Atrial Fibrillation (AFib) Support Group
Atrial fibrillation (AF or afib) is an abnormal heart rhythm (cardiac arrhythmia) which involves the two small, upper heart chambers (the atria). Heart beats in a normal heart begin after electricity generated in the atria by the sinoatrial node spread through the heart and cause contraction of the heart muscle and pumping of blood.
A noteworthy study was published in the prestigious European Heart Journal last week:
http://www.ncbi.nlm.nih.gov/pubmed/25187524
The authors analyzed how the pattern of a-fib occurrence (i.e., paroxysmal, persistent, or permanent) correlated with stroke risk. Recall the discussions here about whether a 2-hour bout of a-fib is any safer than a week-long bout. So the study is especially noteworthy because they analyzed a large population -- 6563 patients being treated with aspirin and no NOACs.
Yearly stroke rates were 2.1, 3.0, and 4.2% for subjects with paroxysmal, persistent, and permanent a-fib. Age > 75 years, sex, history of stroke or TIA, and AF pattern were independent predictors of stroke, and a-fib pattern, namely persistent a-fib, was the second strongest predictor of stroke.
Here is the final paragraph of the discussion: "Our data show that patients with permanent a-fib are at a higher risk of stroke compared with patients with non-permanent a-fib. Although permanent a-fib increased the risk of embolic events by 50-100% in patients with a CHA2DS2-VASC score of 2 or greater, patients with paroxysmal a-fib still had yearly stroke rates of at least 2%. This confirms the recommendations that patients with a high clinical risk of stroke should be anticoagulated regardless of their a-fib pattern. However, in deciding whether to offer anticoagulation to low-risk patients, where the risk to benefit ratio of anticoagulation is less clear, it may be useful to consider the pattern of a-fib occurrence, or perhaps more simply, whether the patient is currently in sinus rhythm or not."
Some insightful nuggets in there. Most intriguing to me is the final sentence, which suggest to me that the study authors are advocating for a pill-out-of-pocket approach for anti-coagulating younger subjects with paroxysmal a-fib and low stroke risk.
Sean
http://www.ncbi.nlm.nih.gov/pubmed/25187524
The authors analyzed how the pattern of a-fib occurrence (i.e., paroxysmal, persistent, or permanent) correlated with stroke risk. Recall the discussions here about whether a 2-hour bout of a-fib is any safer than a week-long bout. So the study is especially noteworthy because they analyzed a large population -- 6563 patients being treated with aspirin and no NOACs.
Yearly stroke rates were 2.1, 3.0, and 4.2% for subjects with paroxysmal, persistent, and permanent a-fib. Age > 75 years, sex, history of stroke or TIA, and AF pattern were independent predictors of stroke, and a-fib pattern, namely persistent a-fib, was the second strongest predictor of stroke.
Here is the final paragraph of the discussion: "Our data show that patients with permanent a-fib are at a higher risk of stroke compared with patients with non-permanent a-fib. Although permanent a-fib increased the risk of embolic events by 50-100% in patients with a CHA2DS2-VASC score of 2 or greater, patients with paroxysmal a-fib still had yearly stroke rates of at least 2%. This confirms the recommendations that patients with a high clinical risk of stroke should be anticoagulated regardless of their a-fib pattern. However, in deciding whether to offer anticoagulation to low-risk patients, where the risk to benefit ratio of anticoagulation is less clear, it may be useful to consider the pattern of a-fib occurrence, or perhaps more simply, whether the patient is currently in sinus rhythm or not."
Some insightful nuggets in there. Most intriguing to me is the final sentence, which suggest to me that the study authors are advocating for a pill-out-of-pocket approach for anti-coagulating younger subjects with paroxysmal a-fib and low stroke risk.
Sean
My concern with the theory is that anticoagulants don't break up clots, they only prevent them (usually). What if you were asymptomatic as they say most symptomatic afibbers are? And how would you know when to stop anticoagulation? Remember that most paroxysmal clots are thrown after the afibber returns to NSR. Cardioversion has resulted in strokes a month after a person is back in afib. While this study shows that more persistent afib has higher risk annually, it also demonstrates that paroxysmal afibbers are more likely to have a stroke around the time (and after) a person is in afib with a daily stroke risk so high that it almost equals afib that is 24/7/365. So the PIP NOAC management is super critical in these dangerous times. If you had 12 episodes evenly spaced out during the year, you probably would have to be on the anticoagulant all the time.
I read that Coumadin/Warfarin has a rebound effect when you stop. So there's another problem. They haven't studied the NOACs in that regard.
Silent afib, when to stop, and possible rebound effect would make me nervous. It seems a low CHA2DS2Vasc score still trumps afib type, no matter what study you use. If your score is zero, your risk is zero. If your score is 1, your risk is pretty close to 1.
My 2 cents.
petey
"Remember that most paroxysmal clots are thrown after the afibber returns to NSR. Cardioversion has resulted in strokes a month after a person is back in afib."
I recall being told this as well by a Dr. in the hospital that the danger zone is that small window of time returning to NSR after being in AFiB.
I also recall being told late during the very first night I spent in the hospital after being admitted via the ER by an EP, that I had a 40% chance of having a stroke sometime during the night.
This was very comforting information and did wonders for my stress levels and inability to get any sleep whatsoever. Lol.
D.
I should have fron-tloaded my post with my main intention: to empower the patient with the latest, good science. To be discussed with the docs. Often times, the EPs just don't have time to keep up with the emerging scientific literature.
Petey, you make several good points. I just wish we knew more about how long the window of extreme stroke risk is following a bout of a-fib. Indeed, the clots can lodge in the left atrial appendage, and there may very well be no calculated rhyme or reason to how long it will take for the clot to emerge and set a course to the carotid artery. The clot should, theoretically, though degrade over time -- this is our vascular system's default activity -- to begin breaking down clots once they have formed. A clot should not reside long in the appendage.
I'm seriously considering have my left atrial appendage closed off during the surgery that I am evaluating. Seems like the right thing to do. I just don't understand how that clipped appendage doesn't become necrotic and fall off some decade much further in to life. Decades after clip or closure which have not been studied yet because the procedure is relatively new.
Cheers,
Sean