AF & Strokes: Who's the Real Daddy?

Very interesting new video from Sanjay Gupta, York Cardiology (UK).

[www.youtube.com]

Makes case that atrial myopathy (atrial wall weakness) is the actual cause of clots/strokes and NOT Afib itself. Says treatment (specifically anticoagulation) needs to be looked at differently, targeted differently in terms of who does and does not need it. Atrial size, strength, fibrosis needs to be assessed. Comorbidities too of course, as is now the case. Afib itself not that relevant. He says AF itself is NOT the cause of clots. It was an eye-opener for me.

Worth a watch! 15 minutes.

kim

Funny thing.... Susan I joked about this in PMs - "what if Eliquis is the cause of afib"

I had the one event, got put on eliquis and more events until persistent af.

I haven't watched video yet but I will

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NotLyingAboutMyAfib
Funny thing.... Susan I joked about this in PMs - "what if Eliquis is the cause of afib"

I had the one event, got put on eliquis and more events until persistent af.

I haven't watched video yet but I will

I think Sanjay Gupta's point was that people who have atrial myopathy but not afib probably do need anticoagulant. and people who have afib but no evidence of atrial myopathy and no comorbitidites don't. atrial myopathy can be measured in various ways that exist.

My recollection of AFFIRM that Gupta mentions (I read many years ago and did not reread), is that it was based on "intention to treat." That is rate vs. rhythm control. So on the rhythm control arm, people were given rhythm meds, but they weren't necessarily in NSR, just given the meds. In other words, just because someone was in the rhythm control arm, it doesn't mean they were actually in rhythm.

That being said, my strategy for nearly 17 years has been to minimize my time in afib as well as controlling all the controllable factors (with lifestyle, not meds) in CHA2DS2-VASc, such as hypertension, T2 diabetes (or its precursor of metabolic dysfunction). Also keeping NT-proBNP (as Dr. Gupta mentions) low. My values in 2020 were 32 & 41 pg/mL with < 253 being good per Cleveland Heart Lab.

I tried relying on the UK Gupta when I first got AF and even reached out to him a few times, no response, no results.

IMHO he should have spoken very strongly for continuing anti-coagulation for those that are already on it. AF is a hassle, taking pills everyday or 2x a day is a hassle, atrial myopathy may be the daddy, but stroke is the mother-in-law from hell or the uncle that molests your children.

If yanking a fingernail out with pliers every month would prevent strokes, I'd gladly do it. Pills don't look too bad in comparison.

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NotLyingAboutMyAfib
IMHO he should have spoken very strongly for continuing anti-coagulation for those that are already on it. AF is a hassle, taking pills everyday or 2x a day is a hassle, atrial myopathy may be the daddy, but stroke is the mother-in-law from hell or the uncle that molests your children.

I have a friend who said his resting and exercise heart rates have materially increased (20 for resting, 40 for exercise for same effort). At some point a doc had seen afib. I urged him to get a workup from a cardiologist post haste, could be afib or flutter. As his CHA2DS2-VASc is at least 2, anticoagulation is likely indicated.

Atrial myopathy is an interesting theory as the genesis of a-fib, but I’m confounded by the notion that it could be the cause in the athletic community. How does exercising the heart create myopathy?

I’m not sure a-fib has a singular cause.

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wolfpack
How does exercising the heart create myopathy?

Well, overuse is a common cause of muscle injury, is it not?

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wolfpack
Atrial myopathy is an interesting theory as the genesis of a-fib, but I’m confounded by the notion that it could be the cause in the athletic community. How does exercising the heart create myopathy?

Maybe exercise creates more pressure - as in more blood pressure, more volume of blood pumped. and I got the impression that increased pressure on/in the heart is what stretches the atrial walls since they are thinner than ventricular walls so they give way first when whole system under pressure - his balloon on garden hose metaphor. and that once the atria start stretching... that can lead to myopathy?

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" (...) Another interesting observation was that when you take young healthy people who have AF, they seem to tolerate it very badly but don't tend to have strokes whereas if you take older sicker patients, they may not even know they are in AF yet they seem to be at a much higher risk of strokes. Same AF but very different stroke risk - that again does not fit. (...)

I think intense exercise creates a lot of inflammation that damages the heart. Cycling is one of the worst sports as the ability to coast and draft for recovery leads to repeated and very high levels over longer periods than running and other sports. When competitive, I had blood lactate > 18mmol tested at the Olympic training center. Easy to imagine that other inflammation markers were also greatly elevated. The diet needed to create this kind of performance is also very inflammatory.

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PoetKim

Maybe exercise creates more pressure - as in more blood pressure, more volume of blood pumped. and I got the impression that increased pressure on/in the heart is what stretches the atrial walls since they are thinner than ventricular walls so they give way first when whole system under pressure - his balloon on garden hose metaphor. and that once the atria start stretching... that can lead to myopathy?

I agree with you. I got here from 40+ years of vigorous exercise, just finished a triathlon 6 months prior to my first afib. My poor atria has been stretched to the limit and can now support fibrillation. My Atria seems to have heeled to some extent from detraining; I only do moderate exercise (walking at least 1 hr. per day). I had 77 afib episodes my first year. Now I get one every 5-7 months usually after too much indulging (food, alcohol, exercise, stress). In terms of evolution, humans have just recently started doing recreational vigorous activities. I think our hearts have not evolved to do the day in day out pounding that I did thinking it was healthy.

On an anecdotal note, I am 65 and know personally four people who have died from heart attacks. All four were endurance athletes.. One died while running (very close friend), one while biking and one swimming. I don't know of any smokers or overweight people who have died from heart issues. Find that odd...

Hi, I am 65 and I do triathlons (73 and counting) I’ve had symptomatic AF once 21 months ago - during a triathlon in Russia!
I await ablation. Echo and perfusion found no abnormalities in my heart. I’ve had asymptomatic AF 3 or 4 times since - I use a KardiaMobil 6 lead ecg device after every training session. On your view on evolution - surely natural selection has seen those who can fight and flight the best prosper? I wonder if the higher number of sedentary older people who suffer heart problems avoid AF detection by not testing their hearts ie their hearts may be more AF prone but they never find out? I continue to do triathlons but with a watchful eye - I do less intense training, monitor my heart during and after and ease off when HR exceeds a given limit. But I am interested in others experiences and fully aware I could be wrong. Nb cardiologists, including second opinion, agree with my approach whilst caveat that optimum for survival would be more moderate forms of exercise (yoga and walking). Nb2 I only do the shorter triathlons - up to 3 hours and train up to 10 hours a week (3.5 hours average across the year). Nb3 I think Joe Friel, triathlon coach, and many ageing specialists, would assert that some intensity is very good for a long healthy life.

I'm bicycling for years, but without excess. My heart was perfectly normal in late 2015, when I had my first afib episode. Back then, I was riding 5 to 7000 km/year, at the quiet AVG speed of 22-24 km/h. Since then, I've been 4 times ablated, and I barely rode 1000km/year, except for 2020 (2000km). May I say I detrained?
I'm 63, I've still afib, and my heart is still perfectly normal. Everything is normal. I've no known reason having afib.