Dr John M

cardiac electrophysiologist, cyclist, learner

Survey for Athletes with AF

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Hey Athletes:

My colleague, Professor Rachel Lampert, from Yale, along with the StopAF.org patient group, seek to learn more about how atrial fibrillation (AF) and its treatments affect athletic people.

If you are an athlete or if you regularly exercise vigorously, please give the Yale researchers a few moments of your time.

Here is the link to the survey.

Since I had AF in the past, I filled it out. It takes only a few minutes.

Prof. Lampert’s research into this area is important because AF affects people in vastly different ways.

It’s weird; while most AF stems from advanced age or lifestyle diseases (obesity, high blood pressure, alcohol excess and sleep apnea), endurance sport represents a special circumstance.

The added problem for athletes with AF is that most doctors do not (really) understand our goals and expectations. This sort of research sheds light on the inner workings of the athletic persona.

The other reason to do the survey is that Prof. Lampert is really nice.

JMM

Statins, Like All Medicines, Are Neither Good Nor Bad

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We have to talk about drugs.

No, not illicit drugs, but medications used by doctors and patients.

Plaintiff attorneys run ads on TV that fool people into thinking certain meds are bad. The current one I deal with is the clot-blocking drug rivaroxaban (Xarelto.) Before that, it was dabigatran (Pradaxa). If, or when, the makers of rivaroxaban settle a class action suit, you can bet apixaban (Eliquis) will be next.

These ads are a problem because they use fear persuasion (see Scott Adams’ blog), and because they can induce patients to stop taking or not start a beneficial medicine.

Lots of other medications suffer from a “bad” or “toxic” branding. Some people think statins are bad; many people think amiodarone is toxic. Warfarin (Coumadin) still suffers from the branding of rat poison.

I want to be clear: medications are neither bad nor good. Medications are chemicals that act on cells in the body in an attempt to create benefit. All medications can be toxic.

Toxicity turns mostly on dose. (Chance can also play a role in toxicity.)

Warfarin kills rats because the rodents keep eating the pellets and the drug builds up to high doses. In humans, we adjust the dose.

When patients tell me certain medications are toxic, I remind them that too much water, taken by endurance athletes, can cause dangerously low sodium levels that may lead to seizures. Oxygen given at high doses for too long in patients on ventilators can damage the lungs. Life saving-antibiotics can cause life-threatening colon infections.

I would urge doctors and patients to frame medications with the big four questions:

Four Crucial Qustions

As an exercise, let’s apply the four questions to the statin drugs (we exclude from this discussion people with familial hypercholesterolemia):

What are the benefits of taking statins?

There is only one benefit of statins: to reduce the future probability of a heart attack, stroke or death. Do not make the mistake of thinking statins are for cholesterol lowering. The drugs do lower cholesterol levels, but that’s a mere blood test. There are plenty of drugs that lower cholesterol but do not reduce the risk of heart attack or stroke.

The benefit of statins, therefore, is a probabilistic one. It’s like a lottery. You take the pill every day in hopes it will prevent a serious cardiac event in the future.

Numerous randomized controlled clinical trials (the highest level medical evidence) confirm that statins do reduce the probability of a cardiac event.

In absolute terms, the degree of statin benefit depends on whether a person has had a cardiac event.

For those without a previous heart attack, stent, bypass or stroke, statin benefits are small—no mortality benefit and about a 1% reduction of nonfatal cardiac events over the next 5 years. Doctors call this primary prevention.

For people with a history of a cardiac event or stroke due to a blockage of some sort, statin benefits are greater—about a 1.2% lower risk of dying and 2.5-3% lower risk of a non-fatal heart attack over the next 5 years. Doctors call this secondary prevention.

What are the harms of statins?

The best known harm of statins are muscle issues. I use the word issues rather than damage because true muscle damage is rare—about 5 in 10,000.

The actual frequency of muscle symptoms is hotly debated. Randomized controlled trials (in which patients don’t know whether they are taking the statin or placebo) report very small increases in muscle complaints—about a 1-2% increase. Observational studies, however, reveal higher rates of statin muscle complaints—in the range of 10-20%.

The second potential harm of statins is a small increase in diabetes. One of the smartest doctors on the Internet, Dr. Richard Lehman, says “the issue of [statin] induced type 2 diabetes is just an artifact of the way we define the threshold for T2DM. Statins often cause a small rise in blood sugar, which would only be of significance if it was associated with an increase in macrovascular or microvascular disease. On the contrary, statins reduce macrovascular disease end-points, and there is no evidence to suggest that they increase eye or kidney microvascular disease (which are very rare in the glucose range we are talking about).”

A third potential harm of statins is the burden of taking a pill every day. Scientists call this pill “disutility” and its measured in how much extension of life one would trade for taking a pill every day. People have different feelings about pill burden.

Another possible (emphasis here on possible) harm of statins is that the drugs may interact in a negative way with lifestyle. In a 2014 theheart.org | Medscape Cardiology column that went a bit viral (647 comments), I cited two observational studies, one that reported a higher calorie intake of statin users and the other less physical activity in male statin users.

Are there simpler safer options?

Opinion alert here: I strongly suspect that a healthy lifestyle delivers similar benefits.

Eating modest amounts of real food, not processed food in packages, doing regular exercise and managing stress would likely deliver lots of probabilistic benefits for reducing the odds of having heart disease.

This “intervention” however, has not been compared to statins in randomized controlled trials. Cardiologists Aseem Malhotra, Rita Redberg and Pascal Meier, writing in the British Journal of Sports Medicine, point to the obvious reason for this: “There is no business model or market to help spread this simple yet powerful intervention.”

What happens if I do nothing?

The most likely outcome of not taking statins is the same as if you take one—nothing. In the best case, that of secondary prevention, the risk reduction for nonfatal cardiac events is about 2.5-3%. That means one has to treat about 39 patients for five years to prevent one event. The odds are you would be in the 38 of 39 category, but you don’t know.

Doctors think this is a good trade. If these stats are applied to populations, many heart attacks can be prevented.

The ultimate decision is up to you. You are not a population.

JMM

You can do this exercise for any medical intervention or medication. Why we don’t do it more often is hard for me to understand.

Graduation Day… From Blogger to Author

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Hi all,

I have graduated from blogger to author. My first book is now available. It’s called the Haywire Heart. I co-wrote it with Chris Case and Lennard Zinn. VeloPress is the publisher.

The Haywire Heart by Lennard Zinn, Dr. John Mandrola, and Chris Case

The Haywire Heart by Lennard Zinn, Dr. John Mandrola, and Chris Case

The book deals with one of my favorite themes: heart conditions in endurance athletes.

Although exercise is a key component of health, excess exercise can lead to heart problems. In nine chapters and about 300 pages, the Haywire Heart attempts to be a comprehensive review of the topic. Chris and Lennard are terrific writers. All three of us are endurance athletes. Lennard had to stop racing because of atrial arrhythmia.

The book is available now at VeloPress. It’s being made into electronic format, which is expected soon. Runners World and Triathlete Magazine have featured the Haywire Heart as picks for 2016. That’s nice.

I hope you enjoy it.

Thanks for your support through these 6 years.

JMM

AF ablation still has a role

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I have been seeing a new trend in the AF clinic.

I never thought this would happen, but I’d estimate that at least once daily, often multiple times daily, a patient says they have read this blog before the visit. That is nice.

Many of these patients, some who have traveled across the country, or even from outside the US, say that they were drawn to my conservative approach to AF. That is also nice.

The (new) trend is that many of these patients are excellent candidates to consider ablation.

I still ablate AF. Ablation of AF has an important role. Yes, it is true that good sleep, weight loss, regular exercise, drinking less alcohol, stress reduction and control of blood pressure do wonders for atrial fibrillation; but these healthful behaviors don’t always eliminate AF.

I’m seeing patients who have symptomatic episodes, failed trials of drug treatments, and addressed their lifestyle factors, and still have symptomatic episodes of AF.

My friends, if these episodes reduce your quality of life, an ablation is reasonable. Notice I did not use the word, necessary. AF ablation is never necessary; it’s always a choice.

I’ve even seen patients with the common form of atrial flutter who have been reluctant to have ablation. Atrial flutter is much easier to ablate than AF. It may not always prevent AF from occurring. About half of patients who have flutter ablation still get AF. Half don’t. And I strongly believe that if you combine lifestyle measures after flutter ablation, the odds of AF are less. (That’s opinion, but would be a good study.)

This is not a flip-flop post.

I don’t mean to say AF ablation isn’t a big deal. It is. The procedure has not changed in 2016. We use general anesthesia; we do two trans-septal punctures; we make 50-80 burns in the left atrium of the heart; we keep patients overnight, and maddeningly, we must redo the ablation in about 20% of cases.

The treasure of AF ablation (plus lifestyle measures) is no AF. The cost is the risk. Published complication rates approach 5%. I’m proud of our complication rate; it’s about 1%. The point is it’s not zero. And the complications can be terrible–stroke, esophagus damage and perforation of the heart, for example.

I’m glad people come to see me because I’ve promoted a conservative approach, one that sees AF not as a disease, but as a symptom or sign of other diseases. It’s vital to treat the underlying causes of AF. If the atrium is under stretch (high blood pressure, obesity, sleep apnea, too much endurance exercise) or inflamed (obesity, sleep apnea, alcohol, too much exercise, lack of sleep, constant stress), it’s hardly the right idea to burn the heart.

Another reason to consider rhythm-control treatments of AF, such as ablation and drugs and cardioversions, is that it’s harder to lose weight and exercise if you don’t feel well. The holistic idea of ablation plus lifestyle measures: You get people out of AF; that improves their sense of well-being; then they are more apt to do the things that keep AF away.

An important study that I keep on the wall of my exam room is the ARREST-AF trial. In this study, Prash Sanders and Rajeev Pathek and others showed that lifestyle measures before and after the an ablation procedure increases the odds of success 5-fold.

Given the modest success rates, costs, and risks of AF ablation, it’s imperative to improve the odds of the procedure.

JMM

The cardiac dangers of excess exercise

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Regular exercise is essential for health. I’ve taken to prescribing daily exercise as a drug. I’ve even written it on a prescription pad for effect.

I see exercise as medicine, a safe medicine, an effective medicine.

That means, like all drugs, exercise can be overdosed. The challenge is knowing the upper limit. How much is too much?

Screen Shot 2015-07-30 at 6.26.03 AMRecently, I helped Chris Case, a writer at VeloNews, put together a magazine-length article on the cardiac effects of extreme exercise. He did a great job with an immense topic.

It’s worth a read: Cycling to Extremes

Two other reads:

This February, I wrote a review article on AF and endurance athletes. Athletes and AF: Connecting the Lifestyle Dots

Another review comes from the Lisa Rosenbaum, writing in the New Yorker: Extreme Exercise and the Heart. Lisa is a friend and a talented writer. She is now the national correspondent for the New England Journal of Medicine.

If you are curious, you will be drawn to this paradox. Athletes should not get heart disease. They are fit and lean. They don’t smoke or drink alcohol excessively (usually). They don’t have high blood pressure or diabetes. The only risk factor most athletes with heart disease have is athletics.

JMM

Update: Social justice of AF care, NOAC monitoring, population health and two new podcasts

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Hi All,

Here is a short update of the past week.

The first thing to say is the Atrial Fibrillation Care: Put the Catheter (and Rx Pad) Down post has gotten a lot of attention. It stayed on the most popular list all week. It has over a 130 comments, and I have received many emails on it. It is a big moment in AF care.

Screen Shot 2015-04-16 at 2.29.45 PMI would also point you to an interview I did with Dr. Prash Sanders from Adelaide. Prash is the senior researcher on the LEGACY trial. His team’s work has been most responsible for the change in thinking of AF care. The title of the post: LEGACY PI Throws Down the Gauntlet to US Physicians

Is AF care fair?

One aspect of AF care that I discussed recently with one of my partners was the notion of social justice. An AF ablation costs $100,000; a redo ablation costs $100,000. That is a lot of money. And now we know that in most cases, lifestyle changes either eliminate the need for procedures or render them more likely to succeed.

So…how fair is to spend $200,000-plus to treat a patient with AF? Think of what could be accomplished if that much money was used to care for the needy in our community? Is it right or just to allocate that many resources to a disease that is most often due to life’s excesses?

Population Health?

This leads me to population health–a hot topic in the hospital these days. The thinking goes that hospitals will be charged with delivering health to the population it serves. That is funny. As if health comes from hospitals. My mantra on the matter of health in populations: #BuildParksNotCathLabs.

Monitoring of NOAC drugs:

My column last week delved into the issue of monitoring patients who take the new anticoagulant drugs dabigatran, rivaroxaban and apixaban. Conventional wisdom–powered by marketing–has it that these drugs are more convenient than warfarin because less monitoring is required. A new study suggests otherwise. Researchers from Stanford looked at 67 VA medical centers and found great variation in patient’s adherence to the drug (dabigatran). They also discovered a yet unappreciated benefit from pharmacists.

The title and the link of the post is here: Should NOACs Be Monitored Like Warfarin . . . and by Pharmacists?

Two new podcasts:

In This Week in Cardiology for April 17th, I discussed NOAC monitoring, news from the FDA, including a warning on two new diabetes drugs, the future of cardiac devices and physicians’ view of electronic health records.

In This Week in Cardiology for April 10th, I discussed cooling after cardiac arrest, sports-related cardiac arrest, young adults and statins (ouch), antidotes for Factor Xa anticoagulant drugs and Staci’s letter to cardiologists on palliative care.

Great read of the week:

The best medical writing of the week came from my colleague and fellow writer Dr. Melissa Walton-Shirley. Trust me. Read her stirring essay A Death Well Lived. 

JMM

P.S. I rode 80 miles Saturday. It felt great.

Athletes, AF, Anticoagulants, Statins, Peanuts, and Dishwashers

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Here is an update on my recent writing.

Athletes and AF:

I was honored to be invited back to the Western AF symposium in Park City, Utah. Last year, I presented on social media. This year, Dr. Nassir Marrouche (University of Utah) asked me to tackle the topic of atrial fibrillation in athletes. This is no small matter.

In the process of putting together the 20-minute talk, I wrote an essay as a guide. In Athletes and AF: Connecting the Lifestyle Dots, I review the evidence, mechanisms, and treatment considerations of the endurance athlete with AF.

My argument in the talk and essay is that AF happens for a reason–even in athletes. We are at an inflection point in the way we think about AF. I made the case that the exercise-AF narrative fits with this new thinking.

AF and anticoagulant drugs: 

In The Gambling Game: Clot vs Bleeding, I address the issue of preventing stroke in patients with atrial fibrillation. The stimulus for this essay was a new study from Sweden that reported lower than expected stroke risk in non-treated AF patients with only one risk factor. (CHADS-VASC-1).

This is important data because knowing the risk of stroke without treatment informs the decision on whether to take an anticoagulant drug. It is definitively not a yes or no call. The tradeoff is always the same: anticoagulant drugs lower the risk of stroke but increase the risk of bleeding. You need stats (and a good adviser–doctor) to make the best choice. And it is your choice.

Statin drugs:

In the post, Statins in Primary Prevention: Welcome to the Gray Zone, I discuss the issue of predicting the future–at least, as it pertains to cardiovascular events. A recent study suggested that standard CV risk calculators overestimate the chance of a future heart event. That is big news because it affects the controversial decision to use pills to prevent heart disease.

For instance, statin drugs, like any medical or surgical treatment, force a patient and doctor to make a gamble. Does the benefit of the drug—a lower chance of a heart attack or stroke—outweigh the risks and costs of the drug?

Recently, guideline writers suggest statin benefit turns to the good when 10-year risk is greater than 7.5%. My post deals with the problem of knowing your future risk, and the wide swath of gray area in the use of statin drugs for primary prevention.

Peanuts, Fats, Dishwashers and Health Advice:

Being wrong about health topics is like the new normal.

For years, children’s health experts scared parents about peanuts. Don’t let your baby near peanut products until they were three. Now it looks like the opposite is true.

For years, nutritional experts warned us that eating fat would make us fat–and give us heart disease. That, too, looks wrong.

And in recent years, experts have created a systemic phobia of all things dirty. Bacteria and viruses are to be feared. Makers of hand sanitizers have cheered the new aversion. Now we learn that leaving a little bacteria on your dishes and utensils (and eating fermented foods) may help prevent allergies. Simply…you might be too clean.

How is this happening? How can experts have been so wrong about such basic things?

You can read the entire post here: Peanuts and More: When Health Advice Is Wrong

Thanks for reading.

JMM

I hope to post the Athletes and AF PowerPoint soon.

A new way to think about curing atrial fibrillation

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The problem with AF treatment is that we do not (really) understand the underlying causes of the disease.

Why does the heart fibrillate? What gets those pesky premature beats started? Why do intermittent episodes persist? Why does AF come back after shocks or ablation?

AF has been thought of as its own disease. You have high blood pressure and AF, diabetes and AF, depression and AF. And when there are no other obvious diseases, we used to say “lone” AF, which wrongly assumed that AF was its own disease.*

Atrial fibrillation was just another problem on a list of things to address. It was in a silo–cardiac.

That mindset is changing. And it is a good news/bad news thing.

The good news is that we are finding answers to the basic questions of AF. We are closer to a cure. Really, we are. I have seen cure happen.

The bad news is that there will be no single pill or procedural cure. That is because atrial fibrillation is (most often) an effect not a cause. The top chambers of the heart, with their thin walls and closeness to nerve endings and exposure to blood volume and pressure 100,000 times per day, are like a window onto overall health.

When we are well, our atria are well.

When the balance is perturbed, our atria will tell us. The nerve endings that connect the brain and heart fire. Premature beats begin. Initially, the premature beats are extinguished. They are just single beats, a thud and that is it.

Over weeks, months and years the premature beats wander out into the atria and find diseased cells and pockets of scar tissue (fibrosis). We name this process remodeling. Single premature beats can now start rotating around the sites of disease into rotors. (Picture an eye of the storm and hurricane.) AF starts.

The remodeling process is complex. It happens inside the atrial cells (ion channels), between the cells, in the scaffold surrounding the cells and in the nerve endings connected to the cells. It is so NOT one thing.

But why it occurs is not mysterious at all. Remodeling occurs because everything in our body is connected. The brain and the heart are connected. The lungs and the heart are connected. The immune system and the heart are connected. And so on.

Dr. Prash Sanders and his team of scientists are getting doctors to pay attention to the entire patient–not just her atria.

Listen to my friend explain this new way of thinking. In the Q & A after his lecture, the second question leads to a very disruptive thought for cardiologists.

JMM

* In very rare cases, AF can be its own disease, sort of like a fluky atrial tachycardia.

Endurance exercise and the heart — a mention in the New Yorker

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Do you exercise a lot?

Have you been at it for years?

Are you the type that rides around the neighborhood to make a 98-mile ride into a century?

Do you get squeamish if you can’t exercise for 24 hours?

Are you curious about that beautiful machine in your chest? You know, the rhythmic coordinated pump that squeezes 100,000 times daily–and never gets a pause.

You have read here, and elsewhere, that exercise is vital for wellness. But could exercise have an upper limit: a point in which the rhythmic pump says enough to the unremitting inflammation and stress.

If you care about this topic, read this New Yorker piece from Dr. Lisa Rosenbaum. The title and link are as follows:

Extreme exercise and the heart.

Dr Rosenbaum does an incredible job of putting together a complex topic, one that challenges our intuitions and attachments. Plus, she is both a beautiful writer and nice person.

Thanks Lisa. That was something.

JMM

CardioStim 2014 Recap

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Promenade des Anglais

Promenade des Anglais

CardioStim is the name given to the biennial gathering of the European Heart Rhythm Association (EHRA) in the Mediterranean resort city of Nice, France.

This was my first (ever) trip to France. As most of you know, I write an electrophysiology column (blog) called Trials and Fibrillations over at theHeart.org, which is now called Medscape | Cardiology.

My assignment at meetings is to cover relevant topics from the sessions. This year in Nice, theHeart.org also sent a real journalist, my friend Michael O’Riordan. It was good to have company. I also had the chance to see my dear friend and recently retired colleague, Dr. David Mann, who now lives in Paris and took holiday in Nice last week.

Here’s a picture of the three of us at the Place Massena.

IMG_20140620_231718584

I thought it might be useful to introduce the columns I wrote at this year’s CardioStim.

Day One: A new brand of pacing lead — Could more be better?

A study presented on Day 1 of CardioStim showed patients with congestive heart failure who were implanted with a cardiac resynchronization device (CRT) and a specific sort of left ventricular pacing lead had an 18% lower risk of dying. Although this was an observational trial, which does not prove causation, only association, the reduction in mortality was remarkable. The specific lead used in the trial (made by St. Jude Medical) is novel in design. Its main feature is that it has four electrodes (quadripolar) rather than the typical one (unipolar) or two (bipolar) electrodes seen in LV leads. It’s rare for me to favor brands in cardiac devices, but this quadripolar lead has a real head start. I’ve used the lead, and it works well. The post is titled: CardioStim, Day 1 2014: Does ‘Brand’ Choice Of Implantable Cardiac Devices Matter?

Day Two: EP on the cusp of disruption

Electrophysiologists, like cardiologists, have been mired in a slump in recent years. There hasn’t been any real paradigm-changing developments. The rule has been incremental improvement only. This may be about to change in the field of pacing.

The Achilles heal of pacemakers is the lead–the means of transferring electrons from the generator in the chest to the heart. The development of nano and wireless technology has allowed the possibility of tiny leadless pacemakers, which can be imbedded in the wall of the heart. The post is titled: CardioStim 2014, Day 2: Nano, Mobile, and Wireless . . . Is Electrophysiology on the Cusp of Disruption?

Day three: Treating atrial fibrillation

One of my favorite types of sessions at medical meetings is the pro-con debate. This one was provocatively titled: In the era of catheter ablation of atrial fibrillation, anti-arrhythmic drugs will become obsolete.

Yeah, right. The debate featured two giants of the field of atrial fibrillation therapy, one from Minnesota and the other from Germany. The title of the post is: CardioStim 2014, Day 3: Treating Atrial Fibrillation: Drugs, Ablation, or Neither?

Day four: Defining normal in the athlete

I know; that sounds comical. Athletes and normal?

A major area of angst in sports cardiology is the gray area between normal adaptations of the athletic heart, such as chamber enlargement, and true heart muscle disease, which we call cardiomyopathy. A couple of years ago, a group of sports cardiology experts met in Seattle to define normal findings on the ECG of an athlete. Numerous studies have shown that if these “athletic” changes are considered normal, fewer athletes will be misdiagnosed with heart disease.  The title of the post is: CardioStim Sports Cardiology Report — Seattle ECG Criteria: What’s Normal in an Athlete? This is an especially worthy topic because, in an era of direct-to-consumer advertising and disease mongering, “normal” can be a hard sell.

This weekend, I submitted a top-ten poster review from CardioStim. It’s an utterly biased selection of posters that caught my eye. If the editors approve this post, I’ll tell you about it as well.

And… on a closing note, I am sure you know Nice, France is close to Provence. I am also confident you know there is a big hill in Provence. I’ll try to put together a report on my experience there as well.

Here is a teaser I took from my iPhone:

IMG_3881

JMM

Exercise, over-indulgence and atrial fibrillation — seeing the obvious

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If you like thinking and writing, few topics are better than the excess exercise and heart disease story. Indeed it is a matter for the curious.

Two studies published last week in the British journal Heart addressed the relationship of exercise and heart disease. (See references below.) Although these studies garnered mainstream media attention they added little to what is already known. Namely, that moderate exercise is protective and excessive exercise is detrimental. This has been dubbed the J-curve of exercise. You could also call it…obvious.

I’ve been to this place so many times, I was going to leave it alone this time.

Two things changed my mind.

One was a series of comments on my Is Atrial fibrillation Necessary post on theHeart.org. The post describes the fact that lifestyle factors, not bad luck, play a central role in atrial fibrillation and its treatment. I believe this research, from scientists in Adelaide Australia, is the most important work in all of electrophysiology.

The Australians are exposing our blind spot. Their findings force us to look at AF as a modifiable acquired disease. Modifiable not with drugs, or freezes, or burns, but with simple lifestyle choices. What we eat, how we sleep, how much weight we carry–these are the things that matter to the health of our atria. What makes the Australian work so compelling is that they connect basic science and physiology to real-world clinical outcomes.

It’s important to note that the Adelaide brand of lifestyle intervention is aggressive. They enroll overweight patients in a physician-led clinic where multiple areas of health are addressed. These patients get results. Their weight drops, BP falls, sleep improves, blood sugar decreases, alcohol intake plummets. Through these anti-fibrillatory effects something else happens: they feel better. Go figure.

So, yes, the Australians are reversing AF in a population that is over-indulged.

Many of the readers here are endurance athletes. And when viewed from a distance, athletic people do not appear over-indulged, eg, they are not overweight. This sort of thinking came through in a number of the comments on my THO post.

“There are some skinny normal-BP people with AF and  no valvular defect. Lifestyle modification will help many, but not all.”

And this one:

“Strange thing is though, a remarkably high level of “super fit” people get Afib too…”

Can you see the intuitive (fast) thinking? That skinny and athletic equates to “healthy.” Most doctors, those who don’t roll with the athlete crowd, think this way.

I, and most of you, know better. Many, if not most, masters-aged athletes are completely and utterly, micro (last few weeks) and macro (last few decades) over-indulged. We’ve been at the train-like-Lance-ride-like-Lance game for a lifetime. Exercise is our drug. When we don’t race fast, we train more, not less. A brisk 10K run isn’t enough, we need to run a marathon, then two, and of course, many, like I once did, move to triathlon. Always more inflammation, not less.

The steady stream of athletes I care for in my AF clinic are far from healthy. Sorry about the cliché but it’s important here to see more than the just the tip of the iceberg. Consider that only a select few middle-aged athletes are trust-funders who have the entire day to rest and recover from a training session. Most athletes add their over-training to a job, marriage, and parenting. And then there is perhaps the biggest misconception about the non-obese older athlete: they got that way with a good diet. This is rarely true. Many of these folks deal with the pangs of intense calorie depletion by gorging on insulin-spiking carbohydrates, including carbs-with-alcohol. Again, more inflammation.

Now to the second thing that pushed me to revisit this worn canvass.

Last week at the 2014 Heart Rhythm Society Sessions in San Francisco, a group of researchers from Barcelona Spain reported a study that confirms the athlete-is-over-indulged thesis.

This group was interested in how the dose of exercise relates to the risk of atrial fibrillation. Previous work suggests that long-term endurance exercise increases the risk of getting AF (over the general population) by a factor of five. The studies that show this are often criticized because they are retrospective and observational in nature. Many experts have trouble believing that sportsman could be anything other than healthy. So the Spanish team enrolled 115 cases of athletes with AF and compared them to 57 age-matched control subjects. They did regression analysis (statistical way of looking for relationships) on the two groups. They found interesting odds ratios (OR):

  • OR for height: 1.06 (Tall people were 6% more likely to have AF. I see this often.)
  • OR for obstructive sleep apnea: 5.04 (Subjects with sleep apnea were 5 times more likely to have AF.)
  • OR for cumulative heavy sport activity (>2000 hours): 4.52 (This was quite in line with previous research.)
  • OR for sedentary individuals: 3.85. (Again, we knew sedentary is bad–see Australian work.)

The most striking finding came when they compared the AF risk of heavy exercisers with ‘normal’ (light to moderate) exercisers. Here they found a nearly six-fold fold increase in odds for AF (OR = 5.89) in the heavy exercisers.

To the group of regular doctors at the Heart Rhythm Society meeting, the researchers emphasized the well-known J-curve of exercise, where light to moderate exercise protects against AF and heavy exercise increases the risk.

But I ask you to move into slow-thinking analytical mode. Did you notice that over-indulgence in endurance exercise exposes one to the same AF risk as being an overweight sleep-apnea patient? Did you see the obvious:

That skinny and athletic are not necessarily healthy. And that AF is a disease of excess–of always being on the gas.

The reason this message is so important is that failure to see the big picture means patients are exposed to serious risks of treatment. I like to tell patients with AF that the disease gets most scary when doctors get involved.

But this wouldn’t be the case if we stopped seeing AF as a disease that always required treatment with drugs or procedures, but rather a disease amendable to good old common sense.

JMM

References:

Atrial fibrillation is associated with different levels of physical activity levels at different ages in men.

A reverse J-shaped association of leisure time physical activity with prognosis in patients with stable coronary heart disease: evidence from a large cohort with repeated measurements