The skeptical cardiologist is a firm believer in the benefit of maintaining normal rhythm in most patients who develop atrial fibrillation (AF, see here.)
Sometimes this can be accomplished by lifestyle changes (losing pounds and cutting back on alcohol , treating sleep apnea, etc.) but more often successful long term maintenance of normal rhythm (NSR) requires a judicious combination of medications and electrical cardioversions (ECV).
It is also greatly facilitated by a compliant and knowledgeable patient who is regularly self-monitoring with a personal ECG device.
My article on electrical cardioversion (see here) was inspired by a patient (we’ll call her Sandy) who asked me in April of 2016, “how many times can you shock the heart?”
In 2016 I performed her fifth cardioversion and last week I did her sixth.
Her story of AF is a common one which exemplifies how excellent medical management of AF can cure heart failure and mitral regurgitation and create decades of AF-free, happy and healthy existence.
A Tale Of Six Cardioversions
Sandy had her first episode of atrial fibrillation in 2001 and underwent a cardioversion at that time and as far as she knew had no AF problems for 14 years. I’ve seen numerous cases like this where following a cardioversion, patients maintain NSR for a long time without medications but I’ve also seen many in whom AF came back in days to months.
In 2015 she saw her PCP for routine follow-up and AF with a rapid rate was detected. She had been noticing shortness of breath on exertion and a cough at night but otherwise had no clue she was out of rhythm.
When I saw her in consultation she was in heart failure and her echocardiogram demonstrated a left ventricular ejection fraction of 50% with severe mitral regurgitation. She quickly went back into AF after an electrical cardioverson (ECV) and reverted to AF again following a repeat ECV after four days on amiodarone.
Since amiodarone can take months to reach effective levels in the heart we tried one more time to cardiovert after loading on higher dosage amiodarone for one month. This time she stayed in NSR
Following that cardioversion she has done extremely well. Her shortness of breath resolved and follow up echocardiograms have demonstrated resolution of her mitral regurgitation.
She had purchased a Kardia mobile ECG device for personal monitoring of her rhythm and we were able to monitor her rhythm using the KardiaPro dashboard. Recordings showed she was consistently maintaining NSR after her 2016 ECV
Image from my online KardiaPro Dashboard showing the date and HR of patient’s home ECG recordings leading up to the cardioversion and following it. The orange dots were Kardia diagnosed AF and following the cardioversion the green dots are NSR.
I’ve written extensively on the great value of KardiaPro used in conjunction with the Kardia mobile ECG device for monitoring patients pre and post cardioversion for atrial fibrillation. Sandy does a great job of making frequent Kardia ECG recordings, almost on a daily basis so even though she has no symptoms we are alerted to any AF within 24 hours of it happening.
Amiodarone-The Big Medical Gun For Stopping Atrial Fibrillation
The recurrence of AF Sandy had in 2016 occurred 8 months after I had lowered her amiodarone dosage to 100 mg daily.
Amiodarone is a unique drug in the AF toolkit.
It is the by far the most effective drug for maintaining sinus rhythm, an effect that makes it our most useful antiarrhythmic drug (AAD).
- It is cheap and well-tolerated.
- Uniquely among drugs that we use for controlling atrial fibrillation it takes a long time to build up in heart tissue and a long time to wear off.
- It is the safest antiarrhythmic drug from a cardiac standpoint. Unlike many of the other AADs we don’t have to worry about pro-arrhythmia (bringing out more dangerous rhythms such as ventricular tachycardia or ventricular fibrillation) with amio.
- Amiodarone, however, is not for all patients-it has significant long term side effects that necessitate constant vigilance by prescribing physicians including thyroid, liver and lung toxicity.
I monitor my patients on amiodarone with thyroid and liver blood tests every 4 months and a chest x-ray yearly and I try to utilize the minimal dosage that will keep them out of AF.
In Sandy’s case it was apparent that 100 mg was too little but with an increase back to 200 mg daily, the AF remained at bay.
In early 2017, Sandy read on Facebook that amio was a “poison” and after discussing risks and benefits we decided to lower the dosage to 200 mg alternating with 100 mg. It is common and appropriate for patients to be fearful of the potential long term and serious consequences of medications. For any patient taking amiodarone I always offer the option of stopping the drug with the understanding that there is a strong likelihood of recurrent AF within 3 months once the drug wears off.
In October, 2018 with Sandy continuing to show normal heart function and maintain SR as documented by her daily Kardia ECG tracings we decided to further lower the dosage to 100 mg daily.
Six months later she noted one day that her Kardia reading was showing a heart rate of 159 bpm and diagnosing atrial fibrillation. AF had recurred on the lower dosage of amiodarone. She had no symptoms but based on prior experience we knew that soon she would go into heart failure.
Image from my online KardiaPro report on Sandy showing all green dots (NSR) until she went into AF (orange dots). Upon discharge from the hospital the daily Kardia recordings now show NSR (green dots).
Thus, her amiodarone was increased and a sixth cardioversion was performed. We could find no trigger for this episode (unless the bloody mary she consumed at a Mother’s Day Brunch 2 days prior was the culprit.)
Medical Management With Antiarrhythmics Versus Ablation
Many patients seek a “cure” for atrial fibrillation. They hear from friends and neighbors or the interweb of ablation or surgical procedures that promise this. Stopafib.org, for example, promotes these types of procedures saying “Catheter ablation and surgical maze procedures cure atrial fibrillation”
In my experience the majority of patients receiving ablation or surgical procedures (Maze procedure and its variants) ultimately end up having recurrent episodes of atrial fibrillation. Guidelines do not suggest that anticoagulants can be stopped in such patients. Often, they end up on AADs.
I’ve prepared a whole post on ablation for AF but the bottom line is that there is no evidence that ablation lowers the AF patient’s risk of dying, stroke, or bleeding. My post will dig deeper into the risks and benefits of ablation.
There is no cure for AF, surgical, catheter-based or medical.
In the right hands most patients can do very well with medical management combined with occasional cardioversion.
Who posseses the right hands?
In my opinion, most AF patients are best served by a cardiologist who has a special interest in atrial fibrillation and takes the time to read extensively and keep up with the latest developments and guideline recommendations in the area. This does not need to a be an electrophysiologist (EP doctor-one who specializes in the electrical abnormalities of the heart and performs ablations, pacemakers and defibrillators.)
I have a ton of respect for the EP doctors I work with and send patients to but I think that when it comes to doing invasive, risky procedures the decision should be based on a referral/recommendation from a cardiologist who is not doing the procedure.
In many areas of cardiology we are moving toward an interdisciplinary team of diagnosticians, interventionalists, surgeons and non-cardiac specialists to make decisions on performance of high-risk and high-cost but high-benefit procedures like valve repair and replacement, closure of PFOs and implantation of left atrial appendage closure devices.
It makes sense that decisions to perform high-risk , high-cost atrial fibrillation procedures also be determined by a multi-disciplinary team with members who don’t do the procedure.
This is a rule of thumb that can also be applied to many surgical procedures as well. For example, the decision to proceed to surgical treatment of carotid artery blockages (carotid endarterectomy) is typically made by the vascular surgeons who perform the procedure. In my opinion this decision should be made by a neurologist with expertise in neurovascular disease combined with a good cardiologist who has kept up with the latest studies on the risks and benefits of carotid surgery and is fully briefed on the latest guideline recommendations.
Unbenightedly Yours,
-ACP
23 thoughts on “Enlightened Medical Management of Atrial Fibrillation: Part I. Amiodarone, Kardia And Cardioversions”
Had lots of debilitating short runs of tachycardia mixed with plenty of PVCs this last early Spring. Was put on the large “loading dose” of amiodarone a couple of weeks later. Was on ZIO patch at the time, so everything was documented.
Wonderful! The arrhythmias stopped cold the next day.
Not so wonderful: One week in I utterly stopped sleeping.
Each time I might have nodded off I startled awake, adrenalin pumping my heart – though not not tachycardia. After three days of this I quit amiodarone temporarily and ten days later went back to four half-pills a week (400mg/week). Naturally, after another ten days I wound up in ER with continuous tachy of 130 to 140. That didn’t last long because I had taken 400mg at a pop before getting driven in to ER. Up & down. In & out. I seem to be very sensitive to the stuff. My window of treatment is very narrow. Currently, at 900md/week, I have just a few arrhythmia runs that I can cope with, but my sleep debt is getting me down.
Ever seen this response before? Wondering what to do now, as amio has been characterized to me as my last resort. (already had four ablations.)
Jeff,
Amiodarone can cause neurologic disturbances like your sleep problem. Usually this is at higher dosages and it has been rare in my patients.
900 mg/week is on the lowish side. I think your approach is the best one-titrating the dosage to minimize the sleep disturbance while keeping the arrhythmia disturbance at bay.
dr. P
Amiodarone: scary. But effective.
You refer to younger patients with heart failure being transitioned to flecainide when function improves.
Would it be true to say that, with artificial support of normal sinus rhythm, reverse remodeling could be expected – to some degree?
Jeffrey,
Yes. With long term maintenance of SR we will see resolution or improvement in LA enlargement, LA function and other cardiac effects created by atrial fibrillation (mitral and tricuspid regurgitation)
All of this (plus lifestyle changes hopefully) mean we are less likely to need the big gun, amiodarone, and can switch to the smaller gun, flecainide
Dr P
I have been reading through some of the older stuff, a treasure trove of great information, so thankful for your blog.
Amiodarone is a really fascinating compound, I thought it was interesting that it is classified as K+ channel blocker but actually exhibits characteristics of all 4 classes of AAR drugs. It made me wonder if that quality is what makes it so versatile especially for AF. In learning more about action potentials of CMs, the slow vs fast, in theory, I thought it was intriguing how a drug like amiodarone could potentially impact slow action potential CMs since K+, Na+ and Ca++ all play a part in the depolarization of the SA node CMs. I know AF has many etiologies and still much of it is idiopathic but thought there had to be some explanation why amio is efficacious in conversion. Do you have any insights or theories as to why it is so efficacious and do you think its cross the board influence on multiple ion channels and adrenergic receptors is a reasonable thought as to why it so efficacious in converting AF to SR?
I have also read/heard that amio is really harsh on lungs, liver and thyroid (it apparently is very close in chemical structure to T4). You mentioned that you think amio is a good drug and that you are aware of these side effects and that you use the lowest dose possible to try and alleviate potential SEs. I am curious what is your experience, have you seen these side effects play out or do you think it is overblown? I know its varies from person to person regarding SEs but is there a dosage where you start seeing much more pronounced SEs in general?
Christian,
Yeah, amiodarone is unique and has been very helpful in my difficult afib patients. It is also a mainstay in the treatment of ventricular arrhythmias.
If I had to guess about its mechanisms I would agree with your thoughts. I find the mechanistic categorization of antiarrhythmics however (like Vaughn-Williams) not to be clinically helpful so most of that information drifts out of my brain very quickly.
Although it has clinically important side effects I would not describe it as “harsh” on any organ system.
I had held off on posting your comment because I was hoping to use it as a launch point to fully discuss side effects in a blog post but …time flies and it will likely be a while until I get to that.
I’ve probably touched on this in my afib posts or comments a few time but I find that in hundreds of patients on amiodarone for afib over 3 decades of treatment with an approach that utilizes quarterly lab tests and annual chest x-rays combined with regular follow up visits to discuss any possible side effects I have had no significant liver or lung issues. Hypothyroidism is not uncommon and easily treated with thyroid hormone and is typically ascribed to the iodine in amiodarone.
A few patients of developed hyperthyroidism and I have typically stopped the drug in them and with treatment they revert back to normal.
Dr. Pearson
I thought you’d be interested in this paper – just out:
“The Impact of Repeated Cardioversions for Atrial Fibrillation on Stroke, Hospitalizations, and Catheter Ablation Outcomes”
http://www.jafib.com/published.php?type=full&id=2164&is=previous_issue&f=full
Jeff,
Thanks for pointing this out for me. After scanning the paper and the journal it is in I don’t think we can obtain any useful information on repeat cardioversion.
It’s an extremely limited observational study. The factors that make a patient have multiple recurrent atrial fibrillation episodes that require recurrent cardioversions (confounding variables) are also the factors associated with worse overall outcomes.
I’ve written about the rise of bogus scientific journals and the weak papers that appear in them and this paper would not have been published in a strong cardiology journal.
Just had a cardioversion this last weekend. Fixed an atrial tachycardia one-to-one to the ventricles of 173 BPM.
First, however, the on-call cardiology resident in the ER was keen on trying adenosine. That was a strange and challenging experience. Stopped my heart for about 5 seconds. It felt as you might expect it to. He called it a “chemical cardioversion”. Didn’t work after two tries. Neither had the dilt drip. My systolic went low, scaring them into doing the electrical cardioversion promptly. Worked like a champ.
Next day the on-call electrophysiologist told me he would never have tried either dilt or adenosine considering my history.
Here’s the problem: If I had gone in to the arrhythmia clinic in this hospital during weekday business hours they would have popped me an electrical cardioversion on the spot. On the weekend however, I had to go to the ER where there is no EP on hand – only enthusiastic but less than fully knowledgeable cardiology residents. Far from ideal circumstances. Should they have a better arrangement?
So now I’m pondering requesting a “note” from my EP explaining specifically what the on-call people should and should not do next time this might happen on a weekend. They’re not gonna take MY word on what to do.
Reasonable?
The whole issue of how ER personnel should handle afib/flutter/atach is one worthy of deep analysis.
Your case is clearly a complicated one with an atrial tach that mimics another type of fast narrow complex rhythm, AV nodal re-enetry tachycardia or AVNRT. AVNRT response very nicely to adenosine but atach won’t. Complicated cases are always best managed by getting the input of an enlightened general cardiologist or an EP but garden variety AVNRT (the most common type of SVT) can easily be handled with adenosine without any consultation.
So if a patient knows that they are more complicated it makes sense to provide that guidance to the ER. Perhaps a copy of your 12 lead ECG in the atach rhythm with notation by your EP that says something like “this is atrial tachycadia with 1:1 conduction and should not be treated with adenosine or diltiazem. Call this number for on-call EP assistance in managing the case.” would be appropriate.
I am not a big fan of ER cardioversions of atrial fibrillation. I believe these should only be done under the supervision of an enlightened cardiologist. I’ve been meaning to write about that.
Just got back from a follow-up. The EP said, in no uncertain terms, that a “note” would not be forthcoming. To second-guess a future event in terms of the past is to risk missing something that might be more serious.
And, of course, therefore, there’s physician liability to consider.
I’m told that my arrhythmia clinic has EPs on call 24/7, so, if I wind up in a different hospital I can instruct that ER to “Call this number for on-call EP assistance in managing the case”, as you suggest, wherever I might be.
So, I’m… not quite… on my own.
The success of my AF ablation ended for me with atrial flutter about 8 months later – the reverse sequence of what you describe. How typical is that? Is there a logical sequence?
Thank you for the article and would the same treatment apply to atrial flutter?
Cantrell,
You’re welcome. Thank you for the great question.
For the most part atrial flutter can be handled as atrial fibrillation, however, there is one big difference and several smaller differences.
Ablation for atrial flutter is much more successful than that for atrial fibrillation. That being said, the two often coexist and I’ve seen lots of patients undergo flutter ablation only to end up with atrial fibrillation which requires another ablation.
Just to let you know (again) how much I appreciate this blog. Great stuff, as usual.
Dr.Pearson: I am sure Sandy is very grateful for your excellent medical management of her condition. I wish her many more years of a happy and healthy existence.
Thank you for an excellent article. Can you report how old “Sandy” was when you started the Amiodarone?
Kathy.
Thank you. It’s funny you should ask that. When I wrote “How Many Times Can You Shock The Heart?” which was based on her question to me, I apparently described her as “elderly.” She brought this up to me prior to her sixth cardioversion. I’ve found that it is never a good idea to call a patient old or elderly and when speaking to patients I’ll usually couch any discussion of that as “getting older”. And clearly chronologic age and biologic age don’t go hand in hand. In Sandy’s case she definitely met the Social Security and WHO definition of elderly as > than or = to 65 years of age in 2016 when I wrote that post but biologically behaves younger than her chronologic age. In fact, I now meet that definition and personally, I reject completely the idea that I’m old or elderly.
Your question prompted me to do a mini search on the topic and quite a bit has been written….like this…Ageing, an inevitable process, is commonly measured by chronological age and, as a convention, a person aged 65 years or more is often referred to as ‘elderly’.12,13 However, the ageing process is not uniform across the population due to differences in genetics, lifestyle, and overall health.14 Thus, chronological age fails to address the heterogeneity observed among the ‘elderly’, particularly in regard to their pharmacotherapy needs where pharmacokinetic and pharmacodynamic factors necessitate individualisation of regimens.14 However, there are no concrete definitions of ‘elderly’ that appropriately characterise this patient population; in using the generic terms ‘elderly’ and ‘older persons’ (even within this manuscript) there may be variable interpretations of the type of patients that is being referred to, and this is problematic when decisionmaking specifically refers to these. These issues have never been more relevant to clinical practice, given the increasing emphasis on patient-centred care.15 Although, much attention has been paid to developing models and tools which help to individualise therapy (e.g., pharmacometrics16 and physiology-based pharmacokinetic (PBPK) modelling)17, seldom do they account for the diverse range of age-associated factors that influence decision-making in older persons.
Finally, amiodarone is typically considered more for older patients than younger due to concerns about lifelong cumulative exposure and toxicity. I will use it in younger patients however if they have heart failure and then look at transitioning them off it or to flecainide as their heart function improves.
Dr. Pearson: What good advice to make decisions about surgery based on input from doctors who do not do the procedure themselves! Wish we had done that before my husband got pressured (by a surgeon at Methodist Hospital in Houston) into saying “yes” to hip replacement surgery for his 90-year-old mother with dementia. It did not end well.
Jeanne,
thank you. America would benefit from a process that oversees and provides guidance on all risky procedures done on nonagenerians.
Dr. AP: many thanks for the great education.
I have been diagnosed with AFIB. I have a Kardia band. I did see a EP and he thought I I wasn’t a good candidate for the meds. I am considering a Cardiac Ablation. I average AFIB about every 5 days. I am 69, overweight, and diabetic on insulin 4 times a day. My numbers have improved a lot. Female. And I have sleep apnea and use CPAP therapy. I really appreciate your website.
Gladys Addington.
Gladys,
Thank you. Consider a second opinion from a cardiologist who believes in enlightened medical management of AF.