Obesity and atrial fibrillation--New information for the whiteboard

Weighty news was made in the world of atrial fibrillation this month. No, it wasn't a downstream intervention like a new catheter, surgical procedure, or pill. It was better than any of that; upstream things always are.

Let's set the stage. The 5' 8" 260-pound salesman is tired, weak, and really out of breath. The referring doctor sees an ECG with AF. The AF doctor sees a big climb. "Here we go again."

Anyone involved in the care AF patients knows that one of the many challenges of treating this disease is getting patients to help themselves. Successful treatment of AF requires an engaged and motivated patient. It's akin to teacher and student: no matter how skilled the teacher, the student must want to learn. But the chances that the student will learn depend somewhat on the skills of the teacher, right?

Enter obesity. Few conditions test AF patients and doctors more than obesity. As a specialist practicing in the southern US, I am faced with this scenario often. Your experience is probably similar to mine: good information, presented skillfully and earnestly, often make the difference in getting patients on the "program."

Obesity and AF frequently coexist, and it is well-known that obese patients are more difficult to treat. But it's never easy mentioning the elephant in the room. Ablation and anticoagulants are a much easier topic. The master of the obvious in me knows a number of things about this scenario:

• The disabling symptoms of AF do not discriminate.
• Obese AF patients suffer the same as their thinner counterparts.
• Obesity is a risk factor for AF, and if patients weren't fat they might not have AF.
• Obesity leads to numerous conditions that associate with AF—high blood pressure, sleep apnea, and congestive heart failure.
• Lifestyle choices that lead to weight loss favor sinus rhythm.

Here's the problem with the above statements: they don't help you in the exam room. Repeating sterile and general phrases like "lose weight and exercise more" to obese patients is a failing strategy. In AF, specific information works better.

That's why I love these two studies.

Let's start with this sheep study published online in the Heart Rhythm journal. (I know what my journalist colleagues are saying—sheep study? Bear with me for a moment; this is a good stuff. I'll get to the human trial next.)

Australian researchers did a detailed experiment in which they extensively compared the hearts of obese sheep (fattened by overfeeding—go figure) with those of normal-weight sheep. The strength of their methods was the inclusion of the kitchen sink: structural, hemodynamic, electrical, histological, and biochemical data.

Results. Compared with normal-weight sheep, obese sheep were found to have:

• Gained weight with overfeeding (obvious things deserve emphasis).
• Increased atrial volume and mass.
• Higher left atrial pressure and systemic pressure.
• Slower atrial conduction velocity.
• More disordered atrial conduction.
• Inflammatory infiltrates, disordered cardiac muscle architecture, and an increase in intramyocardial lipidosis.
• Higher profibrotic markers, like endothelin and platelet-derived growth factor (PDGF), among others.
• A much higher susceptibility to spontaneous or induced AF.

Even though this is an animal study, it still offers clinicians important information. We can now point to carefully conducted science that implicates obesity itself (no other confounders like high blood pressure and sleep apnea) in causing structural, electrical, clinical, inflammatory, and biochemical alterations in the atria. Doctors give this process a sterile name—atrial remodeling. Another way to say it is that obesity destroys the atria.

Now the human study . . .

Researchers from the Mayo Clinic studied AF patients referred for catheter ablation. Excluding middle-weight patients, they compared 19 thin patients (BMI <25) with 44 truly obese patients (BMI >30). The experiment included a comparison of both electrophysiologic and hemodynamic (cath and echo) parameters in the two cohorts.

Results (which maintained significance after multivariate analysis):

• Not surprisingly, obese patients were more likely to have hypertension, diabetes, sleep apnea, and persistent AF.
• Electrically, obese patients had shorter atrial effective refractory periods and slower longitudinal PV conduction time.
• Hemodynamically, obese patients demonstrated higher left ventricular end diastolic pressure (LVEDP) and mean left atrial pressure.
• In an echo, the left atrium of obese patients showed higher volumes, increased strain, and lower contractility.

The authors concluded: "Increased LA pressure and volume and shortened [effective refractory period] ERP in the left atrium and PV are potential factors facilitating and perpetuating AF in obese patients with AF."

There's a narrative forming here. And it's not just these two trials. Dr Stanley Nattel's group in Canada has published similar findings in an animal model of sleep apnea and obesity.

Here's how I put it together: We know atrial remodeling occurs; we know scar formation and inflammation perpetuate AF; and now it is clear that that obesity directly causes these damaging processes. It gets to the basics of what we learned in our early training. Reentrant arrhythmias stem from three things: slowed conduction, areas of unidirectional block, and the presence of multiple pathways. Normal atria do not exhibit these properties, whereas the atria of the obese do.

It's settled. I'm using these studies on my whiteboards. Real science is pretty nifty.

JMM

Your comments

	Obesity and atrial fibrillation--New information for the whiteboard
	# 1 of 6	September 19, 2012 09:38 (EDT)
	Don L	Is atrial remodelling permanent?  That is, if an obese patient with AF loses weight and is no longer hypertensive, is it likely that the AF will spontaneously revert to normal sinus rhythm?
	# 2 of 6	September 19, 2012 10:25 (EDT)
	John Mandrola	Don, I don't have a definitive study to quote on this matter, but I have a few thoughts: It's a matter of degree--a continuum. Once remodeling causes heart muscle to be replaced with scar, the 'structural' disease of the atria is permanent. Until stem cells offer heart patients the ultimate mulligan, cardiac scar is permanent. The LA pressure increases, the stretch, and I suspect the electrical conduction abnormalities are all likely reversible with weight loss and treatment of sleep apnea. (The Mayo study demonstrated electrical abnormalities in patients without atrial scar.) This makes sense. We know AF begets AF. It's why there is a time penalty in treating AF. For instance, patients with long-standing persistent or permanent AF are much more difficult to keep in sinus rhythm. We try to intervene early in the courese of AF--before remodeling occurs.  JMM
	# 3 of 6	September 23, 2012 09:58 (EDT)
	DH	I believe the current massive consumption of simple and refined carbohydrates is the proverbial "elephant in the room here" linking obesity and atrial fibrillation.  Almost all obese people - and virtually all persons in Western society with metabolic syndrome qua carbohydrate intolerance - overconsume CHOs.  This leads to salt and water retention, hypertension, inflammation, dyslipidemia, diabetes - and I believe atrial remodelling and atrial fibrillation.  By restricting my patients' consumption of CHO, I am able to reduce their waist circumference/visceral obesity and return all their biomarkers to the normal range (hsCRP, HDL, triglycerides, sdLDL, SBP, DBP, IL-6, insulin, glucose, A1c, etc, etc).  I would be interested and keen to know whether CHO restriction would also halt (and maybe reverse?) atrial remodelling and keep people in sinus rhythm (or perhaps prevent atrial fibrillation in the first place).  It seems that many of the pathways between a.fib. risk factors and a.fib. itself are shared with CHO overconsumption - specifically hypertension, diabetes, obesity, alcohol and immoderate lifestyles.  Seems we can add a.fib. to the cluster of diseases caused by the Western diet.
	# 4 of 6	September 24, 2012 08:30 (EDT)
	Steve	Have any studies been conducted to see if the conditions triggering afib can be reversed by losing weight?   Or is the damage once done, permanent?
	# 5 of 6	October 2, 2012 09:15 (EDT)
	m rothkopf	Is a calorie a calorie?  Those that produce insulin spikes are the most effective in storing abdominal fat.  What about resistance training vs cardio.  Are we advising are patient's properly.
	# 6 of 6	March 23, 2013 05:29 (EDT)
	Sheri Margulies-Semel	Over-Simplification Once again... blame everything on obesity! I developed AFIB when I was IN MY PEAK physical condition, as MANY afibbers do. I was working out 3 to 4 times a week, I was an ideal weight for me, and I BECAME fatter while suffering from this dreadful affliction because I could no longer exercise, was intensely depressed and had no enjoyment in life anymore at all. I also LOST weight and still had afib - paroxysmal LONE AFIB. Sure ... I'm not arguing that some obese people get afib and I'm not saying being obese is good. But don't blame obesity for afib. While sitting in many Coumadin Clinic waiting rooms that I had to frequent in those days, I saw MANY thin patients, few fat ones. I am okay now after several ablations ... sometimes thinner and sometimes heavier. But I will not allow people to get away with a generalized statement about obesity leading to afib. And a BMI of 30 is NOT the same as a BMI of 45! If I am at 27 or I am at 30 I am not taking a huge leap in health or risk factors for anything...experience has borne this out for me. I LIKE being thinner but I know that my health does not change radically from one point to the other. And certainly not my heart rhythms. And don't blame obesity for hypertension either as a FACT! I have had hypertension when thinner and fatter. I have also had NORMAL B/P in both states. Age seems to have more to do with this than weight for me and if that is true for me it's true for others. I am so tired of this endless over-simplification of what causes health problems. I will never say that being obese is better than being at a NORMAL weight, but it may NOT be worse. And to take an arbitrary figure like a BMI of 30 and say if you are OVER that BMI you are going to encounter all kinds of problems that you WON'T encounter at 27 or less...well...that's just ridiculous. Statistics are just numbers...not real lives. Doctors often get so caught up in their 'scientific' training that their good common-sense judgement disappears. Ask a patient if the DRINK, ask them if they SMOKE, ask them if they drink lots of coffee..you'll get closer to the truth with those questions than you will by putting them on a scale and JUDGING them by their weight. There are millions of really obese people who have never had ONE episode of an arrhythmia of any sort and millions of thin people who are suffering with afib, aflutter, and other SVT's. Author's disclosure (Mar 23, 2013) I have no relevant disclosures to make in connection with this topic.

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