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Cabergoline effects on the heart

Rainmanisback

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Aug 23, 2012
Messages
522
I was listening to a podcast last night and the guest mentioned the negative effects of cabergoline on the heart. According to some studies cabergoline is associated with "an increased risk of cardiac valve disease due to increased frequencies of valvular thickening, calcifications, fibrosis, and increased mitral tenting area." and since this product so widely used among our community, I thought it was a good idea to share/talk about it. If any of you guys have any knowledge about this might be worth the conversation.

"Cabergoline, a dopamine receptor-2 agonist used to treat prolactinomas and Parkinson's disease, is associated with an increased risk of cardiac valve disease due to increased frequencies of valvular thickening, calcifications, fibrosis and increased mitral tenting area. These fibrotic changes cause thickening, retraction, and stiffening of the valves, which result in incomplete leaflet closure with poor coaptation, and, mostly asymptomatic, clinically relevant regurgitation but sometimes if unrecognized earlier can lead to symptomatic heart failure. Here we present a case of cabergoline induced symptomatic right heart failure."

Cheers
 
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The contingency of valvulopathy from cabergoline is spewed-out as absolute.

Incidentally, these individuals that continually regurgitate thee-lore of absolute have not looked at clinical data.

This same homology is spoken by the unscholarly stating testosterone replacement is a common theme for CVD.

I'm sure my commentary will be taken out of context by those whom choose to rebuttal.

If it's not warranted to use a D2 agonist, don't take it recreationally in hopes to set your libido a-blaze. Not a smart idea.

Here's a good start to further your reading pleasures.


"The Third Case of Cabergoline-Associated Valvulopathy: The Value of Routine Cardiovascular Examination for Screening"

"In conclusion, it is reassuring to endocrinologists (and patients) that the prevalence of CAV in patients with prolactinoma is extremely low."

"Given this low prevalence, routine screening with echocardiography is not indicated. The recommended screening procedure should be an annual cardiovascular examination, with echocardiography reserved for patients with a murmur or those with high cumulative cabergoline doses."


"Cabergoline appears to be safe in patients with prolactinoma up to the cumulative dose of ~300 mg. The screening for valvulopathy should be restricted to those with higher cumulative cabergoline exposure."

By cumulative, there's several different longitudinal studies looking at structural changes, some of these patients were Rx'd 6-12grams per day (Parkinson's disease dosages) exceeding an cumulative dosage of >1000 mg without or very minimal, reversible valvular disease. Then there's been similar studies showing permanent structural damage. These were dosages that were taken for years. Not some miniscule 0.25mg (twice-weekly) for short periods of time.

It's like saying, "you'll develop cirrhosis if you drink alcohol". Yeah, sure in an abusive manner or you have a genetic predisposition to some hepatic disease, or inclusion of hepatotoxic drugs that potentiate the ethanol damaging effects from alcohol to your liver.

I would be more concerned with my immune system (prolactin facilitates as a hormone and a cytokine) due to pushing my Prl levels too low, rather than placing concerns of the possibility of valvulopathy. As well, chancing a paradoxical effect on my libido by driving my Prl in the dirt.

Our immune system is dependent on physiological levels of prolactin, like with many other hormones, prolactin is a immunoregulating hormone. We have prolactin receptors in our T lymphocytes and B lymphocytes, this also could disrupt macrophage activation. Not a good thing. Both, T and B lymphocytes produce antibodies against foreign antigens, such as bacterial infections. So I'd be a little cautious on long-term hypoprolactinemia. An occasional D2 agonist, isn't a big deal. Long-term, I personally wouldn't use.

And to clear the air on the pathogenesis of valvulopathy via Caber, it's not a relationship with circulating levels of Prl (to the best of my knowledge). It's due to off-site effects by targeting-->5-Hydroxytryptamine 2B receptors (type of serotonergic receptor). In which are highly abundant in heart tissue, this specific receptor regulates cardiac tissue structure and function.
Ecstasy and Fen-Phen (long been banned) are two other drugs that directly express agonistic effects on 5-Hydroxytryptamine 2B receptors.

So don't go banging any Ecstasy with your Caber.
 
So don't go banging any Ecstasy with your Caber.
Unless Ecstacy is the name of a hot stripper.....(listen for rim shot.....)

Stewie.....Do you think p5p has the ability to control prolactin? After searching I found a few members here that had success in using it. Others didnt. I suppose part of their results could depend on the size cycle they were running.
 
Unless Ecstacy is the name of a hot stripper.....(listen for rim shot.....)

Stewie.....Do you think p5p has the ability to control prolactin? After searching I found a few members here that had success in using it. Others didnt. I suppose part of their results could depend on the size cycle they were running.
I've seen some individuals claim this as well. Purportedly pyridoxal-5′-phosphate increases dopamine, in which tames down prolactin.

There's a caveat with this to, possibly. Taking in too much B6 by way of foods and supplementation in conjunction with pyridoxal-5′-phosphate could lead to toxic sensory (peripheral) neuropathy. This is coming by way of scant literature, so take that for what it's worth.
 
I've seen some individuals claim this as well. Purportedly pyridoxal-5′-phosphate increases dopamine, in which tames down prolactin.

There's a caveat with this to, possibly. Taking in too much B6 by way of foods and supplementation in conjunction with pyridoxal-5′-phosphate could lead to toxic sensory (peripheral) neuropathy. This is coming by way of scant literature, so take that for what it's worth.
Thanks for the response. I'll do some searches on possible neuropathy. Ran across this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3805452/ Makes me wonder if the dopamine effect of Wellbutrin might help to keep prolactin in range.
 
I was listening to a podcast last night and the guest mentioned the negative effects of cabergoline on the heart. According to some studies cabergoline is associated with "an increased risk of cardiac valve disease due to increased frequencies of valvular thickening, calcifications, fibrosis, and increased mitral tenting area." and since this product so widely used among our community, I thought it was a good idea to share/talk about it. If any of you guys have any knowledge about this might be worth the conversation.

"Cabergoline, a dopamine receptor-2 agonist used to treat prolactinomas and Parkinson's disease, is associated with an increased risk of cardiac valve disease due to increased frequencies of valvular thickening, calcifications, fibrosis and increased mitral tenting area. These fibrotic changes cause thickening, retraction, and stiffening of the valves, which result in incomplete leaflet closure with poor coaptation, and, mostly asymptomatic, clinically relevant regurgitation but sometimes if unrecognized earlier can lead to symptomatic heart failure. Here we present a case of cabergoline induced symptomatic right heart failure."

Cheers
My endo had me on .5mg cabergoline for a benign macroplactinoma. i have been on it for 8 years same dose once a week. he said this can happen but is very rare and that is only seen in older patients on a much much higher dosage of cabergoline for Parkinson's.

Long-term cabergoline therapy is not associated with valvular heart disease in patients with prolactinomas - PubMed (nih.gov)
 
The contingency of valvulopathy from cabergoline is spewed-out as absolute.

Incidentally, these individuals that continually regurgitate thee-lore of absolute have not looked at clinical data.

This same homology is spoken by the unscholarly stating testosterone replacement is a common theme for CVD.

I'm sure my commentary will be taken out of context by those whom choose to rebuttal.

If it's not warranted to use a D2 agonist, don't take it recreationally in hopes to set your libido a-blaze. Not a smart idea.

Here's a good start to further your reading pleasures.


"The Third Case of Cabergoline-Associated Valvulopathy: The Value of Routine Cardiovascular Examination for Screening"

"In conclusion, it is reassuring to endocrinologists (and patients) that the prevalence of CAV in patients with prolactinoma is extremely low."

"Given this low prevalence, routine screening with echocardiography is not indicated. The recommended screening procedure should be an annual cardiovascular examination, with echocardiography reserved for patients with a murmur or those with high cumulative cabergoline doses."


"Cabergoline appears to be safe in patients with prolactinoma up to the cumulative dose of ~300 mg. The screening for valvulopathy should be restricted to those with higher cumulative cabergoline exposure."

By cumulative, there's several different longitudinal studies looking at structural changes, some of these patients were Rx'd 6-12grams per day (Parkinson's disease dosages) exceeding an cumulative dosage of >1000 mg without or very minimal, reversible valvular disease. Then there's been similar studies showing permanent structural damage. These were dosages that were taken for years. Not some miniscule 0.25mg (twice-weekly) for short periods of time.

It's like saying, "you'll develop cirrhosis if you drink alcohol". Yeah, sure in an abusive manner or you have a genetic predisposition to some hepatic disease, or inclusion of hepatotoxic drugs that potentiate the ethanol damaging effects from alcohol to your liver.

I would be more concerned with my immune system (prolactin facilitates as a hormone and a cytokine) due to pushing my Prl levels too low, rather than placing concerns of the possibility of valvulopathy. As well, chancing a paradoxical effect on my libido by driving my Prl in the dirt.

Our immune system is dependent on physiological levels of prolactin, like with many other hormones, prolactin is a immunoregulating hormone. We have prolactin receptors in our T lymphocytes and B lymphocytes, this also could disrupt macrophage activation. Not a good thing. Both, T and B lymphocytes produce antibodies against foreign antigens, such as bacterial infections. So I'd be a little cautious on long-term hypoprolactinemia. An occasional D2 agonist, isn't a big deal. Long-term, I personally wouldn't use.

And to clear the air on the pathogenesis of valvulopathy via Caber, it's not a relationship with circulating levels of Prl (to the best of my knowledge). It's due to off-site effects by targeting-->5-Hydroxytryptamine 2B receptors (type of serotonergic receptor). In which are highly abundant in heart tissue, this specific receptor regulates cardiac tissue structure and function.
Ecstasy and Fen-Phen (long been banned) are two other drugs that directly express agonistic effects on 5-Hydroxytryptamine 2B receptors.

So don't go banging any Ecstasy with your Caber.
Well said 👏🏻
 

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