Dr John M

cardiac electrophysiologist, cyclist, learner

Search Results for: alcohol

Writing about lifestyle modification — and blaming the patient

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I was pleased when the editors of the TheHeart.org reposted my recent essay, Let’s Stop the Unnecessary Treatment of Heart Disease. As of this morning, there are 167 comments. The majority of them were positive, and supportive of lifestyle promotion. Negative comments represented a small minority, but were notable in their vigor, and occasionally reached the level of vitriol. (“A self-righteous sanctimonious SOB,” said one nurse of the author.)

I’m glad the post touched a nerve. That was the aim.

This beautiful comment, in particular, indicates the power of a physician’s voice and his or her deeds.

My father’s vascular surgeon told him before he would perform a fem-pop procedure (Ed Note: a peripheral artery bypass) on my father that he had to quit smoking, and he did. His wife quit at the same time. That was 15 years ago and I credit that surgeon for saving my father’s life then and to the fact he is still alive today. Patients want us to be honest and straightforward about lifestyle choices.

That specialist did something special. He transcended his role of skilled technician and embraced the notion of being a doctor.

I’ve had a few similar cases with patients who were referred for ICD implants. I didn’t overtly refuse to implant the ICD if they didn’t quit smoking, but I made it clear that continued smoking in the presence of known heart disease would render the device less likely to benefit. (ICDs don’t prevent death from heart attack or stroke or cancer.) Most of these patients quit smoking—an action that conferred far more health benefit than any ICD. I can probably count on one hand the device patients I follow who still smoke.

Blaming the patient?

Another small but distinct group of commenters felt I was blaming the patient for having disease. This line of reasoning got me thinking.

First, I went back to the piece and reread it a couple of times for tone. And yes, maybe, I was bold, or too definitive in my stance. The Swedish study, however, showed up to 80% of heart attacks might be prevented by simple lifestyle choices. And the investigators weren’t looking at the effects of boot camps or triathlon training, but just 5 simple things: a healthy diet (with fruits and vegetables), moderate alcohol intake, not smoking, being physically active and not having a large waist. I found this study and its results worthy of taking a bold stance.

So why is it that writing forcefully about lifestyle gets interpreted as blaming the patient? I suppose it’s complicated, but maybe I should have been more precise. I could have made clear that lifestyle does not prevent all heart attacks—just four of five. This means some patients will develop heart disease even if they make good choices.

I’ve run into this same issue with AF patients, too. When I advocate for lifestyle measures in the prevention (and now treatment) of AF, many patients write back to say they are doing things right and still getting AF. I see that in my practice; these are the ideal patients for catheter ablation, by the way.

Perhaps I make this error because I take for granted that not all disease is avoidable. There are people with genetic predispositions to disease. There is bad luck. And there is…it just happens.

So skilled doctors will always be needed.

The central problem I want to emphasize is the collective misthink that health comes from healthcare. In the majority of cases, four of five in the Swedish study, being healthy comes from making good choices every day. Stacking together the little things.

Doctors who ignore the huge gut, deconditioned muscles of non-use, or smell of smoke in the exam room do their patients and colleagues a great disservice.

JMM

Let’s stop the unnecessary treatment of heart disease

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There are many reasons doctors suffer from burnout and compassion fatigue. One of the least-mentioned of these reasons is that much of what we do is so damn unnecessary. In the US, the land of excess everything, caregivers, especially cardiologists, spend most of our time treating human beings that didn’t need to have disease.

Let’s be clear and honest: Lifestyle-related disease is largely unnecessary.

These days, there is so much unnecessary disease that caregivers, especially cardiologists, rarely see it. We look past the obesity right to the cholesterol number and ECG. And then we pull out the prescription pad for the guideline-directed pills. Just typing that causes me angst.

A man gets referred for AF ablation for symptomatic AF. Indeed he has many AF episodes. But he also drinks alcohol excessively, weighs 300 pounds, and refuses to wear his sleep apnea mask. You refuse to do a $100,000 procedure and soon the reputation arrives: you are too conservative an ablationist. Mandrola won’t do procedures.

My interventional cardiology colleagues have it much worse. They are roused from sleep and family time to rush in and save people from mostly unnecessary heart attacks (MIs). One way to see the chorus of emergency PCI (percutaneous coronary intervention) treatment of acute MI is with awe. Another is with utter frustration–because in most cases it was unnecessary.

The study:

A recent population-based prospective study of Swedish men suggested almost four of five MIs in men could be preventable. (That’s not a typo.) Researchers from the Institute of Environmental Medicine in Stockholm Sweden followed 20, 721 men from 1997-2009. They specifically asked about five modifiable lifestyle behaviors: a healthy diet, moderate alcohol consumption, no smoking, being physically active and having no abdominal fat (waist circumference.) There were 1,361 cases of MI in the 11-year follow-up period.

Heartwire journalist Michael O’Riordan recaps the details of the study here on Medscape|Cardiology. The short story was that each of the five low-risk behaviors independently reduced the chance of having a heart attack. Not smoking was the strongest risk reducer. Men who combined all five behaviors were 86% less likely than those who had zero behaviors to have a heart attack.

The wake-up call:

I realize everyone knows lifestyle is important to prevent heart disease. It’s so obvious that we (patients and doctors) have grown numb to it. But pause for a moment and think about the finding that four of five heart attacks could be prevented with simple achievable lifestyle behaviors. That is something.

My electrophysiology colleague Dr. Prash Sanders (Adelaide Australia) stands in front of audiences of doctors and says risk factor modifications, such as weight loss and blood pressure control, are easy. The key word, he says, is motivation.

The challenge for caregivers, especially us cardiologists, is to stop suppressing the idea that heart disease can’t be prevented—that people won’t do it. The first definition of the noun motivation is the reason or reasons one has for acting or behaving in a particular way. That’s our job as caregivers.

My experience in the AF clinic in the past few years of lifestyle-enlightenment is that people can change. I’ve posted the lifestyle studies in the exam room. I discuss the biology of how lifestyle disease relates to the atria. I make the case that AF is (largely) unnecessary. I talk about atrial stretch and fibrosis, rotors and inflammation.

We can do the same with vascular disease and diabetes and high blood pressure. Being active, eating well, not smoking, and carrying less body fat work because they favorably affect oxidative stress, inflammation, endothelial function, insulin sensitivity and blood pressure. These are the reasons why people should eat less, move more and reduce their belt size. Reasons and expectations equal motivation.

The low-hanging fruit is right there. I say we reach up and grab it. Just thinking about doing fewer unnecessary things for unnecessary disease is soothing.

JMM

Is this the most important cardiology study of the last decade?

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In recent years, progress in the field of cardiology has been painfully incremental. We have enjoyed small gains–a better ablation catheter and mapping system, a couple of new anti-platelet drugs, maybe better stents, and even the highly touted anticoagulant drugs are within 99% in efficacy and safety of warfarin. Major breakthroughs, though, are non-existent. (And please don’t tell me squishing valves in the frail elderly is a major advance.)

This absence of game-changing type progress has an explanation. Perhaps the answer will be obvious after I tell you about the most important cardiology medical study of the last decade.

Its title includes atrial fibrillation but it is much more than a rhythm study.

Screen Shot 2014-08-27 at 6.03.14 AMEffect of Weight Reduction and Cardiometabolic Risk Factor Management on Symptom Burden and Severity in Patients With Atrial Fibrillation–A Randomized Clinical Trial

This is a trial of a novel treatment strategy for atrial fibrillation. Patients enrolled in the study were overweight Australians referred to an urban arrhythmia center in Adelaide for symptomatic AF. The researchers compared an intensive (physician-led) intervention approach to weight reduction and risk factor (high blood pressure, sleep apnea, alcohol intake, diabetes) management to the standard of care.

The study was born from two facts: One was that there is a long waiting list to get AF ablation in Australia. There was time. The second was that this group of researchers previously discovered (in a sheep model of obesity) that weight reduction had beneficial rhythm and structural effects on the heart. If it worked in sheep, it would likely work in humans, went the thinking.

Patients in the intervention group were referred to a specialized clinic (not an arrhythmia clinic) where a team worked with patients on basic health measures. This meant strict attention to calorie reduction for weight loss, including meal replacement if necessary. It also meant attention to blood pressure, sleep apnea, blood sugar control, lipid lowering and alcohol and smoking cessation. The control group also got excellent care; risk factors were treated and patients were given good advice on losing weight.

I know what you may be thinking: This does not sound like electrophysiology; it sounds like general internal medicine. And it is–and that is the point.

What makes this trial so important are the results–and the implications of the results.

The trial is free on the JAMA website, so you can read it yourself. There is also a 6-minute podcast with senior author, Professor Prash Sanders. Here are the study’s major findings:

  1. BMI and waist circumference decreased in both groups, but the intervention group lost much more. (Patients in the intervention group lost–on average–6 inches in waist circumference.)
  2. AF symptom burden and severity in the intervention group dropped significantly after 3 months and the curves continued to separate over time. (The graphs are impressive. See Fig 2.)
  3. 7-day ECG recordings from the intervention group, taken at baseline and 12-months, revealed significantly fewer AF episodes (3.3 to 0.62) and shorter duration of episodes (1176 min to 491 min). No significant changes were seen in the control group.
  4. On echo, left atrial size and volume, posterior wall thickness, and myocardial mass all decreased significantly in the intervention group. (This is a huge point because it provides a mechanism for improvement.)
  5. Cardiometabolic risk factors improved in both groups, but there was a significant decrease in numbers of patients with high blood pressure, elevated lipids, and alcohol consumption greater than 30g/wk in the intervention group.
  6. Pill burden decreased in the intervention group and increased in the control group.
  7. Catheter ablation was performed in 14/75 patients in the control group compared with 10/75 in the intervention group.

Yes, it’s a small study from one center in Australia. But look at those findings; look past the AF reduction. Think big picture. Consider what these results say about the practice of medicine. It is so clear to me.

For my entire career, the default has been to treat risk factors and late manifestations of disease. We prescribe medication for high blood pressure and diabetes. We ablate the left atrium to treat sources of atrial fibrillation–the irony being that scar leads to AF and burns/freezes create scar. The reason we do all this treating is because we fail to see these diseases as unnecessary. We don’t think it is possible, or worse, we don’t trust people to make good choices. And this failing is mostly on us physicians.

These researchers have shown both doctors and patients that it is possible not to have lifestyle diseases. They have given us proof that, if you try hard enough, structural heart disease and blood vessel disease and insulin resistance may be reversed. The key word: motivation.

Here is where the skeptics come in. They point out that these sort of results are not possible in the real world. They say: in developed societies where food is abundant and technology makes life easy, weight loss is hard. Really hard.

Okay, I get that. But why is it so?

One reason it’s so hard is because the medical establishment collectively gives in. Look at this Tweet from Dr Rajeev Pathak, one of the Australian researchers.

Respect, teach, and convince patients. These are our major roles as professional caregivers. To doctor is to teach. We aren’t just technicians and medication prescribers.

Of course there will always be a need for treating disease. We will need skilled ablation docs as there will still be AF. We will need interventional cardiologists because there will still be heart attacks. And so on for all medical fields. But we have to stop ignoring the obvious.

Respect. Teach. Convince. What makes this study so damn important is it that should change an entire way of thinking about treating people.

And now you can see why progress in cardiology has been incremental. It’s because there are no more antidotes to living so large.

JMM

Blaming the patient…and the philosophy of caring for people with atrial fibrillation

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More than a few commenters recently noted something disturbing in my writing. They said my words are increasingly taking a blame-the-patient tone. That bothers me. Of all people, I know about making imperfect health choices.

These comments got me thinking about striking the right balance in writing about health, say, between apathy and defeatism, (oh well, here is the script, it is hopeless), and overzealous boot camp instructor, (you are lazy and weak, 100 more pushups, then to CrossFit.)

It gets even trickier with atrial fibrillation–a malady that affects people in many different ways, but is so clearly lifestyle-related. We know more than we used to about AF, but we still don’t know essential things.

Consider…

We know the brain and heart are connected; so it’s clear that when the brain is unsettled the heart may be as well. But what is the connection? How does personality type, frowny faces and stress management skills connect to arrhythmia triggers? Something has to trigger those focal impulses. A colleague once wrote to me that he felt neural imbalances were more important than inflammation as a cause of AF. Ok, but the neural ganglia around the heart are connected to the brain.

Then there are the genetics of AF—tall, northern Euro, Type A’s. Sure there are strong genetic ties, but actionable gene information is far off in the future. African-Americans, for instance, have much lower rates of AF despite having a higher prevalence of risk factors, such as diabetes and high blood pressure. Why is that? I wonder—are the genes that predispose to AF inherited along with those that make one think Ironman triathlons are a good thing? (Grin, athletes, grin.)

And of course there is the lifestyle component. Obesity, high blood pressure and sleep disorders stretch and scar the atria, but not every patient with lifestyle-related diseases gets AF. Why not?

Alcohol intake associates with AF in a linear way, but not all who drink get AF. Remember, alcohol also affects the brain, which is connected to the heart.

Finally, we know inflammation plays a role in AF, but inflammation is essential for life. Why do some pneumonias and recoveries from surgery induce AF, and others do not? How much inflammation is too much?

See. We don’t know essential things. I could go on.

The other reason I harp on lifestyle factors is that AF treatments are so lousy. It’s hardly hyperbole to say that AF gets most dangerous when doctors get involved. What is a side effect of a rhythm-control drug? Answer: Sudden death. And, tell me, how is making 60 burns in the left atrium, done to isolate areas that may or may not be driving AF, a good therapy?

The point is that it sucks to have AF. But it also sucks to take AF treatment. So, if AF were unnecessary, this would be a good thing.

If you look at population maps and overlay wealth and rates of obesity, you see clearly that AF is a disease of riches. The more we have as a society, in convenience, in expectations, in longevity, the more AF we can expect. Maybe such wealth distorts the view of what is “normal.”

Here, I will close with a note from Joe, one of my many fine commenters.

At the risk of attracting ire, I’ll point out that most of us (myself included) are very bad at objectively evaluating our own situation. We look around the office and say “I’m not working too hard” when all of us are burning the candle at both ends. We look around the restaurant and say, “see, my diet isn’t so bad” when all of us have 1300 calories on our plates. We look around the gym and say, “see, I’m not that out of shape” when we’re really seeing a typical cross-section of our obese society.

Modern life has eliminated most of the limiting mechanisms that slowed us down as our bodies evolved. We work and play well into the night, we have constant access to abundant food, we typically move via machine instead of under our own power, and we enjoy a longevity of life that is unprecedented. All of this seems ‘normal’ to us, but it’s all very abnormal over the arc of human history.

Simply put, our bodies aren’t designed to handle all of this. Our version of ‘normal’ is quite unusual.

I know that small minority of AF patients exists. I strongly suspect that more than a small minority think they are in the small minority.

Ladies and gentleman, I pledge to stay mindful of tone going forward. Human disease, especially AF, does not fall into discrete boxes.

Yet there is no denying that how we live, the choices we make, affect our health. And that great harm has been done because modern medicine too often ignores this fact.

JMM

Two AF cases — and my changing view of AF

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I receive many emails about AF. I don’t often answer them because it is bad practice to doctor without seeing the person. Recently, however, I received a note with more general questions. The sender suggested I could use the response as a blog post. The reason I am posting these two cases along with my response is that my views on AF are changing. I am in the process of putting these global thoughts on AF together as a more general update, but these cases are a start.

Here is the email from a reader: (a doctor).

Dear John,

What would you recommend?

My med school roommate and I are 69 years old and in good health, normal BMIs, non-smokers, social drinkers. We both exercise almost daily. He takes something for mild hypertension. I’m on no meds.

He has had 3 episodes of PAF in his life–one in 1984 and two in the last few months. They all converted spontaneously to NSR. His doctor worked him up fully including an echo. His heart is structurally sound and no clots were noted. He has been strongly advised to start taking Coumadin or Pradaxa.

I have also had 3 episodes–one at age 26 which reverted to sinus after one dose of quinidine (I am old) and two about 6 months ago a couple of days apart which disappeared in about 12 hours after a good night’s sleep. I did not see a doctor about this. I had a normal echo 10 months ago because a routine EKG done as part of a preop eval for shoulder surgery showed nonspecific changes and I didn’t have a previous EKG to compare it to.

I don’t know if you saw this (http://thehealthcareblog.com/blog/2014/02/01/why-your-a-fib-diagnosis-may-not-be-as-bad-as-you-think-it-is/). It’s not much help.

What would you recommend if we were your patients?

Personally, I have seen so many complications with anticoagulation, especially Coumadin, that I am reluctant to take anything. I should mention that my father died of a stroke at age 76, but he was a heavy cigarette smoker all his life. He did not have A fib.

My response:

Sorry about the AF. (As an AF patient myself, I understand the frustration.)

A few things about treating AF.

First the complications:

The most important complication from AF is stroke—as it is often life-altering, or ending, the former is sometimes worse. The risk of stroke is surprisingly not related to the “amount” of AF a patient has. I often hear, from other physicians, that patients don’t have that much AF so stroke risk is low. There is evidence to support that this intuition is incorrect. Paroxysmal AF patients have as much risk as persistent AF patients.

The risk of stroke depends on the company AF keeps. We use the CHADS-VASC score, which considers the presence of CHF, HTN, AGE > 75 (2 points), Diabetes, Prior stroke/TIA (2 points), Vascular disease, Age >65  and Sex category (females  get 1 point).

Thus, your CHADS-VASC score is 1 and this confers a 1.3% annual stroke risk with no warfarin or other anticoagulants. The stroke risk on warfarin is not much lower — 0.5-6%, but the average risk of bleeding is in the range of 3%. Most guidelines, therefore, do not recommend anticoagulation. That’s a patient level decision though because there is a very small absolute risk reduction in stroke with anticoagulants. An important note is that there is no benefit from aspirin. And my view of the new anticoagulant drugs is that they are 99.3% similar in efficacy and safety but more than 100 times the cost.

Your friend’s risk score is higher because of hypertension. He gets a CHADSVASC of 2, which increases his annual stroke risk to 2.3-2.9% without drug and then 1% on warfarin. (Same 3% risk of bleeding.) His risk reduction is double yours, in the range of 1.5%—or a NNT of about 66. (A note on bleeding risk is that it’s not zero without warfarin; it’s about 1% in the general population but varies on other factors. Patients bleed without taking anticoagulants.)

Recall that almost all patients with bleeding leave the hospital the same person they came in as. That’s not often the case with strokes. ICH (intracranial hemorrhage) is the exception; thankfully, it is uncommon. A quick sidebar on ICH: the last two patients I saw with ICH probably had hemorrhagic transformation of ischemic stroke rather than a primary brain bleed. Meaning, if they had not had a stroke in the first place, they would not have bled into the brain.

Those are the odds that I quote. The risk of stroke and bleeding with different levels of CHADSVASC scores, on or off warfarin, come from population-level data, and have been confirmed in analyses of clinical trials.

Now onto the AF itself:

As for treating the episodes and having AF, it is now clear to me that AF is rarely a primary disease. Meaning, I think AF occurs because of perturbations of other health issues. This may sound pseudo-science-like but I think AF occurs when homeostasis of the mind, body or soul is disturbed. Think brain-heart connection via neural pathways. Poor sleep (?OSA), alcohol, stress, obesity, hypertension, caffeine, travel, worry. recent bronchitis, injury, surgery, etc are all common associated issues. And some individuals are clearly more susceptible than others, likely due to genetic variations in cell functions. Yes, of course, there are those patients who develop AF as a form of a focal tachycardia without any other health issues, a fluke if you will, but these are the small minority.

Research on the role of lifestyle and arrhythmia is beginning to show that AF may be unnecessary.

I like your treatments, which include prn (as needed) things. In your case, time and sleep–beautifully effective strategies for many medical problems. When I use anti-arrhythmic drugs, I often prescribe them as prn therapies so patients aren’t exposed to the drug on days they are not having the episodes. If a patient has one AF episode per month, that’s 29/30 days  she has no episodes. I find focusing on the positive is good for AF patients, as it sometimes helps them avoid over-treatment.

The problem (bias) I have, and other cardiologists too, is that we see a skewed population of AF patients. I, for one, see about 1 AF patient per year with a disabling stroke and a CHADSVASC of 0 or 1. We see the 1%, in other words.

I never “strongly advise” low-risk patients to do anything. Instead, I strongly advise them their statistics. People feel differently about NNTs of > 50 or 100.

Another bias of mine: I have little fear of warfarin. If my AF came back, I would get a home monitor and never have an INR out of range. We now do pacemaker and ICD surgery (and AF ablation with transeptal heart puncture) with patients fully anti-coagulated. There was even a NEJM study showing lower complications with device surgery when patients were left on warfarin.

I realize the anticoagulation viewpoint of other MDs is different from mine.

Hope this helps.

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

2014 Heart Rhythm Society Sessions — My massive recap:

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Hey Everyone,

I recently returned from the Heart Rhythm Society meeting in San Francisco. I attended the meeting as both a physician-journalist-columnist for theHeart.org and as a practicing electrophysiologist. As it so often is with international meetings, I returned energized and rejuvenated about the practice of medicine. Medical meetings are great this way.

It’s quite sad that fewer doctors are traveling to meetings. It’s a missed opportunity for learning, and shall I say, rekindling of the spirit of doctoring. Sure, social media allows a semblance of virtual attendance, and this is better than no attendance, but it is just not the same as in person.

Before I tell you about the topics that I chose to write about, let me share some of the non-technical thrills of the conference, or as my European colleagues call it, the congress.

On writing:

It was a true honor that so many doctors came up to me out of the blue to say, “I read your blog.” Many of them said they enjoyed the writing, but others just left it as: “I read your blog.” This was nice…and humbling. And I am grateful for the chance that Shelley Wood and theHeart.org people took with me. I’ve learned a lot about writing and reporting. I continue to revel in my place on the steep portion of the learning curve. It’s like being a Cat-4 bike racer or medical resident: you can’t stop thinking about getting better. Being a newbie is a fine place to be.

On seeing old friends:

I was able to have dinner with a friend from Germany and his Italian colleague. These guys are leading researchers in the field, but I call them friends. The value of exchanging information in this informal way is immense. We talked late into the night on matters big and small, in electrophysiology, in healthcare, and of course, in life. There’s nothing like learning about healthcare policy from first-hand experiences in other countries. This might sound naïve but I can’t help thinking we don’t look enough to other country’s strengths and weaknesses. I also got a chance to spend time with my two virtual-now real-buds, Doctors Wes Fisher and Jay Schloss. So good, these guys are.

On making new friends from social media friends:

I was able to connect IRL—in real life–with some long-time social media friends. A few of us had dinner and then many met for the first annual Tweet-up session. Meeting in real life can sometimes be tricky–but not with these folks. It seemed we got along better in real life than we do on Twitter.

Now to the reporting:

There was big news made at the meeting. It gets right to the heart of one of my favorite topics: the treatment of atrial fibrillation.

Atrial Fibrillation – A brand new way of thinking about the disease:

As you know, the disease AF afflicts millions of people. Billions of dollars are spent trying to treat this disease. AF ablation costs (charges) up to $100,000 per procedure in the US; the risk of serious complications run as high as 5% in some published databases, and multi-procedure success rates get to only 70-80%.

I’ve long felt that AF is a disease that doctors and patients misunderstand. Rather than see AF as a modifiable problem related to lifestyle choices, both parties look at AF as if it is a fixable problem that can be solved with a pill or procedure. Over the past few years, I’ve found myself doing fewer AF ablations (even though it’s my chief source of income and I’ve grown quite practiced at it) because, in my heart, I know that it’s often too big a hammer for a problem that could be solved with common sense and motivation. I’ve been encouraging the electrophysiology community to see our roles as stewards to patients and the healthcare system alike.

Now a group of prominent and well-respected researchers are proving me correct.

Yes, I believe, we are doing too many AF ablations.

The work of Prash Sanders in Adelaide Australia deserves your attention. They have shown, first in animal models, then in humans and now after ablation, that aggressive—not lip service—attention to weight reduction, sleep, blood pressure, diabetes, and alcohol intake can radically reduce AF burden. It’s real; and it’s not just a blogger who says so.

The president-elect of the Heart Rhythm Society, Dr. John Day, says he thinks AF may be unnecessary.

Here is my report of the most important presentation at HRS2014:

Is Atrial Fibrillation Necessary? The Most Important Study Presented at the Heart Rhythm Society 2014 Scientific Sessions

I also found an example of how wireless digital medicine saves lives. In patients with cardiac defibrillators, a prior (2010) study had shown those patients who used the remote monitoring capability of their device enjoyed a much lower chance of dying. At HRS2014, there were numerous studies that extended these observations to patients with pacemakers and all types of ICDs. I was drawn to this story because of my inherent bias that we may be over-monitoring human life. In the case of implantable cardiac devices, this is probably wrong thinking. Wireless monitoring allows for earlier detection of hardware failures and atrial fibrillation, among other benefits. Here is my piece:

HRS 2014: Remote Monitoring of Cardiac Devices: Hard Evidence for the Digital Transformation of Medicine

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Simple is best:

Another story I covered was the Simple Trial. This was a comparison of doing or not doing a test of a defibrillator at the time of implant. In the old days, when we implanted an ICD, we were not sure the shock would terminate the arrhythmia that might cause cardiac arrest. We called this voltage the defibrillation threshold. So, to determine that a patient would be saved by a future shock, we actually put them into ventricular fibrillation at the time of implant and watched the device work. If the implanted device didn’t work, we’d shock the patient with external pads, and reposition the lead or add more leads.

But then, over the years, device manufacturers beginning making better leads and higher-voltage “cans.” These improvements led to a situation where DFTs nearly always worked. Doctors began not doing DFTs, which was really a remarkable trend given that they were paid to do the easy test.

The Simple Trial, therefore, simply compared two groups of patients (test v no-test) and followed them for three years. They found no difference; in fact, there was a trend to more side effects in the test arm.

I liked this story for a couple of reasons. One is that it was an elegant trial, and the other is that it confirms a practice that we thought we knew was correct. Here is the piece:

SIMPLE Stuff? What We Think We Know

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The first day of HRS 2014 featured too much for me to pick just one story. My choice for a report on Day 1, therefore, was to do a roundup of stories that I found worthy of a paragraph. This included an opening plenary session from four leading futurists in medicine. Dr. Eric Topol, author of the Creative Destruction of Medicine, and editor of theHeart.org, had the line that most struck me: he spoke of  the upcoming “doctorless” patient in the future. And…Who will need hospitals, he asked?

I wrote about this remarkable plenary session along with a paragraph or two on six other selected themes of the day:

  • A Canadian study on the referral bias of electrophysiologists who do ablation; (if you have a hammer study)
  • Multiple studies looking at brain health after AF ablation; (sobering data indeed)
  • Two studies on the results of ablation in patients with hypertrophic cardiomyopathy (thick heart); (also sobering)
  • A Dutch study on the long view of patients implanted ICDs; (No, ICDs do not confer immortality, and all should remember that.)
  • An Australian study on how inflammation, blood vessel disease and atrial fibrillation are connected; (of course, it’s all connected.)
  • A Cleveland Clinic study on the heartiness of the human body.

Here is the link to the 1600-word post: Day 1 Roundup of the HRS 2014 Scientific Sessions. One note is that in the comment section of that post I was brashly and anonymously dubbed the Fox News of EP…neither fair nor balanced. That made me grin.

These were just my takes. Steve Stiles, a veteran journalist with theheart.org, covered the meeting as well. His professionally done news stories are worth a read. They are here at theHeart.org HRS page. 

JMM

AF ablation and the hard truths about AF

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Atrial fibrillation is a mysterious disease. We know a lot but surely not enough. We look at AF but are we really seeing it?

I believe there are hard truths to this disease. Hard in a way that neither patients nor doctors like. More on that later. First to some news on a major AF ablation trial.

AF ablation news:

One of the fundamental questions in electrophysiology today centers on the outcomes of AF ablation. Though most experts agree that AF ablation, when compared with medical therapy, reduces AF symptoms and improves quality of life (important metrics for sure), we don’t know whether ablation reduces the chance of stroke or death. We think it does–preliminary studies look good–but the only way to know for sure is to do a head-to-head comparison.

The long-term outcomes after specific AF treatments are relevant because population data (Framingham Study) show that having AF increases the risk for stroke or early death. So it’s better not to have AF. But populations are not individuals. Some AF patients have little risk while others are quite ill. The vast majority of AF patients are spread across a continuum of risk.

One of the most important AF studies of our time was (or is) the Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial. CABANA is an ongoing multicenter, international study that compares anti-arrhythmic drugs to catheter ablation. Researchers randomize AF patients to either strategy, follow them over years and then count easy things like stroke and death. CABANA aims to tells us whether ablation is just an expensive and invasive way to control AF symptoms or a true disease modifier.

Dr. Wes Fisher broke the story that the leadership of the CABANA trial decided to change its primary outcome from stroke and death to a composite of total mortality, disabling stroke, serious bleeding, or cardiac arrest. I know what you’re thinking…How is this news? As always, Dr Fisher explains it well:

While some may not see this as a significant development, we should understand that clinicians will be left without a definitive answer to which therapy, catheter ablation or anti-arrhythmic drug therapy, will prolong life the best in symptomatic patients with atrial fibrillation. Instead, doctors will have to read tea leaves based on a composite score of several endpoints to make their own personal judgment.

My colleague worries that statistical realities will muddy the issue: that being, of course, the dilemma of how best to approach a not-immediately life-threatening disease with potentially life-threatening treatments (ablation or medications).

I think about this a lot.

Let’s first talk about CABANA and then move on to those hard truths I was mentioning.

The CABANA trial is doomed to fail. Not because it’s a bad trial or bad idea or done by bad investigators. It’s none of that. The problems with CABANA are the following realities:

  • Symptomatic AF patients do not want to be randomized to drugs. AF patients go to AF centers for ablation. Recruitment of study volunteers has been slow and will remain slow.
  • Eligible AF patients have very low event rates–a good thing. This is important statistically because to show a difference in stroke rate or deaths (infrequent events in AF) between the two treatments, you need a lot of patients and a lot time. This is why investigators changed the endpoint and shortened follow-up. They wanted an answer in their career–not their children’s.
  • The techniques of AF ablation will improve. I believe we are on the cusp of big stuff–a new understanding of AF mechanisms, which will lead to better success rates. Consider that the results of CABANA won’t be available for years and by then better techniques will have rendered the results irrelevant.

The Hard Truths of AF:

The second issue is that I’m not sure asking whether AF ablation is better than drugs is the most important question.

My big-picture feelings about AF treatment are evolving rapidly. Let me start this way: Too often AF is treated as if it’s fixable rather than manageable. You have heart disease; heart disease is bad; therefore you need treatment. This logic might be okay if we weren’t prescribing dodgy QT- or QRS-prolonging drugs that fail two-thirds of the time, or if we weren’t delivering burns/freezes in the atrium that fail half the time. Or this: that in most cases, patients with AF could help themselves if we told them the truth—that losing weight and managing major risk factors can reduce atrial fibrillation symptom burden and severity. AF is not appendicitis; there is rarely an easy fix.

More and more, I counsel patients that AF is both a disease and a consequence of actions–your body talking to you. Like it does in the days after lifting weights for the first time in a while. Why else do you think those atrial cells begin to misfire?

Yes, as clinicians in 2014, we aim to prevent complications from AF. We prescribe anticoagulants to lower the risk of stroke and beta-blockers to prevent tachycardia-medicated heart muscle weakness.

But merely prescribing said treatments ignores the inflamed elephant in the room. There is no medical or surgical fix for inflammation overload. And I don’t mean just inflammation from obesity, high blood pressure, sleep apnea, sleep deprivation, alcohol, diabetes, smoking and exercise overload. I mean inflammation from never taking your foot off the gas, physically, mentally or emotionally.

I was recently bragging to a patient about the successful ablation I performed on him. He replied that it may not have been the ablation. “What do you mean”?  I asked. “Well…about that time doc, I retired from working nights; I fixed my relationship woes; and now I come home to peace and quiet and a kid who I love. You think that stuff helped?”

If I had a dollar for every time I have heard a version of that story.

You see what I mean? There’s a common thread here. It’s the inflammation.

For athletes with AF, the issue is years of over-inflammation from exercise and inadequate rest. For the obese and hypertensive, it’s the inflammation of atrial stretch and fibrosis. For the executive or engineer, it’s the inflammation of never having enough, or never being exactly correct enough, or maybe the three–not one–glasses of wine.

You think I’m full of beans. Consider also the common scenario of AF occurring after an infection, surgery or trauma, all of which are indeed big wallops of inflammation.

Doctors look at this picture-in-a-picture everyday. But are we putting it together?

Does AF ablation reduce the risk of stroke or death? Okay, okay, yes, of course, it’s an important question.

But…

That we have to ask it, that we look at the problem of AF without really seeing it, speaks to a collective unwillingness to face the hard truths about this disease. Again, we see a disease rather than a human being.

Is it possible that anti-arrhythmic drugs and ablation may just be imperfect ways to buy time for the patient with AF to modify the inflammation overload that stirs the ion channels of highly connected atrial muscle cells?

With humans, it’s all connected.

JMM

Two gifts and a consolation prize

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President Obama has a few good ideas.

He wants Americans to discuss healthcare this holiday season. That’s actually a really good idea.

This blog aims to do some good in the area of medicine and health. What follows are two incredibly important essays. The consolation prize is an excerpt from my recent Top Ten post. I chose this particular excerpt because in my view the most impactful cardiology study of 2013 involved two prominent themes of this blog–arrhythmia and the power of lifestyle choices.

On over-treatment and the collective inability to give peace a chance:

Dr. Rob Lamberts is a primary care doctor, accomplished writer and full-fledged master of the obvious. His November 20th essay, Gaia and Snake Oil, is an absolute gem. He hits upon the very essence of what’s wrong with the American culture of medicine. He calls it Medicine 101. I call it Medicine 101-through-404. (Staci first discovered this post on KevinMD.)

On the risks of denying death as a natural part of life:

I don’t know Dr. Craig Bowron, but that doesn’t diminish my admiration for his 2012 Washington Post essay, Our unrealistic attitudes about death, through a doctor’s eyes. I’ve tweeted that if I could change one thing about US healthcare, it would be to improve the care of the elderly and dying. End-of-life care is a great American tragedy. Neither the medical profession nor the general public has come to grips with death and dying.

Now for the consolation prize. I believe the most important cardiology study in 2013 involved atrial fibrillation. Here is an excerpt from my Medscape/Cardiology post:

#5. In Electrophysiology, Treat the Underlying Cause of AF

There are a few landmark studies I keep around the exam room for show-and-tell. 2013 brought another keeper. Dr. Prashanthan Sanders and colleagues (from Adelaide, Australia) are authors of the most significant study in all of cardiology in 2013. (Here is the link to the study– JAMA)

Here is the story: Atrial fibrillation is increasing exponentially. Electrophysiologists see patients at the end of the disease spectrum. Rate control, rhythm control, and anticoagulation are each important treatment strategies, but they don’t address the root cause of AF. In previous work in animal models, this group of researchers showed that obesity increases the susceptibility to AF.

The hypothesis was that weight loss (and aggressive attention to other cardiometabolic risk factors) would reduce AF burden. They randomly assigned patients on their waiting list for AF ablation to 2 groups: (1) a physician-led aggressive program that targeted primarily weight loss, but also hypertension, sleep apnea, glucose control, and alcohol reduction; or (2) standard care with lifestyle counseling.

The findings were striking. Compared with the group of patients receiving standard care, patients in the physician-directed program lost weight, reported less AF symptoms, and had fewer AF episodes recorded. Most impressive were the structural effects noted on echocardiograms. Patients in the intervention group had regression of left ventricular hypertrophy and reduction in left atrial size.

Though this is a small trial, it is practice-changing for cardiology. It shows that treating modifiable risk factors remodels the heart and in so doing reduces the burden of AF. In an interview in JAMA, Dr. Sanders says aggressive risk factor treatment should be a standard of care. I agree. Right now, AF ablation is too often thought of in terms of a supraventricular tachycardia ablation — a fix for a fluke of nature. It’s not that way. In the majority of AF cases, the same excesses that cause atherosclerosis also cause AF. Rather than make 50 burns in the atria, it makes much more sense to address the root cause.

JMM

ObamaCare will not make us sick…

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On day 1 of ObamaCare, the headline in our paper said “SHUTDOWN.” It’s here; it’s really here.

You might be wondering what’s been going on in the hospital or office–the contact points where healthcare actually happens.

The funny thing is: nothing seems any different.

And…this is the problem with ObamaCare. It hasn’t, won’t, or perhaps couldn’t, change the fundamental problem with US healthcare. Namely, that it is too big, too disruptive, and too devoid of nuance. In this way, healthcare mirrors modern American culture. We put in too little, expect too much and can’t seem to get by with less.

I realize; that seems awfully negative. So let’s be heart-healthy, and begin with the positives:

ObamaCare does many good things. It was a national embarrassment that we knowingly allowed large groups of fellow humans to go without basic health insurance. Germany, Britain, Netherlands and many other countries provide their citizens healthcare. So should we. Removal of the pre-existing condition barrier to getting coverage may be a challenge from an insurance perspective, but it’s necessary and right.

When Mr. Clinton spoke to us at the Heart Rhythm Society Sessions this year, he was right to say we needed change. Not only is our current system financially doomed, it is neither compassionate nor fair.

My problem with ObamaCare is that it’s like so much of medical care these days: it doesn’t address the root cause of the problem. Does a cardiologist who stents a blockage in an artery fix the problem of atherosclerosis? Does a heart rhythm doctor who medicates a stress/obesity/alcohol-related rhythm issue fix the problem? How do we reward a proceduralist that finds a safe cheaper way to do a procedure, say by avoiding use of an expensive ultrasound catheter? We dock his and his hospital’s pay.

So nothing is changed where the rubber meets the road. In fact, it’s worse. I spoke with a doctor who poignantly spoke of how she spends hours teaching her patients about basic health care behaviors, like good sleep, good food and good exercise, and her productivity has plummeted. “It’s far better to do than to educate,” she said.

Another thing that hasn’t changed is the metastasis of misplaced incentives. Rather than incent caregivers to provide gentle nuanced care, policy makers have imposed dreadful regulations that have only created a culture of checklists. Nothing has been done to curb the fee-for-service model. This is a huge problem because FFS punishes caregivers that practice minimally disruptive care. Do hospitals that employ physicians (and operate on razor-thin margins) want their doctors doing fewer procedures and ordering fewer CT scans and MRIs?

I’m an optimist though. Let’s assume that emergency care remains intact. We’ve always been good at taking care of the sickest. ObamaCare will not change that.

In the care of chronic diseases, the main health issue in America, I ask you to look around and consider whether we could do any worse? Consider mammogram and prostate cancer screening failures, over-treatment of the elderly, the promulgation of unproven drugs for cholesterol and the many pharma-created disease-states. The list of unproven, aggressive and expensive care is endless.

I’ve never been more convinced that good health cometh not from healthcare. The change will be tough, change always is, but Americans will learn that if they take better care of their minds and bodies, they won’t need as much medical care.

The health of our citizens will not go down as access to care decreases. Based on what I see every day, it’s more likely that less access will improve our health.

JMM

P.S. My electrophysiology colleague, Dr Wes Fisher, had the same idea I had this morning. He also penned some thoughts on our new healthcare landscape. Always candid, Wes’ take is worth your time.

Atrial Flutter — 15 facts you may want to know.

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I get a lot of questions about atrial flutter.

Atrial flutter is a common arrhythmia that shares many similarities to its next of kin, AFib; but there are important differences.

Sawtooth appearance of typical atrial flutter

Let’s go over 15 basic facts and important points about atrial flutter. (In plain English.)

1. Atrial flutter is defined as a rapid but organized rhythm (tachycardia) in the top chamber of the heart (either from the right or left atrium). In typical cases of atrial flutter, the atrial are contracting at 200-300 bpm. [Note: Do not confuse atrial rate with pulse rate. The pulse rate (or heart rate, originates from the ventricles, which beat at some ratio of the atrial rate—see numbers 2 & 7]

2. The rapid atrial rhythm of flutter differs from AFib in two important ways: First, when the atria fibrillate, the rate is well above 300 bpm, and this results in quivering, never contracting atria. Second, fibrillating atria have a very irregular rate. In flutter, the atria are going fast but are regular. These two factors have important implications. It’s hard to explain, but the regularity of atrial flutter contributes to more rapid conduction to the ventricles—and this makes it harder to control the pulse rate of atrial flutter compared with AFib.

3. The symptoms of atrial flutter vary widely. On the one end of the spectrum, patients with flutter may report no symptoms, while others report severe problems, like tachycardia, loss of consciousness, chest pain or a feeling of dread. Most flutter patients however report fatigue, shortness of breath, and decreased energy levels. Many say, “something isn’t right.”

4. Atrial flutter is common. It often occurs in conjunction with AFib. Both arrhythmias share similar associated clinical factors, like advancing age, hypertension, obesity, prior heart disease, prior heart surgery, alcohol, stress, endurance exercise, poor sleep, lung disease and thyroid disease.

Typical right atrial flutter5. Think of atrial flutter as a single big (usually) circular circuit. Whereas AFib can be considered chaos from numerous different locales (an oversimplification); atrial flutter tends to be one rotating circle. Usually, but not always, the circuit is in the right atrium. (See image.)

6. Atrial flutter does not occur spontaneously. It is initiated or induced by a burst of atrial arrhythmia. The inducing beats may be merely benign premature beats (PACs or APCs), a short burst of supraventricular tachycardia (SVT), or it may be that a sequence of AFib organizes into atrial flutter. (I know you want to ask why this happens or how often. I urge you not to ask these questions. We don’t know why; and it’s hard to quantify how often AFib organizes.)

7. Atrial flutter creates three problems for patients:

7a. High Heart Rate: An atria in flutter may drive the ventricles too fast. The most common scenario for atrial flutter occurs when the atria are at 300 bpm and the ventricular rate (pulse rate) sticks at 150 bpm. We call this 2:1 A-V conduction. All sorts of rates are possible. It might be an atrial rate of 240 and a ventricular rate of 120. The ratio can vary too. In 3:1 flutter with an atrial rate of 270, the pulse rate would be stuck at 90. You get the picture.

7b. Loss of Rhythm/Synchrony. When the atria beat at a different rate than the ventricles, the cardiac output is reduced. How much less varies a great deal. The reduction might just be 10%, but it could be up to 30-40% less in older stiffer hearts. Most patients notice the difference, though some do not. (See number 3.)

7c. Increased stroke risk: In terms of the risk for clots and strokes, European and North American guidelines do not distinguish between flutter and AFib. Drugs that block coagulation (anticoagulants, ie…’blood thinners’) are recommended in atrial flutter similarly to AFib. The explanation here is beyond the scope of the post, but keep in mind that most patients with atrial flutter also have (at least the tendency for) AFib (See number 13.)

8. The diagnosis of atrial flutter can be tricky. This is important because there are flutter-specific treatments. Atrial flutter is diagnosed from the EKG. It takes some skill. Sometimes it is easy, but it also can be subtle. Over-diagnosis, under-diagnosis and mis-diagnosis are not uncommon. I see coarse AFib diagnosed as atrial flutter. Likewise, I see atrial flutter often called AFib. And I have even seen slower versions of atrial flutter missed altogether. If you are diagnosed with atrial flutter, it’s okay to ask the doctor if he or she is sure. That never makes me mad.

Treating atrial flutter: Let’s first talk about the two similarities to AFib treatment:

9. Heart rate control of atrial flutter: Just like it is in AFib, it is important to get the pulse rate under control. In most cases, this does not have to happen immediately. In fact, attempts at rapid heart rate control can lead to problems. Things that lower adrenaline levels help lower the heart rate in atrial flutter, like peace, quiet and transiently limiting exertion. The most common drugs for rate control are the beta-blockers (by far the best), calcium-entry blockers, and digoxin. Recall that rate control is the means for preventing heart muscle weakness (heart failure). Persistent tachycardia, over weeks to months, can weaken the heart muscle. The good news is such muscle weakness is rarely permanent; the bad news is atrial flutter is tougher to rate control than AFib. (See number 2)

10. Stroke prevention in atrial flutter: The atria in flutter contract rapidly and often ineffectively. This increases the risk of blood pooling, clots and subsequent stroke. Guidelines suggest using the CHADS-VASc score to estimate stroke risk. In patients with CHADS-VASc scores greater than 2, anticoagulant drugs confer a net clinical benefit.

11. Rhythm control drugs rarely work to control atrial flutter. Rhythm control therapy of atrial flutter differs greatly from AFib. In fact, most rhythm drugs (not beta-blockers, Ca-E blockers or dig) can create a favorable milieu for atrial flutter. That’s right; some AF-rhythm drugs (propafenone, flecainide for example) often make atrial flutter worse. This is especially relevant to athletes on AF-drugs. Athletes who take AF-rhythm drugs (without beta-blockers or Ca-E blockers) can sustain dangerously high heart rates during exercise. I tell athletes who take these drugs to either not exercise, or stop exercising, if they feel like their heart is out of rhythm.

Let me explain: remember I told you flutter was a circular circuit. This means the trailing edge of the circle must have recovered from the passage of electricity—or refractoriness. The slower the circuit, the more time the tissue has had to recover, and the more likely it is that the circular rhythm persists. One of the ways AFib rhythm drugs prevent AFib is by slowing conduction. This effect may prevent AFib, but it may also favor the organization of atrial flutter circuits. What’s more, this concept—that slowing conduction favors flutter circuits—is why atrial flutter can complicate AF ablation. Here, the incomplete creation of ablation lines injure—but not deaden—heart cells. An injured group of cells conduct poorly and these areas of slow conduction create anchoring points for circular flutter circuits. (This is less of a problem now that AF ablationists less often make linear ablation lines, and when we do, we work hard to make them complete and durable.)

12. Cardioversion of atrial flutter: A very simple way to terminate atrial flutter is to shock the heart. This sounds awful, but is really quite simple. After a patient has been on anticoagulant drugs (usually up to 3 weeks), a cardioversion can be done safely. Cardioversion takes minutes. The patient is sedated (for a few minutes) and then a shock is delivered. The heart nearly always goes back to regular sinus rhythm. With adequate anticoagulation, the risk of cardioversion is tiny. The problem of course is durability. Atrial flutter recurs after cardioversion in well more than half the cases. The recurrence may be in hours, days, months or years. I frequently recommend cardioversion for newly diagnosed atrial flutter.

13. Catheter ablation of atrial flutter: Before proceeding, it must be stipulated that when I talk about ablation of atrial flutter, I am referring to the typical right atrial version of flutter. This is reasonable because typical right atrial flutter (more accurately referred to as caval-tricuspid-isthmus-dependent flutter) is the most common form of atrial flutter. Patients without prior ablation or heart surgery rarely develop non-right atrial flutters. (Let’s say, less than 10% of de novo atrial flutter is atypical flutter.)

Catheter ablation of atrial flutter13a Catheter ablation of right atrial typical flutter is easy and very effective. It is a focal anatomic procedure that targets one area and requires just a few ablation lesions. The picture on the right depicts the flutter ablation procedure. The isthmus between the tricuspid valve and inferior vena cava is easy to get to, consistent in location and not often near important structures. Ablation there is well-tolerated, and complications from flutter ablation are much less frequent or severe than AFib ablation. Unlike cardioversion, atrial flutter ablation prevents recurrences of flutter.

13b The problem with atrial flutter ablation is not recurrence of atrial flutter; it is recurrence of atrial fibrillation. Recall that I told you atrial flutter does not occur spontaneously; rather it is induced by another arrhythmia. The incidence of AFib after successful flutter ablation ranges from 20-60%. I round it off and tell patients that after successful flutter ablation, there is a 50% chance of developing problematic AFib. This should make sense, right? AFib is more often than not a left atrial disease. Common atrial flutter is a right atrial disease. Ablation of flutter does not target the left atria. The other important implication of this fact, other than post-ablation symptoms, is the risk of stroke. It’s often a tough call deciding on continuing anticoagulation after flutter ablation. The CHADS-VASc score is a good guide, but it is also clear that some patients with atrial flutter do not develop AFib. And if there is no AFib, there is no benefit from anticoagulation.

14. The best approach to patients with both atrial flutter and atrial fibrillation: This is also a tough one. Many patients with atrial flutter also have episodes of atrial fibrillation. In these patients, it’s clear that ablating just the flutter circuit will take care of only part of the problem. Here is where shared decision-making comes in. Although ablation of typical flutter circuit might be partially effective, the procedure is easy and safe. Flutter ablation is a much smaller procedure than AF ablation. So the upside of an incremental approach is symptom relief with a smaller procedure. The downsides are incomplete symptom relief, persistent need for medicine and the possibility of a second procedure (AF ablation.) Some patients seek total elimination and accept the risk of the bigger AF ablation procedure while others like the more conservative incremental approach. There is no right answer here. It’s an individual call, and the doctor’s input is critical.

15. Atrial flutter also responds to lifestyle changes. This is similar to atrial fibrillation, and all of heart disease. Good food, good movement, good sleep and good attitudes help prevent all forms of heart disease, including atrial flutter. It’s silly to medicate, shock or burn the heart and then not do the basic lifestyle things to help prevent recurrences. Yes, it is true that atrial flutter often requires an intervention, but the chances of a second procedure or more treatment decrease with simple lifestyle choices. Athletes with atrial flutter pay attention here. If you keep inflaming yourself incessantly after flutter ablation, do not be surprised that you are in the 50% who develop AFib. (And please do not ask how much exercise is too much. That answer is unknowable.)

I hope this helps.

JMM

P.S.

This is not supposed to be a book chapter, review article or medical advice. It’s just a rough guide.

Atrial flutter therapy should be individualized. There’s no cookbook or protocol. Treating atrial arrhythmia requires nuance and a robust patient-doctor relationship.

If you have a general question that was not answered, feel free to post it. But…Please do your best not to ask questions specific to your case. Of course I can’t give medical advice over the Internet.

 

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