Strophanthin

It is claimed that it helps with certain types of AF? Does anybody know more about it or used it???

Claimed by who? Where? Never heard of it before but a quick googling suggests it's a rather dangerous substance.

My gosh! Used in historic period in Africa as an arrow poison. I can see why you might be interested as a cardiac remedy
[www.ncbi.nlm.nih.gov]

BUT it’s so dangerous!! It’s a rat poison. They tested it on rats.



Edited 1 time(s). Last edit at 07/13/2022 02:30AM by susan.d.

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susan.d
My gosh! Used in historic period in Africa as an arrow poison. I can see why you might be interested as a cardiac remedy
[www.ncbi.nlm.nih.gov]

BUT it’s so dangerous!! It’s a rat poison. They tested it on rats.

My interpretation of your link is that it is a very interesting substance. Obviously, as in many substances (including water), the dose makes the poison.

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Carey
Claimed by who? Where? Never heard of it before but a quick googling suggests it's a rather dangerous substance.

By a German doctor being interviewed on a Swiss channel. Unfortunately it's in German. The doctor had a heart attack in his early 40s and is still going strong at mid 70 with a special interest in Strophantin. Apparently it was used many years ago but has fallen out of favour/use - i'm not quite sure why but suspect it might be because of the critical dosing required or better safer drugs since? Of course, no money in promoting it either if one looks at it cynically.
It's important that he mentioned it's effect on helping AF only in passing.

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Joe

Claimed by who? Where? Never heard of it before but a quick googling suggests it's a rather dangerous substance.
By a German doctor being interviewed on a Swiss channel. Unfortunately it's in German. The doctor had a heart attack in his early 40s and is still going strong at mid 70 with a special interest in Strophantin. Apparently it was used many years ago but has fallen out of favour/use - i'm not quite sure why but suspect it might be because of the critical dosing required or better safer drugs since? Of course, no money in promoting it either if one looks at it cynically.
It's important that he mentioned it's effect on helping AF only in passing.

Dr. Kern?
[www.faim.org]

[www.linkedin.com]
(Last sentence)

Or German doctor Edens?
[www.linkedin.com]

Thank you for the links Susan. It wasn’t Dr Kern but this organisation was mentioned. Please I wasn’t dreaming re AF.

Might as well mention it - 3 days ago I had a 6 months routine Cardiologist appointment. I asked him about Strophanthin and he said that he had no idea about it. Maybe he just thought that I'm wasting his time and should go away?
Anyway, i don't think I'll go back to him. He is an arrogant bugger offering strict workshop manual advise only. I'd be better off consulting with an AI algorithm if there were one available.

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Joe
. I'd be better off consulting with an AI algorithm if there were one available.

It can’t be any different to two virtual cardio phone appointments this week. One was a video pre TEE physical (6 month watchman tee) and the other a phone audio Dr appointment. If you don’t get a physical exam or at least an ekg there isn’t any difference between an AI or phone IMHO.

Had a few AF episodes lasting for 8 to 12 hours in the last few months, but got into NSR with 100 to 150 mg Flec. My AF is not getting better that's why i look at everything i come across. The majority of time we are in NSR so some imbalance must be the trigger. Why is it so difficult for all these smart medicos and researchers to work that out (maybe they aren't that smart?). Ablation, to me, is just treating the symptom...

Given that AF is due to cardiomyopathy and Strophanthin is said to improve cardiac circulation an plays a role in acting on certain ion channels of cells (as does Flec.) it would be nice if one could find some trail data or even case experiences. I get that no Pharma will pay for any trail since the substance is not under patent.
Bit frustrated so please excuse my rant.
[journals.physiology.org]

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Joe
Given that AF is due to cardiomyopathy and Strophanthin is said to improve cardiac circulation

Not exactly. AF is thought to be due to atrial myopathy, which isn't the same thing as cardiomyopathy and may not be caused by the same factors. Specifically, unlike the ventricles, it may not be due to circulatory issues at all but more likely atrial stretch and fibrosis. So improving cardiac circulation may not be helpful.

It would really help if you would point us to the sources that make these claims that it improves "certain types" of AF, and what's meant by "certain types."

Try these:
[www.sciencedirect.com]
[pubmed.ncbi.nlm.nih.gov]
[pubmed.ncbi.nlm.nih.gov]

I am personally a fan of cardizem. A 15mg IV push over a 8 minute period (drip is ineffective) usually converts me.

[www.aafp.org]
They recommend 5-15mg IV drip spread over an hour. For me it’s 100% ineffective. Just give me my 15mg push (straight into the vein) slowly for 8 minutes does the trick. A 1/4” push of the syringe every minute is what I instructed the ER…and for me it is 100% effective. But everyone is different

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Mechanism of Action
Primarily, diltiazem inhibits the inflow of calcium ions into the cardiac, smooth muscle during depolarization. Reduced intracellular calcium concentrations equate to increased smooth muscle relaxation resulting in arterial vasodilation and, therefore, decreased blood pressure.27 Aug 2021

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Not exactly. AF is thought to be due to atrial myopathy, which isn't the same thing as cardiomyopathy and may not be caused by the same factors. Specifically, unlike the ventricles, it may not be due to circulatory issues at all but more likely atrial stretch and fibrosis. So improving cardiac circulation may not be helpful.

It would really help if you would point us to the sources that make these claims that it improves "certain types" of AF, and what's meant by "certain types."

I'm only thinking out loud from a lay's point of view hoping to find some answers.
After my aprx 4 month of permanent AF in 2015 i was told that my left atrium was very large. After a year or so of being in NSR and having another US i was told that my left atrium was almost back to normal. At the beginning of this year i had an US and was told (after specifically asking) that my atrium was only slightly larger than normal. No mention of fibrosis (possibly not visible on an US?).
Still, even if i have fibrosis - why is it that I only at certain times (meeting certain parameters?) i go into Af? Got to have to do with cellular condition and or intracellular environment, or perhaps an imbalance of my nervous system? Why else would cardizem work for Susan the way it does? Or Flec with me - it also modifies polarisation and/or depolarisation of the atrium's (and other?) cells?
Carey, hope you don't get frustrated with my uninformed rambling, it certainly is not my intension to do so.

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Joe
After my aprx 4 month of permanent AF in 2015 i was told that my left atrium was very large. After a year or so of being in NSR and having another US i was told that my left atrium was almost back to normal. At the beginning of this year i had an US and was told (after specifically asking) that my atrium was only slightly larger than normal. No mention of fibrosis (possibly not visible on an US?).
Still, even if i have fibrosis - why is it that I only at certain times (meeting certain parameters?) i go into Af? Got to have to do with cellular condition and or intracellular environment, or perhaps an imbalance of my nervous system? Why else would cardizem work for Susan the way it does? Or Flec with me - it also modifies polarisation and/or depolarisation of the atrium's (and other?) cells?
Carey, hope you don't get frustrated with my uninformed rambling, it certainly is not my intension to do so.

That enlarged left atrium causes stretching, stretching causes fibrosis, and fibrosis causes afib. And then afib causes more atrial enlargement, so it's a vicious cycle. Atrial stretch is why endurance athletes, weight lifters, and people with hypertension get afib -- because all those things stretch the atrial walls. No, fibrosis can't be seen on ultrasound. To see fibrosis you would need what's known as a delayed enhancement MRI.

If you ever figure out what actually causes afib to start and stop at certain times, publish immediately and collect your Nobel Prize. :-)

I'm not the least bit frustrated with your questions. That's what this forum is for!

Just throwing out my 2 cents on this. I agree with Joe --"Got to have to do with cellular condition and or intracellular environment". I think it's the cellular changes in electrons (the calcium/sodium, mag and potassium) which makes the heart tissue/cells more subject to excitability.

Quoting Mildred Seelig's (MD, MPH) book, The Magnesium Factor : "The normal concentration of magnesium ion inside cells is easily 10,000 times that of intra-cellular calcium ions---under healthy conditions. But if the amount of magnesium in a cell falls, for any reason, calcium ions flow into the cell. Higher than normal calcium inside a cell excites a LOT of reactions. It puts the cell into a hyperactive state. (Heart and blood vessel cells are especially excitable because of their biological need to react rapidly in fight or flight situations)."

Wouldn't it be nice if just getting/keeping our body stores of magnesium 100% might solve afib?