John Mandrola

DisclosuresApril 07, 2015

My approach to patients with atrial fibrillation has changed. Completely and fundamentally. This is a before-and-after moment in AF care.

Before: We saw atrial fibrillation as a disease rather than seeing it as a result of other diseases. That explains why our treatments (drugs and ablation) have performed so poorly. It is a wrong-target problem. It is akin to stenting an artery and saying atherosclerosis is fixed or prescribing an antipyretic for bacterial infection.

After: Atrial fibrillation in the vast majority of patients (excluding those with brief episodes that are a form of focal atrial tachycardia) is a sign that something is awry in the body—usually exposure to an excess. The atria, with their sensitivity to stretch, neural connections, and plastic cells, are a window onto overall health.

Year after year I have watched the drugs fail and the AF return after ablation. It is a relief to (better) understand AF and to be able to cite evidence that supports the concept that the atria fibrillate for a reason. And that reason is the main therapeutic target.

You know the story. A group of researchers in Adelaide have shown—first in animal models[1,2]and now in humans [3,4]—that promoting basic health dramatically improves AF burden. Their methods and results have taught us how AF happens. Although work remains, it is clear that lifestyle diseases, via pressure- and volume-induced atrial stretch, inflammation, or neural imbalances, induce disease in and around the cells of the heart.

The coolest part about these data are that treatment of lifestyle diseases—mostly, the removal of excesses—not only reduces AF burden but also improves the structure of the heart. Even fibrosis (aka scar) can regress, which is a novel way to think about cardiac biology.

This “upstream” approach to AF is no longer a radical idea. Nearly all the leaders in cardiologyagree. It changes the way doctors should treat people with AF. Namely, the idea that AF is fixable with rhythm drugs or ablation is as wrong as thinking a stent fixes atherosclerosis or that treating fever cures infection.

Before I go on, let me make a note of caution. I am not saying AF drugs or ablation have no role. They do. But their (much smaller) role now is similar to stents or beta-blockers in patients with coronary artery disease: to stabilize an acute situation or to help transiently restore regular rhythm so that patients can feel well enough to exercise and enjoy life—things that make the atria healthier.

I no longer think of an antiarrhythmic drug as long-term therapy. For instance, I cardiovert and medicate so that patients can feel well enough to exercise every day they eat. I buy time. Then patients can lose weight or address other lifestyle issues, such as sleep disorders, alcohol intake, and perhaps overexercise and overwork. This improves glucose handling, lowers blood pressure, and relieves inflammation. People start to feel better. When they come back for follow-up, I discuss stopping the rhythm drugs—because they have served their adjunctive purpose.

On the matter of stroke risk: think about what it means to improve high blood pressure, diabetes, inflammation, and hyperlipidemia. Now think what it means to do so in millions of people.

You can see how this new approach upends the role of AF ablation. It is one thing to prescribe a pill; it is yet another to deliver 60 to 80 burns to the left atrium. Recall that patients who choose AF ablation walk into the hospital the morning of the procedure. They may not be perfect, they have AF after all, but they are alive and functioning. What awaits them in the EP lab is nothing small. They will endure 2 to 3 hours of general anesthesia, vascular access in both legs, two transseptal punctures, a fluid load, and purposeful damage to the heart done in proximity to the esophagus, phrenic nerve, pulmonary veins, and the thin left atrial appendage.

And . . . that $100 000 procedure, with its (real-world) 5% to 7% risk,[5] often fails. Repeat procedures are required in one of four patients. Even when the procedure is done well, recent research [3] shows that long-term success is fivefold lower when patients do not remove excesses from their lives.

This new approach to patients with AF has significant implications for the cardiology and healthcare community.

Consider those affected:

• Hospitals invest in expensive ablation labs. They have banked on the epidemic of new atrial-fibrillation patients who will “need” procedures. Recently, I did a marketing video for my hospital on AF treatment. We filmed in our EP lab, the ablation machines as the backdrop. I was excited to speak about the new discoveries in AF care. But I stammered when the interviewer asked me about the “procedures we do here.” I thought to myself: we do procedures here, we do them well, we do them safely, but we are sure to do a lot fewer in the future.

• Doctors—like me—have reaped the rewards of AF misthink. We are paid well to do and redo AF ablation. The financial reward for helping people help themselves pales in comparison. Yet I urge you not to blame overtreatment on fee for service. The main reasons doctors overtreat are do-somethingbias and the disease model of care. First, doing things is what we are taught, and it is what society expects. We might give cursory mention to lifestyle but then we rush to drugs and procedures. Second, the disease model of care tricks us into putting problems—like AF—into silos (cardiac, renal, pulmonary, etc), which we treat in isolation. So ingrained is the silo model that it has been daring to use the word holistic. As if things are not connected in the body.

• Workforce needs will be disrupted. A few years ago, cardiology groups and hospitals felt like they needed more electrophysiologists to handle the epidemic of atrial fibrillation. Now it is clear that what we need more of is not people with catheter skills, but people with people skills. The painful truth is that American cities and American hospitals do not need more EP labs.

• Policy makers and payers are bound to notice. Think about the billions of dollars spent to care for the millions of patients with AF. Why would any insurer pay for drugs and procedures that are doomed to fail unless lifestyle measures are addressed? I wonder whether this could be the spark that gets payers to see the value of helping people live healthier lives?

• Industry will have to adjust. Imagine the boardrooms of pharmaceutical and medical device companies in the past decade: they saw atrial fibrillation as a major opportunity. We will develop drugs, catheters, and mapping systems to treat the millions of afflicted patients. What these companies should see now is that AF drugs and ablation will go the way of renal denervation—useful in very selected cases, but no gold mine.

• Patients are most affected by this new discovery. Although there will be small numbers of people afflicted by fluky focal AF (a confusing fact), the vast majority of patients with AF will enjoy the best results when they and their caregivers treat the root causes. From now forward, when a patient with AF sees a doctor who recommends rhythm drugs or ablation without first exploring how that person sleeps, eats, drinks, moves, and deals with stress, it will be a signal to get another opinion. Rushing to drugs or ablation will be as wrong as prescribing antibiotics for a viral infection.

This discovery about atrial fibrillation teaches us that focal (easy) solutions for systemic diseases due to lifestyle are destined to fail. Given the rise of lifestyle-related diseases, this is a critical lesson, one we should learn sooner rather than later.

JMM

References

1. Abed HS, Samuel CS, Lau DH, et al. Obesity results in progressive atrial structural and electrical remodeling: Implications for atrial fibrillation. Heart Rhythm 2013; 10:90-100. Article

2. Mahajan R, Brooks AG, Shipp N, et al. AF and obesity: Impact of weight reduction on the atrial substrate. Heart Rhythm Society 2013 Annual Scientific Sessions; May 8-11, 2013; Denver, CO. Abstract YIA-01

3. Pathak RK, Middeldorp ME, Lau DH, et al. Aggressive risk factor reduction study for atrial fibrillation and implications for the outcome of ablation: the ARREST-AF cohort study. J Am Coll Cardiol 2014; 64:2222-2231. Article

4. Pathak R, et al. Long-term effect of goal directed weight management in an atrial fibrillation cohort: A long-term follow-up study (LEGACY Study). J Am Coll Cardiol 2015; DOI:101016/jacc.2015.03.002. Abstract

5. Deshmukh A, Patel NJ, Pant S, et al. In-hospital complications associated with catheter ablation of atrial fibrillation in the United States between 2000 and 2010: Analysis of 93 801 procedures.Circulation 2013; 128:2104-2112. Article

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