has a point. One of the trials for Apixaban was Averroes which compared it to aspirin, which it had no trouble beating. Its trial against warfarin (Aristotle) was sponsored by the makers, Bristol-Myers Squibb and Pfizer. It was criticised as there was apparently fraud associated with part of the trial:
and also the peer review process was poor and the TTR for warfarin users was only 62%:
As regards what causes strokes, there is still no clear answer but it seems more associated with the inflamed inner surface of the heart rather than just a plumbing issue. That is why ablations tend not to reduce stroke risk.
I graduated with a degree specialised in human nutrition. In the pathology unit i did, all the disease states have very detailed flow chart. I am quite surprised to still be unable to find such details regarding AF causing a stroke. The details i am hoping to find is regarding what factors increases the risk of pooling of blood in the atria, how long does it need to remain stagnant to form a clot, can initial pooling be cleared by the heart naturally in the next few beats, whether regular exercise reduce risk of pooling, what about those af patients that ate plenty of carotenoids and anti oxidants from fruit and veg (can there be a protective effect?), whether there is any interactions between certain food with apixaban. From what i found so far, no studies has ever compare the blood levels of apixaban on subjects eating varied amount of fresh fruits and veg. Given that this diet is protective in many ways, but many fruits and veg also contains natural substances in high enough amount to affect several detoxification pathways in the body.
I didn't want to take anti coagulants but I was told I may not even feel the AF episode and a clot could form in minutes. It can stick to the inside of the heart and break away later.
I have been on Wafarin for 3 years. I use a home INR tester and test 2x a week to keep it well controlled. I buy test strips on eBay.
Why not apixaban instead? U dun need to test anything.
Exactly like Kaz I had a clot in LAA found by a TOE before an ablation. I think it formed in the 5 days I was off warfarin. That's how quick it can happen. It was 6 months before they were happy that it had dissolved and went ahead with ablation.
I had a patient once who was an engineer. He sounds very much like you. Unfortunately human beings are idiosyncratic and so are their responses to medication. I too like to know how things work but moderation in everything ( even my thirst for knowledge!) leads to a balanced outlook.
I am fortunate to have few hiccups with my ailments so in spite of popping on here regularly and another forum, I have come to the conclusion some things just can't be explained completely........yet.
General anaesthetic is another conundrum.
I am a scientist and decided to have a look at the data -- the Framlingham study.
What that shows is that if you have (or have had) a) coronary heart disease b) hypertension (increased blood pressure) or c) cardiac failure then you are more likely to have a stroke. If you have none of these conditions then there is no data in from that study.
The risk that AF (and NOT the 3 factors above) is causing the stroke only become important once you are over 80 years old, although at >70 there is some slight increased risk down to AF.
I am not aware of any data to support the use of medication or its effectiveness in reducing this risk. There may be additional data on both points but I am not aware of it.
Many of the above comments are based on "what seems to make sense" but that is a poor way to do things. The Greeks did that and during the 1800s people realised that logic and argument must be supported by observation.
A healthy lifestyle is worth a lot...
I hope this helps
Hi Whiteface there is no mention of CHA₂DS₂-VASc Score for Atrial Fibrillation Stroke Risk in your post which includes other risk factors in addition to medical comorbidities.
It is recommended by NICE and my doctor that I take an anticoagulant based on a CHADS score of 3 which includes 1 point for being over 65, 1 additional point for being female+over 65 (neither of those factors seem to be on your list) and 1 point for having a comorbidity ie high blood pressure.
Bob D has explained in his post above about the possibility of blood pooling especially in the left atrial appendage during AF allowing clots to form and I have seen the same information repeated many times in articles and on stroke and heart advisory sites and it seems logical to me that this could happen. Even if my CHADS score was 0 it would still seem possible to me that pooling blood in the atria could make me more susceptible to strokes and I would feel happier taking an anticoagulant.
So regardless of the Framlingham study, I prefer to make my own decisions on anticoagulation based on the advice of doctors /common sense/logic/my own research and the experience of other members here.
There is logic in the analysis of the many different reports on stroke risk. However all l I can say is that there are many forum users myself included, who have non of the other stroke indicators such as high weight, high blood pressure, high cholesterol etc . Because of our low risk we were not given an anticoagulant and unfortunately we went on to have strokes or TIAs really soon afterwards. I read somewhere recently that people with a certain shape of left atrial appendage have more chance of developing and retaining a clot and I must admit that this makes sense to me. X
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