Endurance Sports and Atrial Fibrillation – WHY?

Endurance Sports and Atrial Fibrillation – WHY?

starting a long run on the local PCT. We saw a bear that day – fun.

Exercise is supposed to be good for you, good for your heart, right? Then why is that endurance athletes have two to ten times the rate of developing atrial fibrillation compared to “normal” people? Is a little or moderate exercise good but excessive exercise bad? As an endurance athlete (marathons, trail running, long distance mountain and road biking) who has permanent atrial fibrillation (AF) I would certainly like to understand “WHY?”

There is a terrific article on Europace entitled Endurance Sport Practice as a Risk Factor for Atrial Fibrillation and Atrial Flutter . By internet standards it’s a long read but I will review it here.

The studies aren’t large, and male athletes predominate – but it is clear that endurance athletes have, as mentioned above – 2 to 10 times the likelihood of developing AF. It is not actually known why but it is thought that ectopic atrial beats, chronic inflammation, and larger atrial size are all risk factors.

Personally – the story checks out – I started having runs of “premature atrial contractions” years before ever going into AF, and because endurance athletes train more frequently and tend to avoid rest the atria are chronically inflamed, which leads to fibrosis (scarring) of the atrial muscle. And of course my left atrium has been severely enlarged for decades – not as much because of sports but because I had previously had mitral regurgitation (repaired surgically 1994 but the atrium never shrunk back to normal).

But even without the mitral valve issues endurance athletes tend to have enlarged atria. And we don’t rest enough leading to inflammation and scarring. The Europace article cites several studies that link long term endurance sports with AF, compared to sedentary individuals.

Moderate exercise may actually protect against AF.

Ringo after a long run – Fremont Trail

The Europace article also cites studies that show a correlation with “occupational physical activity” and AF – meaning people that have difficult, physically demanding jobs are also in the same boat as endurance athletes.

I didn’t know this – there is also a higher rate of AF related to how tall a person is – damn! I’m 6’3” (or 6’4” – depending on what year was measured.)

The article discusses, speculates, as to the mechanism of AF in the athlete’s heart but much of this is a bit technical for this blog. Feel free to explore the article if you are curious.

The typical clinical profile of sport-related AF or atrial flutter is a middle-aged man (in his forties or fifties) who has been involved in regular endurance sport practice since his youth (soccer, cycling, jogging, and swimming), and is still active. This physical activity is his favourite leisure time activity and he is psychologically very dependent on it. 

Interestingly the AF rarely occurs during running:

They almost never occur during exercise. This makes the patient reluctant to accept a relationship between the arrhythmia and sport practice, particularly since his physical condition is usually very good. The crises typically become more frequent and prolonged over the years and AF becomes persistent. Progression to permanent AF has been described by Hoogsteen et al .

Again, for me, the story checks out. I certainly recall long episodes of palpitations at rest that I now can identify as AF – until the day when it became (dreaded) permanent AF!

The article suggests that abstinence from sports is helpful for athletes having episodes of AF, although it isn’t curative. The problem, as any endureance athletes knows, is that it is nearly impossible to get us to give up our long runs, bike rides, etc.

Other therapeutic measures are also discussed – but that is a talk that is best left to the runner and the cardiologist.

Although ablation seems to be quite effective, endurance sport cessation associated with drug therapy seems to us a more suitable approach as an initial therapy, particularly in non-professional, veteran athletes.

To conclude I’m just going to quote their conclusions right here:

Vigorous physical activity, whether related to long-term endurance sport practice or to occupational activities, seems to increase the risk for recurrent AF. The underlying mechanisms remain to be elucidated, although structural atrial changes (dilatation and fibrosis) are probably present. There is a relationship between accumulated hours of practice and AF risk. Further studies are needed to clarify whether a threshold limit for the intensity and duration of physical activity may prevent AF, without limiting the cardiovascular benefits of exercise.

I’d be interested in others opinions and experiences with these issues. Reading this article was a little emotional for me – like I said – the story checks out! I guess that if I knew what I know now I might have cut down a little on the endurance sports before I was forced to do so by permanent AF. Truly, for me, a day long run with my dog, on a trail, in a local wilderness area was the most enjoyable thing I can imagine. And at this point it isn’t even the AF preventing me from still doing it – it’s the  high dose of beta blocker I take for rate control – really takes the wind out of my sails.



“C’mon Boss, let’s go for a trail run!”


Warfarin Withdrawal in Patient’s Awaiting Surgery Increases the Risk for Stroke


Last April Dr. Adnan I. Qureshi reported on research, at the 67th Annual Meeting of the American Academy of Neurology, that has shown that atrial fibrillation patient’s who are taken off of warfarin for surgical procedures have an increased likelihood of having a stroke.

Subjects included in the analysis had atrial fibrillation plus at least one additional risk factor for stroke or death: age >65 years, systemic hypertension, diabetes, congestive heart failure, transient ischemic attack, prior stroke, left atrium diameter 50+ mm, left ventricular fractional shortening <25%, or left ventricular ejection fraction <40%.

Specifically atrial fibrillation patients who discontinued warfarin for surgical procedures had a 1.1% rate of stroke while atrial fibrillation patients who remained on warfarin had a 0.2% rate of stroke.

Read more here:

Warfarin withdrawal in atrial fibrillation patients awaiting surgery dramatically ups stroke risk

Well, this seems like one of those articles where you read the headline and think, “Duh!” Like the article about how obese children have a higher chance of hypertension – No kidding?

Obviously if you are on a medication, in this case warfarin, to prevent having a stroke, and you stop taking the medication, well, you have an increase likelihood of having a stroke. I think everybody suspected this – but what we see here is that the rate of stroke increases five-fold. Wow – that seems incredible!

This article reinforces my strong belief that strict compliance with taking my medications, especially warfarin, is a good idea!

As far as surgery is concerned, clearly, if you need to have the surgery and you need to go off the warfarin, then so be it. The article didn’t mention anything about bridging with Lovenox. You might want to ask your surgeon about that. And also – consider how important the surgery is to your general health. Is the surgery truly necessary? Is it worth risking a stroke?

La Muerte Tocando Guitarra

What is the ACLS Approach to Atrial Fibrillation? (Advanced Cardiac Life Support)

A week or so ago I re-certified in ACLS – Advanced Cardiac Life Support. ACLS is a set of emergency clinical interventions for cardiac arrest, stroke, respiratory arrest, etc., which is basically a step above BLS (Basic Life Support – formerly known as CPR). ACLS certification, in my case anyway, is done through the American Heart Association, and is only open to health care providers: doctors, nurses, dentists, advanced practice providers like PAs and nurse practitioners, EMTs, respiratory therapists, pharmacists, and so on.

I thought I’d write about it in this blog so people might know what to expect as far as the type of treatment they might experience if they have an unstable episode of atrial fibrillation.

I’m in permanent atrial fibrillation, so when I’m in one of these classes I’m glad I’m not hooked up to an EKG – I don’t feel like getting medicated or shocked!

ACLS deals with various problems using algorithms, so let’s look at the “Tachycardia with a Pulse Algorithm” which would generally apply to acute atrial fibrillation.


So basically we start with a person with a fast heart rate. Tachycardia is, by definition, a pulse over 100 beats per minute, but for ACLS purposes it generally means a pulse over 150 bpm. Obviously not all tachycardia (fast heart rate) is atrial fibrillation.

For this article I am not discussing the other types of tachycardia, even though they are in the algorithm. I assume most people reading this blog are dealing with atrial fibrillation.

The first step is to assess the patient, identify and treat any underlying cause, make sure the patient is breathing effectively, assist if necessary, and give the patient some oxygen.

Now the next step is very important – is the patient stable? Five things: 1.) Is the blood pressure too low? 2.) Is there altered mental status (confusion)? 3.) Is the patient going into shock? 4.) Chest pain? 5.) Heart failure?

Even though I am in atrial fibrillation, all the time, I don’t have any of these symptoms. But if the patient is unstable and have tachycardia, basically, they are going to be getting some electricity! That means synchronized cardioversion, and in the case of atrial fibrillation (see “narrow irregular”) that means 120-200 joules – that’s a big shock!

Check out this video of cardioversion for atrial fibrillation – yikes!

Notice that it says “consider sedation.” Sedation can be considered, but not if it interferes with getting the unstable patient shocked as soon as possible. If you go into unstable atrial fibrillation at a race expect that the sedation will likely be skipped and get ready to be ZAPPED.

Photo by Ted Friedman.

Photo by Ted Friedman.

This is for unstable tachycardia – that means the patient is in some sort of crisis that may eventually be life threatening.

For an episode of stable atrial fibrillation expect vagal maneuvers and a referral to a cardiologist. Vagal maneuvers include firm carotid sinus massage, coughing, gagging, valsalva maneuver (holding your breath and “bearing down”), and placing your face in ice water (snow also works). A lot of people with intermittent atrial fibrillation already know how to do this.

For a great article about her episode of unstable atrial fib see Run, Smile, Drink Water and Don’t Die – A Guest Post by JoAnna Brogdon.

I’d be very interested in anybody else’s experience with unstable atrial fibrillation and what type of treatment was administered. Please comment below. Thanks.

Does Drinking Coffee Cause Atrial Fibrillation?


It has often been said that drinking coffee is related to developing atrial fibrillation. How about people who already have a history of atrial fibrillation? Can coffee trigger an episode?

A recent large study from Sweden shows that coffee consumption does not increase the chance of developing atrial fibrillation, even if quite a bit of coffee is consumed.

So coffee does not cause atrial fibrillation; not in people who have no history of atrial fibrillation.

But what about people who already have a history of atrial fibrillation? Can coffee trigger recurrence of atrial fibrillation?

The answer to that is probably yes, but more research needs to be done. In this study it was found that people who already had atrial fibrillation tended to drink less coffee than people without atrial fibrillation – probably to prevent triggering the arrhythmia.

As for me, I’m in permanent atrial fibrillation and it really doesn’t make much difference – I drink my normal amount of coffee and don’t worry about it.

Here are some excerpts from an article, by Colleen Mullarkey, in Consultant360:

After analyzing data from nearly 250,000 individuals, researchers found no association between coffee consumption and an increased risk of AF, according to the findings in BMC Medicine.

“This is the largest study to date on coffee consumption in relation to risk of atrial fibrillation,” says lead study author Susanna C. Larsson, PhD, associate professor in the Institute of Environmental Medicine at Karolinska Institutet in Stockholm, Sweden.

Larsson and her colleagues investigated the association between coffee consumption and incidence of AF in two prospective cohorts who had provided information on coffee consumption in 1997 and were followed up for 12 years—41,881 men in the Cohort of Swedish Men and 34,594 women in the Swedish Mammography Cohort.

Using the Swedish Hospital Discharge, they identified 4,311 and 2,730 incident AF cases in men and women, respectively, in the two cohorts. The median daily coffee consumption was 3 cups among both men and women.

In their analysis, the researchers found that coffee consumption was not associated with AF incidence, even in more extreme levels of coffee consumption.

They confirmed this lack of association in a follow-up meta-analysis that included both of these two cohorts along with four other prospective studies, which amounted to a total of 10,406 cases of AF diagnosed among 248,910 individuals.

“These findings indicate that coffee consumption does not cause atrial fibrillation,” Larsson says. “However, high coffee consumption may still trigger arrhythmia in patients who already have atrial fibrillation.”

While the researchers could not examine this possibility in the present study, they observed that participants who had AF at the time they completed the questionnaire about their coffee consumption drank, on average, less coffee (mean of 2 cups/day) than those who did not have atrial fibrillation (mean of 3 cups/day).

Data in the study suggests that some individuals who had AF at the start of the study may have quit drinking coffee or cut down their consumption because of an arrhythmic-triggering effect.

“Further study is needed to assess whether coffee consumption may trigger arrhythmia in patients with atrial fibrillation,” Larsson says.

Larsson SC, Drca N, Jensen-Urstad M, Wolk A. Coffee consumption is not associated with increased risk of atrial fibrillation: results from two prospective cohorts and a meta-analysis. BMC Med. 2015 Sep 23;13(1):207.

Now the next question: Does running really ruin your knees? (Ha ha)

Update Part 2 – Atrial Fibrillation, Pradaxa Fail, Transient Ischemic Episode, Blood Clot in Left Atrial Appendage

Jimi Hendrix sang, “manic depression’s a frustrating mess.” Well, I think the same can be said of atrial fibrillation!

mountainbikingwringoRingo and Me – Photo by Ben Vallejos

It’s been a while since I have written and I have to say the last couple of months have been nerve-wracking. As I posted in a previous entry I had a TIA (transient ischemic attack) while running a couple of months ago, had a normal carotid scan, but a TEE (trans-esophageal echocardiogram) showed that I had a small blood clot in my left atrial appendage.

In other words I had a “mini-stroke” and was at risk of having a full on stroke.


This TIA occurred while I was on Pradaxa, a newer, novel anticoagulant. At that point I was taken off Pradaxa, started on Lovenox (low molecular weight heparin) injections, and warfarin (Coumadin), and also aspirin. I was instructed to discontinue running, and bicycling, and limit my activity to easy walks, and a repeat TEE was scheduled two months after the initial one.

I won’t hold back any longer regarding the surprise ending – I never had a second TIA “mini-stroke” (that I know of) or stroke and the follow-up TEE (trans-esophageal echocardiogram) showed that the blood clot inside my heart is now gone. Hooray!

appendagePhoto – The little cul-de-sac is the LA appendage

Just to review how this happens: when you are in atrial fibrillation your atria is beating so fast it’s like it isn’t beating at all, just sort of vibrating. There is a part of the left atrium (the “appendage”) where the blow flow is extra sluggish, and this is where clots can form. When a tiny piece of clot breaks of and goes into the brain that’s a TIA. If a big clot is present and breaks of into the brain that’s a stroke, which of course can be disabling and even fatal.

It goes without saying that I am disappointed that this occurred while I was on Pradaxa. I figured that as long as I was taking it I was safe, and I liked not having to watch my diet or have blood tests constantly. Taking Pradaxa is easy – “set it and forget it.” Now I’m on warfarin (Coumadin), a royal pain in the butt, and have to micromanage my diet constantly – this drug is not an easy choice for a vegetarian! Eating too many greens (think kale) is dangerous as is not eating enough greens. Imagine trying to eat about the same amount of kale or broccoli or spinach each day.

zaPhoto – vegan pizza

My target INR is between 2.0 and 3.0, but seeing as I have had a TIA while on an anticoagulant I am trying to keep it nearer to 3.0 or even higher (3.0 – 3.5).

The two months between echocardiograms was an era of angst – anxiety and fear – for me, especially the first several weeks. Every symptom, no matter how minor, seemed like stroke. For example – lie in bed trying to get to sleep and your hand becomes numb – normal, right? Not when you know you have a blood clot in your heart – that seems like a stroke! Jump up from bed, start testing the muscle strength in each arm and leg, recite the alphabet, smile, frown, move eyebrows up and down checking for asymmetry. Do you think I’m exaggerating?

Every once in a while a person stammers or mispronounces a word. Normal? Maybe, but not when you are obsessed with a gigantic blood clot lodging in your brain.

As far as exercise was concerned at first I was limiting myself to short, easy walks more appropriate for a non-athlete. Eventually I became a bit bolder and started doing longer (but slow, especially up hills) hikes of an hour or two. It took me three weeks (!) to bridge to a therapeutic INR, so I was on warfarin and Lovenox for all that time. Once I was off the injections I started doing bike rides – but they were on non-technical trails and were slow, especially while going uphill.

My brain never got the memo that I was no longer a long distance runner/cyclist so I still ate like I was, and consequently I’ve gained some weight.

At this point, after finding out the clot is no longer present, I have started increasing the intensity of my bike rides, but mostly I’m still doing bike rides. I haven’t yet started running again – but I will.

I am mountain biking again, but not on any trails that would be considered challenging. Well, that’s not 100% true, I guess.

awol-1-2Photo – “Adventure Without Limits?”

As far as mountain biking is concerned I am phasing out technical trails (gradually). I made a deal with my self that if I didn’t have the blood clot on the second TEE I would get a new bike – and I did. I got a Specialized AWOL, which is a “gravel grinder.” That’s sort of a cross between cyclocross bike and a loaded touring road bike – basically a bike designed for gravel or dirt roads – we have an infinite supply of these around here so I have a lot of exploring ahead of me.

As far as that blood clot is concerned I’m very pleased it has gone away – but I am not fooling myself that it is gone forever. It could return at any time. It wasn’t there when I had my second TEE, but it could actually be there right now – how would I know? How long had it been there and how many times have I had a clot in that area? There’s no telling without doing a ridiculously expensive, somewhat invasive test over and over. I guess all I can do is stay vigilant, take my meds, watch the diet, and keep on trying to run, hike, and ride, even if it is at a reduced level.

Re A-Fib: 5 Things I’ve Learned in 10 years… A Guest Post by David Grayson Lees


I’m a 64 year-old road/trail runner, marathoner and weight lifter diagnosed with atrial fibrillation more than a decade ago. I’ve had three ablations and as many cardioversions, plus I’ve swallowed the usual assortment of prescription meds. Now my a-fib has become paroxysmal atrial flutter—about one episode every two weeks or so, usually lasting a few hours—and while my running days seem to be over, I still regularly make it to the gym and I’m discovering the joys of walking and hiking.

Through trial and error—plenty of each, actually—as well as a fair amount of research, I’ve come to a handful of conclusions that may be useful. While I believe them to be true, keep in mind that my observations are true for me; your experience may well be different. Finally, since I’m not a physician, nothing here is intended as medical advice.

And now: 5 things I’ve learned in 10 years of dealing with the always-entertaining world of cardiac arrhythmia.

A-Fib won’t kill you…even though a diagnosis of a-fib—and its symptoms—can be very scary, barring underlying cardiac disease, a-fib is not inherently life-threatening. And so if you have just been diagnosed, relax as best you can.

…but a stroke could. Pay rigorous attention to your anti-coagulation regimen. Even if your CHAD score is zero, at least take a low-dose aspirin every day. Personally, I find Coumadin to be a true pain, what with blood monitoring, dietary restrictions and the like. I much prefer the newer meds, especially Xarelto. It acts quickly, and as an added bonus you don’t have to be continuously concerned with your INR numbers.


Your EP isn’t interested in prevention. Typically, EP’s are all about fixing stuff rather than prevention. Which is weird, because unless you’re on the younger side of 40 and/or your a-fib has been freshly discovered, one ablation usually won’t do the trick. Of course, I’m grateful to my two EP’s, one rated among the best in California and the other acknowledged as one of the best in the world. It’s just that neither one has ever expressed any interest in the contours of my life, including what my exercise habits happen to be, what sorts of supplements I take, or what my days are like. Now, I’m not looking for a new best friend, but it’s clear that for them I’m a unique problem to be solved rather than a unique human being. I’m not angry about it; after all, these docs chose a field in which their major interaction with patients occurs when the patient is unconscious.

Still, I believe the implication is clear: you are pretty much on your own when it comes to figuring out how to modify your life style, exploring vitamin/mineral supplementation, and gathering the latest non-nutsy information.

(BTW, in terms of info, two websites I recommend are Dr. John Madrola and The A-Fib Report. Dr. John is a younger EP who always has a thought provoking take on new developments in a-f treatment and research and The A-Fib Report is a readable compendium of international a-f research, written in lay language. It requires a nominal membership fee that’s well worth it.)


Supplementation could work for you. I haven’t thrown out my beta blocker (Sotalol AF, not regular Sotalol) but along the way I have had excellent results in controlling the frequency and duration of my atrial flutter episodes by supplementing with 200 mg of magnesium citrate in a pill taken at lunch and ¼ teaspoon of potassium citrate dissolved in water taken in the morning and again at dinnertime (Please note: ingesting too much potassium involves some quite severe health risks, so be careful.)

Life is good. But first, the bad news: as near as I can tell, nobody knows what causes atrial flutter. The gang of suspects spans endurance sports (!) to mysterious biochemical mechanisms that somehow encourage the formation of tissue substrates that make the electrical system of the heart go haywire. Researchers—and your EP, too–are just guessing, leaning on statistical correlations rather than employing demonstrable causal connections. Maybe cutting out caffeine will help you; maybe it won’t. Maybe abstaining from demon rum will prove to be the answer; maybe not. Obviously, if you are over-drinking, over stressing (like many of us who are into enduro sports) under sleeping or happen to be engaged in other deleterious deeds, changing your behavior is simply a good idea, a-fib or no a-fib. Just don’t expect that any one thing will be the answer.

The good news is, you can have a great life even with a-fib and a-flutter. No, I don’t love my a-flutter episodes; they are annoying and sometimes, even after a decade, still frightening. I don’t run anymore, but a long walk or a moderate—I know, I know, not my favorite word, either—hike turns out to be a lot of fun. No, I can’t put the same hemodynamic load on my heart that I used to, but I can still work up a nice funky sweat underneath the weight machines at the gym.


Besides, working out is only a part of life. My friendships, relationship with my son, work, and my love life (I’m getting married again, and I’m stoked!) are just as satisfying as ever.

Maybe more so.

Those of us with a-fib or a-flutter aren’t sick, not truly. Nor do we need to afraid.


(Thanks to Linda for the inspiration. Thanks to you for reading.)