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A new way to think about curing atrial fibrillation

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

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

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

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

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

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

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

When we are well, our atria are well.

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

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

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

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

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

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


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

7 replies on “A new way to think about curing atrial fibrillation”

OH MY!!! Dr. SH……I was in the middle of a long-winded reply and just gave up… one is listening…..And there you are…..actually LISTENING….as a
72 YO patient….I can count on one hand the docs who just shut up and
listen to what the patient is saying! And yes….with big pharma bought and paid for studies influencing how you treat us “civilians”…’s a losing battle.

What are your thoughts on fibrotic atrial cardiomyopathy as a primary disease process in patients with lone af?

Great presentation. Eye opening!
Can you provide links for Prash’s other presentations? Presentations by others at this symposium?

Hello Dr. John – that second question at the end of Dr. Sanders’ presentation is a biggie (asking at what point does a physician say to a patient: “Until you get your weight/sleep apnea under control, we won’t do an ablation..” )

Reminds me of a former colleague who was told by her orthopedic surgeon a few years ago that, until she lost at least 30 pounds, he would not do her knee surgery (because her recuperation/outcomes would be compromised with extra weight burden).

So she did, and then he did.

As a primary care physician educator – What I LOVE about your message John on the importance of Lifestyle Change for control of AFib (which you have been actively conveying for quite some time now) – is that: i) There IS now something patients can do for themselves that may be at least comparable to whatever the cardiologist might do; and ii) There IS an important message for primary care clinicians to be delivering to their many patients with AFib – especially since my perception is that not all cardiologists are yet “on board” with the importance of your Lifestyle Change message.

I found the data presented by Dr. Prash Sanders to be fascinating – showing a real effect that being overweight may convey – including anatomic LA atrial enlargement – increase in atrial pressures – fostering fibrosis and delay of atrial conduction times – all of which serve to perpetuate the vicious cycle of “AFib begetting AFib … “. THANKS for presenting this!

As a 65-year-old AF patient seeing very well trained doctors at a highly regarded clinic, I have to say that not only has no doctor ever talked to me about risk factors, they avoid the subject when I bring it up. I have none of the usual risk factors (and as far as I can tell I’ve been in normal sinus rhythm for at least 8 months now without any AF, on Flecainide), but instead of helping me try to identify what the substrate is for my AF, my doctors spend their time trying to persuade me to start OAC. I would love to have a doctor talk to me about modifying my risk factors because then he or she would not have to talk to me about what those risk factors are. When I ask, they say I might have fibrosis, but since I’m normal weight with normal echo and no coronary artery disease, no diabetes, physically active, etc. etc., why assume I have fibrosis?

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