Dr John Mandrola practices cardiac electrophysiology in Louisville, KY. He finished training at Indiana University in 1996. His practice encompasses catheter ablation, including an eight-year experience with AF ablation, device implantation, and consultative EP. Outside of the EP lab, Dr Mandrola's two hobbies include competitive cycling and writing. He has maintained a medical, fitness, and cycling blog, Dr John M, for the past two years.
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Obesity and atrial fibrillation--New information for the whiteboardSep 18, 2012 22:25 EDT
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.