This post is in introduction to my most recent column over at Trials and Fibrillations on Medscape | Cardiology.
If I had just one thing to say to patients and doctors about the disease atrial fibrillation it would be this:
Be as scared of AF treatment as you are of the disease.
Yes, it is true: AF can make people feel bad. (It sure did that to me.) It induces fear in both patients and caregivers. And, AF also increases the risk for stroke and heart failure in the future. The emphasis being on the future–as in weeks, months, and years, not usually tomorrow.
One striking aspect of the mainstreamâ€”non-electrophysiologyâ€”way of treating AF is the urgency. It seems everyone is in a rush. This is not good, especially when the topic of shocking the static fibrillating atria back to regular rhythm is concerned. Here I am talking about cardioversion, which is a severe euphemism for high-voltage shocks. (Wait. can euphemisms actually be severe?) But make no mistake; shocking the heart is no small thing, especially when patients are not taking an anticoagulant drug.
As an AF doctor, I spend endless hours undoing fearâ€”and the dangerous stuff that comes from fear. One is surely the rush to get people out of AF quickly. These are busy people who are feeling terrible, after all. They need to get back to their inflamed lives.
There exists this legend that if AF has been ongoing for less than 48 hours, it is safe to shock (cardiovert) the patient without using an anticoagulant drug.
A new study from a Finnish research group, published today in the Journal of the American Medical Association, sheds important light on this frequently encountered scenario–a decidedly cautionary light.
Many years ago, I was involved in the care of middle-aged professional man who died after such an unprotected cardioversion. This case, and the new data, moved me to write about the matter of shocking people without the protection of anticoagulant drugs.
Here is the link and title of the post: Cardioversion for New-Onset AF: Time to Hit the Pause Button?
7 replies on “Shocking AF — What’s the rush?”
Thanks for calming everybody down on this subject…
Dr John, for general information, can you say how far atrial remodeling might proceed in the three to four weeks you suggest waiting?
Might you also be able to say if you’d recommend the same patience before cardioverting for atrial tachycardia?
The above 2009 article makes the case that more than half of the cases of afib that present in an ER self- convert within 48 hours anyway. It also says for those with persistent afib, cardioversion doesnâ€™t result in maintenance of NSR in other than the short term. So there is little value from an NSR standpoint. Then he goes on to say, what really matters is that afib is a risk â€œmarkerâ€ not a risk â€œfactorâ€, and therefore, maintenance of sinus rhythm has little effect on outcomes: death, stroke, ventricular function/heart failure, and symptoms.
Note that this article is broader than just cardioversion. But the point is that, in most cases, cardioversion has little effect on NSR maintenance and, more importantly, outcomes.
Further, â€œUrgently terminating AF has at least 1 other potential drawback. One of the scourges of electrical cardioversion is immediate or early recurrence of AF. It turns out, somewhat unexpectedly, that immediate or early recurrence of AF is more common the sooner after the onset of AF that one is electrically cardioverted.â€
Wow! Thatâ€™s a big statement!
To me, putting myself at risk for stroke by not waiting to be properly anticoagulated before they perform a procedure that has little effect on long term outcomes anyway, seems foolish.
I agree with youâ€¦
For most with afib-â€¦ cardioversionâ€¦whatâ€™s the rush?
To me, personallyâ€¦ cardioversion- whatâ€™s the use?
In regard to the other comment on Medscape: Note that heart disease isn’t the only thing that ups your risk for stroke. Many at high risk for stroke will not self convert in 18 hours because they don’t have heart disease.
Jeff: If Dr. John has a definitive answer on extent of remodeling in 28 days, I will be shocked and astounded.
Remodeling. That and time is what leads from paroxysmal to persistent and permanent.
How much time, more-or-less? Weeks? Years?
It leads to fibrosis, and you don’t reverse that so easily.
What factors might influence that?
I’m just asking if our Dr John might be able to say what his ideas are.
Maybe there’s something a bit more clinical than the four table legs – which I’ve paid great attention to since well before he ever expressed the concept:
Good food, mellow attitude, exercise – all in moderation, of course – and good sleep.
Of course. Might there be any better ways to avoid inflammation?
( Could? Might? Maybe? I’m not asking for definitive. But who better to ask for educated guesses?)
I meant “even though” they don’t have heart disease (not “because”).
The one case that shocked me was a patient who came for a second TEE after 4 weeks of anticoagulation with a NOAC because on the first TEE we had found a thrombus in his LAA. Well, it was still there, so no cardioversion this time either, but had we not done the first TEE, he would have had his cardioversion with a thrombus. Makes me want a TEE if I ever get AF.
Would a TEE be sufficient?