The safety of AF ablation depends greatly on the adequacy of blood thinning. AF ablation is no cardioversion.
The choices of blood thinning regimens include either warfarin or dabigatran (Pradaxa)–and soon perhaps rivaroxaban or apixaban. The advantages of warfarin include the ability to confirm the level of thinness and its long-acting properties lessen after-procedure gaps when a patient has no blood thinner on board.
On the other hand, contrary to mass media reports, thousands of AF patients are taking dabigatran without any issues. When these patients come for ablation, a decision has to be made: do they switch over to warfarin (and risk the volatility of the switch) or do they stay on dabigatran.
This choice represents a great debate in electrophysiology. It sure would be easier to keep dabigatran-treated patients on the drug before ablation procedures. But it’s not only just the convenience; dabigatran’s success or failure around the time of an AF ablation speaks to its prowess as a blood-thinner. If it can protect patients in such a thrombogenic (clot-risk) procedure as left atrial ablation, well then, that says something about the drug.
Going into the Heart Rhythm sessions last week, the prevailing wisdom held that warfarin was the better choice for patients set to have AF ablation. The negativity of dabigatran stemmed from only one trial. The eminent authors of this trial voiced strong negative opinions on dabigatran. I read the paper and was less negative, but I’m far less eminent.
At last week’s HRS sessions, there were eight abstracts on dabigatran as a periprocedure blood thinner, and six of the eight directly compared dabigatran with warfarin.
In my most recent Trials and Fibrillations post over at theHeart.org, I summarized the pre-HRS trials, the eight abstracts presented at HRS and then even add a little “Mandrola” statistics on the summation of the six comparison studies.
Though the post is a tad long, I believe it encompasses most of the known evidence base on this important and increasingly frequent conundrum.
Head over to see how it ended up.
Keep in mind that this hot topic will likely grow hotter as more AF patients pursue treatment with non-warfarin blood thinners, like rivaroxaban and apixaban.
JMM
8 replies on “Is dabigatran (Pradaxa) acceptable as a periprocedural anticoagulant for AF ablation?”
Nice discussion by Dr. Mandrola at theHeart.org site – which to me is balanced and completely appropriate in its conclusions. Dabigatran is not superior (compared to warfarin) as a perioprocedure anticoagulant prior to AFib ablation. It is difficult to know at this time if it is worth switching anticoagulants (if the patient has been on dabigatran) prior to the major procedure of AF ablation.
THANKS for synthesizing and putting data-to-date in perspective!
Thanks Ken. If we ever meet in person, I’m buying coffee. I appreciate your supportive words.
Dr John-
Long time reader of your blog.
Just my 2 cents.
Last July 17 I had ablation at a very competent hospital here in Michigan with a very highly rated/experienced/recommended EP.
Had been on Pradaxa about 3 month.
1 hr into procedure bleed began. Difficulty reversing blood thinning effects of Pradaxa. 5 litres of blood fluid products, 3 days cardiac ICU, plus nearly 1 yr to get back to normal.
4 earlier ablations with warafin with no bleeding.
No absolute proof. But no doubt in my mind that Pradaxa is a high risk drug treatment.
No science here. Only happy to be alive and not interested in coming anywher e near Pradaxa again.
Bob…
Sorry about your mishap.
You bring up a valid concern about dabi’s lack of reversibility. Thanks for doing so in a calm and measured tone. I appreciate that.
@Bob – All I can say is “Wow” … Brings up the truism of “n=1” (the “odds” not important if the one time it happens is you … ).
The “old school” in me is much less enthusiastic for new drugs and treatments until they’ve established a ‘track record’. That said – Dr. John does a GREAT job on this site presenting his views on the new with the old in proper perspective. The reality is that non-coumadin alternatives to anticoagulation are here to stay – though time clearly needed to figure out what their ultimate role will (should) be.
Final Thought on YOUR Case: Truly highlights the importance of collaborative decision-making together with the informed patient – since others on this site have shared very positive experiences with Pradaxa – whereas your experience is clearly reason to stop and rethink …
Back when I was on warfarin, I had to take about 7 mg per day to stay in the therapeutic range (which is remarkably narrow; my INR was 1.7 when I had a post ablation stroke). My elderly father only needs about 3 mg. .
Why is there such a huge difference? I only outweigh him by 20 lbs, so it can’t be just a simple matter of body mass.
How does a doctor determine the initial dose?
I am on dabigitran now, where one dosage fits all.
Your question about warfarin is an excellent one. Warfarin is notorious for its great individual variability of metabolism. Based largely on genetic makeups of liver enzymes, individuals process the drug differently. That’s why some need higher levels than others. Also, other medications and diet play a role in determining the correct dose of warfarin. Lately, genetic tests have been studied as a means to pick a low or high starting dose. I have little need for warfarin susceptibility tests because I just start low and work the dosage up according to the INR. Dabigatran and rivaroxaban work as standard dose agents because they lack warfarin’s variability of metabolism–though its important to note that patients with impaired kidney function require lower dosages.
Hi, I ‘d like to know if there are any anti-arrthymic drugs that dnt affect blood pressure?