Atrial fibrillation

New post up over at — Rethinking on old drug for atrial fibrillation

Hey all,


I just published a new post on an old drug–digoxin.

“Dig,” as it is shortened to in medical-speak, originally came from the foxglove plant.

A recent analysis of the landmark AFFIRM trial has questioned the wisdom of using this decades-old medicine.

I know; dig isn’t as interesting as ObamaCare, ICDs or AF ablation, but it is an important topic. Estimates have nearly a third of AF patients in the real world on digoxin. But is this wise? What are the real outcomes?

I kept the post short. I mixed in a few bike racing references, some history, a little botany and of course, a reference to less-is-more thinking.

Here is the title and link: It’s time to rethink the role of digoxin




7 replies on “New post up over at — Rethinking on old drug for atrial fibrillation”

John- I agree with your post, “It’s Time to Rethink the Role of Digoxin” – and also with your words of caution, “It’s a pretty plant, but we must be careful with it” – though not necessarily with your path to these accurate conclusions.

I totally agree with your caveat and personal anecdotal experience: “IV Digoxin remains useful for the acute and short-term control of rapidly conducting atrial tachy-arrhythmias, esp. in hospitalized patients with low BP”. During my years of practice – my anecdotal experience was the same.

The post-hoc analysis of the AFFIRM Trail by UK researchers is problematic – despite the seemingly large increase in mortality. Mortality from Dig was not a primary end point of this retrospective analysis – plus NO Dig levels were required – NO monitoring of renal function was required – there was NO check on compliance – and “HF” was loosely defined as EF <40%. So while the conclusion of this study might be true – in NO WAY does this study prove it. It can't given the above methodologic flaws.

Similarly – I have trouble with the Van Gelder NEJM study finding "lenient" vs "strict" rate control didn't matter – since to me a non-inferiority assessment of "resting rate <110/min" vs "resting rate <80/min plus moderate exercise rate <110/min" simply looks at two ends of the spectrum without allowance for individualized middle ground rate control. I realize objective and prospective analysis of an "individualized rate control regimen" would be a nightmare to study – but I don't think one should generalize the subject of rate control to "all or none" which is what (to me) this NEJM article does. I believe the entity of tachycardia-related cardiomyopathy (from persistent uncontrolled rapid AFib) is real – so hard to believe that some attenuation of rate (even if it doesn't achieve resting heart rate < 80/min) is not beneficial, at least in some subsets of patients.

All of the above said – the reason why I have shared the views you state here is simply because the newer generation of physicians just don't have (and won't get) the experience needed using Digoxin to be able to master the intricacies of that drug. Though my specialty was not cardiology – I cared for hundreds of patients (in-hospital and out-of-hospital) in my family medicine practice who have been on Dig, or who I started on Dig. It was the "bread and butter" of my cardiology rotation during residency. Though possessing a very narrow "therapeutic window" – mastery of Dig therapeutics and ongoing patient-involved follow-up can minimize the incidence of Dig toxicity. It just requires time and effort. Alas, in my last few years of teaching – I'd find even senior residents able to count on the fingers of one hand the number of patients they started on Dig. Without thorough appreciation of how to use this drug – it is DANGEROUS.

The clinical reality is that in 2012 – the experience needed to attain competency in using Dig has become elusive. It is for that reason that I no longer think of it as a drug that should be used in the non-cardiologist's armamentarium.

In closing – in addition to being a "pretty plant" – the foxglove gave us art (What could be more classic than Van Gogh's portrait of his personal physician Dr. Gachet – with all wavy yellow-lines suggesting Van Gogh lived his later years in a Dig-toxic state from use of that drug in attempt to control his depression and seizures – GO TO: ).

The other major continuing use of Digoxin in 2012 – is that our collection of Dig-Toxic arrhythmias (albeit mainly of tracings from years past … ) – still serves well for teaching the new generation much about arrhythmia interpretation from our fascinating array of Dig-toxic arrhythmias.

There’s a study that reported beta blockers and digoxin were effective for rate control in about equal numbers of people, and neither is effective in everyone. When my husband was suffering from atrial flutter and concomitant heart failure, his cardiologist ran him rapidly through several doublings of carvedilol dose, up to the highest dose recommended for rate control under the European guidelines. This brought his briefly successful weight loss to a screeching halt and left him unable even to rise from his couch without pausing to sway for a minute to avoid passing out, but reduced his ventricular rate from 140 only to 125 or so. The cardiologist then proposed yet another doubling. He dug in his heels at that point, and his GP prescribed a low-dose digoxin which rapidly dropped his rate down into the 80s and below. The digoxin also countered the carvedilol toxicity enough that he was able to walk for exercise.

Now, even if the data you cited were very solid, we would still say that using digoxin would have been the right call for him. It would have been accepting a tiny risk of death in exchange for the avoidance of a 100% risk of worsened side effects and the possibility of reversing his heart failure through a program including physical activity – as he in fact did – which probably gives him in the long-term a much lower risk of premature death. If your drugs turn you into a blob on the floor, you are pretty well guaranteed not to get better. (It has been my experience that many cardiologists believe, and often state explicitly, that patients can never get better, and therefore they can’t see your point when you try to explain that their proposed regimen would make it harder to get better. Even the best cardio my husband saw thought he should never, ever cut back his QOL-reducing beta blocker dose after the flutter had stopped. Instead he stopped seeing cardiologists. No offense. 🙂 )

Your case illustrates an important point that I made at the end. Paraphrasing here: In “selected cases when the benefits of the drug outweigh its burdens, I’d lean towards lower dosages and close monitoring of levels.” This means dig can be helpful. The point of my article was to temper its widespread use and educate on its potential danger.

Fair enough. But another of my husband’s doctors made repeated efforts to pressure him to take amiodarone, which has been found in more solid studies to double the death rate. If digoxin should be a last resort for patients who are doing very badly with beta blockers and willing and able to make noise about it, then you’d think that rhythm control should be even more unacceptable for anyone but the most desperate. (I know YOU do not support the folly of trying to coerce every AF patient into lifetime rhythm control – but an unfortunately large number of your colleagues still do.)

Ken – Yes, and Dr. Mandrola is one of them – which naturally means that our insurance wouldn’t cover him, alas! Fortunately, my husband now has no active heart problems, and if they should recur in the future he’s going to choose the sort of very conservative management that could be handled by his primary care doctor.

Jane – Amen! As a teacher of family medicine for many years – I heartily support the premise that with no active cardiac problems, a good family physician will hopefully be all that your husband needs for the collaborative conservative approach you both favor.

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