Antiarrhythmic drugs, what and why...

Nothing new for many on here but it's all in one talk. It all seems to me treatment of the symptom(s). Wonder if anybody has come across treatments of the cause(s) of AF?
[www.youtube.com]

The short answer is no because no one knows for sure what the causes of afib are. There are some good suspects, but the real culprit hasn't been identified.

Nearly 7 years since my first episode. I'm now close to my 500th one, and I still don't know why they come and go.

Joe,
Yes, there are pockets of research scientists around the world searching for the actual cause of PAF rather than treating the symptoms. Looks like they are always battling for funding. Who wants to find the cause and cure of PAF when at the moment it is such a fantastic money spinner for the medical profession and drug companies??

Professor Svetlana Reilly of Oxford Uni in England discovered that the heart produces a bone hormone called Calcitonin. Calcitonin was thought to be only produced by the thyroid gland until Prof. Reilly found the heart producing it in quantities much greater than the thyroid.

“Professor Svetlana Reilly, BHF Intermediate Fellow at the Radcliffe Department of Medicine, said: “Discovering that calcitonin is released by the heart should open new doors for developing heart treatments.

“It looks as though calcitonin and its receptor might have been an important missing piece to the atrial fibrillation puzzle.
“We now need to explore how we can best restore the actions of this hormone to treat people with this type of AF, and to understand when the best time to treat someone would be."

Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, said: “Many of the treatments available for AF focus on restoring a normal atrial rhythm, controlling the rate at which the heart beats or thinning the blood to reduce the risk of stroke - but they do not tackle the atrial scarring seen in people with severe AF.

“These discoveries could be game-changing for the management of AF. Developing a new treatment to prevent or reverse atrial scarring could provide a lifeline to many people at risk of or living with AF.”

[www.rdm.ox.ac.uk]

Dean in Aussie

They have the research funding for expensive race horses who have afib.

[vetmed.umn.edu]
comparison between humans and horses.
Snippet of article:

“There are genetic mutations in horses that, when they occur in the same place in humans, cause irregular heartbeats,” says Molly McCue, DVM, MS, PhD, DACVIM, associate dean of research at the CVM and principal investigator on a forthcoming paper on the subject. McCue is collaborating with Sian Durward-Akhurst, BVMS, MS, DACVIM, PhD candidate at the CVM, to potentially solve the sudden cardiac-related death issue for horses on the racetrack by investigating similarities and differences between how human athletes and racehorses experience cardiac arrhythmia.

“Our early research suggests that arrhythmias are tolerated better in horses,” says McCue. “Understanding why that is the case is important for horses. It is also important because if we can understand why horses tolerate it, it could point to therapies for humans.”

Athletic horses die of cardiac dysfunction less regularly than human athletes, but horses develop cardiac arrhythmias more frequently than human athletes do. Horses typically survive arrhythmias of greater magnitude than those that humans can survive. The team doesn’t know how many forms of atrial fibrillation there are in horses, but in humans there are multiple—some are caused by abnormal heart structure, but there are also those that develop without any pre-existing structural abnormalities.

Since arrhythmias are more prevalent among human athletes with larger (but still healthy) hearts than among human athletes with smaller hearts—and because racehorses are specifically bred to have larger hearts—the researchers suspect that horses with larger healthy hearts are also more likely to experience atrial fibrillation than their counterparts with smaller hearts. The scientists are on the hunt for ways to effectively measure heart size in athletic horses and will use ultrasound to eliminate horses with any cardiac abnormalities from the study.

Physicians can assess human athletes’ electrocardiogram to determine when they should retire. McCue and Durward-Akhurst are trying to develop similar testing in racehorses to help them retire before they develop a catastrophic arrhythmia. And understanding the mutations could help veterinarians anticipate problems, treatment, and prognosis for a racing career’s longevity and risk of sudden death.

“We have also already found mutations that could be causing atrial fibrillation,” says Durward-Akhurst, “Our most recently funded projects will allow us to prove which of those potential culprits are causing it and other cardiac arrhythmias.”



[training.arioneo.com]

[www.ncbi.nlm.nih.gov]. Same study a peer article

[pubmed.ncbi.nlm.nih.gov]

[thehorse.com]


[twin-cities.umn.edu]
Snippet:
“Our goal is to develop screening diagnostic tools to identify horses at high risk of sudden cardiac death. This would allow us to monitor these horses more closely and only allow them to race when they are safe to do so. Additionally, once we identify the genetic cause of these arrhythmias, we will be able to develop a genetic test that allows breeders to make educated breeding decisions to reduce the frequency of arrhythmias and sudden cardiac death in racehorses.”

Sian Durward-Akhurst is an assistant professor of genetics, genomics, and large animal internal medicine. Her primary interests include cardiovascular disorders, in particular cardiac arrhythmias that contribute to sudden cardiac death. Her research focuses on understanding the genetic and electrophysiologic mechanisms of these arrhythmias in horses. She also investigates other detrimental diseases in horses that are similar to simple inherited diseases in humans.”



Edited 3 time(s). Last edit at 11/12/2022 10:41PM by susan.d.

Interesting Susan! Racehorses might solve AF burden

Thank you for the link Dean! Now, how can we increase our calcitonin output?

Looks like they are onto something. Recently i had a bone density scan and found that i have Osteopenia. Left femoral neck is 0.682gm/cm*2 which is a T-score of -1.7 and a Z-score of -.08 (normal BMD: T-Score more than -1.00; Osteoporosis: less than -2.50.
And i thought i was ok at 72 yo, BMI 21, low visceral fat and active .

As for AF research funding i'm afraid you are spot on. Why bother when they can make immense fortunes selling a non sterilizing vaccine and be totally liability free and have a chorus of powerful people promoting it . Naturally, funding will go in the direction where the money is. Capitalism at it's best

Google says:

Quote

How do you increase calcitonin?
What stimulates calcitonin release? Your thyroid releases calcitonin based on the level of calcium in your blood. When your blood calcium levels increase, your thyroid releases calcitonin in higher quantities.3 Feb 2022

Yet others on this forum find that high calcium intake makes AF worse - go figure
In the last few weeks i began eating milk products again (after the bone density scan )and i suspect my AF propensity has increased.

Quote
Joe
Google says:How do you increase calcitonin?
What stimulates calcitonin release? Your thyroid releases calcitonin based on the level of calcium in your blood. When your blood calcium levels increase, your thyroid releases calcitonin in higher quantities.3 Feb 2022
Yet others on this forum find that high calcium intake makes AF worse - go figure
In the last few weeks i began eating milk products again (after the bone density scan )and i suspect my AF propensity has increased.

It's likely related to quantities. Some is good, some more is already too much, and too much may be bad.
How much is too much is likely very individual.

In regards to my AFIB treatment path, I can say one of the most uncertain, frightening and stressful periods was when my local EP (at the time) essentially started down the list of AA's for me to sample. Every one was a combination of ineffectiveness and side-effects, like 3-4 second conversion pauses and 4 day hospital stays. Hindsight is indeed 20-20, and if I could, I'd go back and go to Texas Cardiac Arrthymia first. Cause or symptom...at the time a patient mostly just wants sinus rhythm.

Quote
Joe
Looks like they are onto something. Recently i had a bone density scan and found that i have Osteopenia. Left femoral neck is 0.682gm/cm*2 which is a T-score of -1.7 and a Z-score of -.08 (normal BMD: T-Score more than -1.00; Osteoporosis: less than -2.50.
And i thought i was ok at 72 yo, BMI 21, low visceral fat and active .

Thoughts on osteopenia.

See the stuff on boron in this post: [forums.apoe4.info] May have a hard time getting boron/borax in Oz.

Stuff on strength training in this post: [forums.apoe4.info]

This book on osteogenic loading: [www.amazon.com] On this, the author's company has an iOS app, Fractureproof. [www.jaquishbiomedical.com] The research suggests that a load of 4.2 times your wieght must be applied to stimulate bone growth - I think this is one way but other strenght training will also do IMO. Anyway the app can use the phone's accelerometer to sense the load if you connect the phone to your body. I have a case with a holster & will put it on a tight belt on one hip. Then I will jump rope and come down as hard as I can on one leg till I get to > 4.2 x. Then reset the app and repeat on the other hip. In my case, I weigh around 170# (77 kg) so 4.2 times is 714#'s (324 kg). I usually strive for 800#'s (363 kg). This might be not appropriate for everyone. I do this about once a week, only rep on each side as long as the force is high enough. In the US the book author has a company, Osteostrong, where they use isometric loading at their facilities to generate these forces safely.



Edited 1 time(s). Last edit at 11/13/2022 08:08AM by GeorgeN.

How do you know how many # you are generating by jumping?

I too have osteopenia. I can’t jump rope and avoid enriched calcium (tachycardia) and am dairy free. Problem. I switched almond milk brands and have had flutter since 10am yesterday. Back to Whole Foods brand.

I choose not to get injections my oncologist recommended for now because of the risk of jaw fracture.

[www.mayoclinic.org]

The type of calcium one takes is important. There are several companies - one is Algae Cal - that recommends plant based calcium. Calcium supplements made from rocks (which several due) are problematic for arteries and heart issues. I have osteopenia/osteoporosis. I can tell you from my own experience that my spine went from osteoporosis to normal within 2 years using plant based calcium. Still working on hip improvement numbers, which typically take longer. I have not experienced any changes in my AFIB issues with calcium either plus or minus.

My rheumatologist was impressed with my numbers, but still recommends one of those drugs to speed up the process for hips. The newest drug Evenity states risk of heart attack or stroke. Why would I want to take that if I already have a risk? Also jaw fractures and femur fracture risk.

Also started Osteostrong treatment to speed up the process.

Here is an article that reviews this topic:

[www.trioplantbased.com]

I have been down the RX path for over 40 years. Unfortunately, I have found I have to choose between side effects even after ablations. I have a strong belief that in folks like me who were diagnosed at a young age - 30 for me - there is a genetic component. In the meantime, we have what we have for treatment options. I hope I live long enough to see a significant breakthrough.

Quote
Dean
“These discoveries could be game-changing for the management of AF. Developing a new treatment to prevent or reverse atrial scarring could provide a lifeline to many people at risk of or living with AF.”

My report from Natale on my ablation from a few days ago says “moderate atrial scarring.” I was surprised as my Afib had been pretty well controlled by drugs until recently. What are the implications of the scarring and is there any evidence that it could be reversed?

Quote
susan.d
How do you know how many # you are generating by jumping?

The iOS app I mentioned, Fractureproof, uses the phone's accelerometer to figure it out. I actually think they put this in the app as a marketing ploy to show that for most people, it can't be done. I commonly put on a weightlifting belt to connect the phone tightly to my body (put the phone in between the belt & my hip.

In this link I posted above: [forums.apoe4.info] there is information on Doug McGuff MD's strength training approach. For many, it is probably a safer approach than my slamming my leg down (the research on this was done looking a the strength of gymnasts' bones from doing their dismounts). McGuff's approach is superslow strength training to failure. Here is a quick overview: [kadavy.net] It can also be done isometrically as in "timed static contractions (TSC)." This is an isometric protocol with 90 second isometric holds. 30 seconds at perceived 50% exertion then going to 30 seconds at 75% perceived exertion and 30 seconds at 100% exertion. No rest between the 30 second periods. It is mentally very demanding, I use TSC as a part of my isometric workouts.

The Osteostrong folks use isometric loading with their equipment at their facilities as their protocol. Doesn't have to be long duration or frequent.

Susan, I have Osteoporosis (along with severe Osteoarthritis) and I was on Prolia injections for some years before I began experiencing pain in my upper thighs. Dr immediately stopped the injections as the risk of fracture of the Femur was apparently high ( apparently a side effect of the drug, which no one told me about prior to starting ) My bone density had improved somewhat so I did stop.
Fast forward 10 years and the latest Dexa Scan showed my Osteoporosis has returned again, my pelvis is demineralized and my bones are worse than ever.
My Doc wanted me to start Prolia again despite me telling her about the problems I had the first time around. She insisted I start the injections again, and I didn't argue. I just didn't fill out the script.
Also, the issue with Prolia is that once you stop, your bones lose any gains very quickly and continue to lose density at a faster rate (another side effect I wasn't advised about)

So we are damned if we do and damned if we don't

[quote Daisy My report from Natale on my ablation from a few days ago says “moderate atrial scarring.” I was surprised as my Afib had been pretty well controlled by drugs until recently. What are the implications of the scarring and is there any evidence that it could be reversed?


Daisy, I am wondering if Dr. Natale talked to you about this or if you just read it on the report.



Edited 1 time(s). Last edit at 11/14/2022 11:55AM by Pixie.

Quote
Daisy
My report from Natale on my ablation from a few days ago says “moderate atrial scarring.” I was surprised as my Afib had been pretty well controlled by drugs until recently. What are the implications of the scarring and is there any evidence that it could be reversed?

The scarring may be why you have afib, not a result of it. What caused it? Who knows. A viral infection at some point you weren't aware of, possibly, and that could have been years ago, long before you developed afib.

No, there's no way to reverse scarring.

Interesting--so I had it backwards and the scarring probably caused the Afib. I saw this in my report after Natale had left the room but thinking back, what he had told me earlier now makes more sense--I'd guess that mitral valve prolapse and regurgitation were the culprits:

Quote

Atrial fibrillation (AF) is a common sequela of degenerative mitral regurgitation (DMR) and is frequently present in patients referred for surgery for DMR.(1) DMR may lead to the development of AF via left atrial (LA) volume and pressure overload, progressive atrial fibrosis, LA enlargement, and electroanatomic remodeling.(2–5) Progressive LA enlargement and remodeling – hallmarks of long-standing DMR – promote AF substrate by affecting cell coupling, altering conduction velocity, and promoting reentry.(6)

[www.ncbi.nlm.nih.gov]

He had told me that because of my history of mitral valve disease, he expected that he would need to do a more aggressive ablation--I just didn't understand why, but this article lays it out.

Quote

Surgery may prevent the progression of scar formation in the atrium but is not expected to eliminate fibrosis generated by DMR-induced pressure and volume overload. In fact, once AF develops, it probably leads to an increasing degree of fibrosis - AF begets AF- which in turn results in increased substrate for AF.(30) This vicious cycle is likely to lead to continued worsening of the AF burden despite valve surgery and to reduce survival compared with patients free of AF, as described above...The presence of AF in patients with DMR is currently rated as a class IIa recommendation for MV surgery in the both American and European guidelines on valvular heart disease.(17,18) A class I recommendation can be applied when there is strong supportive evidence that a treatment option is beneficial, even if obtained from a non-randomized study (i.e., class I, level . Given the strength of the above evidence from Grigioni and colleagues, it may be time to re-evaluate the guidelines regarding the presence of AF in DMR patients.

This is interesting as it looks like mitral valve repair should be done earlier rather than later if the patient has Afib. Wish I had had this information sooner!

Quote
Joe

Thank you for the link Dean! Now, how can we increase our calcitonin output?

Vitamin K2 which Natto has lots of.



[dralexrinehart.com]

In terms of the role of the thyroid releasing calcitonin, I have hypotherydism (low functioning thyroid) and elevated TSH levels. I'm on levothyroxine.
Does a low functioning thyroid therefore release less calcitonin? That's would be a contributing factor to AF.
Am I reading that correctly?
Thanks Blake

Sorry, bit late - Covid positive for the last 6 days and fairly sick with it (ok now).

Thank you everybody for the advise on Osteopenia!
I have been adding a little Borax (and colloidal silica, selenium, lithium, K and Na,) to my distilled (to take the fluoride out because of my elevated TSA) drinking water for over a year.
Perhaps my Osteopenia is on the improve anyway - will find out in another 2 years when i'll get another test.
The weight exercise advise from George i'll take on board.
Natto has also been on my regular diet for well over a year. On days when i don't eat it i take K2/MK7 - at least 180mg

Since I've been diagnosed with osteoporosis (at a relatively-young age - 61) I've started eating a spoonful of natto every morning. In addition, I try to eat some form of leafy greens every evening (spinach or kale or arugula). This is despite doing weight training since age 25. My doctor tells me it's due to my urine leaking excess calcium. She put me on hydroxochlorothiazide (25 mg. once a day) which has gotten my urinary calcium in range. It doesn't appear to be making my afib worse (although I should watch it since it can lower potassium and cause dehydration).

In reading through this thread and links, I'm highly motivated to stay of Prolia and the other bone drugs. It's alarming that once you start, if you get off of them you lose bone faster. So far my doctor hasn't told me I need to go on it yet. So hopefully the natto helps. I'm also continuing weight training but pushing harder and really trying to go to failure.

I looked up bioDensity but there aren't any places in my area for it. There were two about an hour from my place, but they've gone out of business apparently (their websites didn't work and the bioDensity webpage is out of date since it's still listing them). I looked up another similar type of program (Osteostrength I think), but, same issue, none anywhere near where I live (the closest one is in Texas).