Not bicuspid?!?

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preciosa1974

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So I had 2 echos done before surgery. I did have different statements. one said tricuspid, one said bicuspid valve. I had a ct, and an angiogram done as well. Anyways, I was told my valve was bicuspid. But it turns out it wasn’t. I just read the report and the surgeon notes he can’t discern what caused the severe aortic insufficiency. He did think about repairing, but wasn’t able to so continued with the replacement. I’ve had some symptoms for years, but recently the symptoms escalated which caused me to get treatment so quickly. I am wondering if, even though it wasn’t bicuspid, I had some type of congenital issue. All of the doctors who saw me said this is something my heart has been dealing with for a very long time. I just thought it being bicuspid was the reason. I will ask the surgeon when I see him. Interesting.
 
Sounds familiar. I had many echo's, CT's, TEE's, and they all said bicuspid aortic valve. Not until surgery when the surgeon got in there, did he discover it was unicuspid. You may have severe calcification. Further tests and evaluation needed. Good luck!
 
I already had it replaced and it was tricuspid with no calcification. His notes said he couldn’t discern what caused the severe AI and regurgitation. 🙃 I’m so young for valve disease, I thought for sure it was a congenital defect. Who knows?!?
 
Great to hear that all worked out. What valve did you end up getting?
 
But it turns out it wasn’t
this is good news in some ways; for now you are less likely to have the connective tissue disorder which is associated with BAV (aneurysm).

Have you had Lp(a) tested. Some cause for the stenosis exists and you should now start slowly researching and thinking about that.

Are you "pre-diabetes" (sheet, I'm sounding like @Chuck C now). But I'm an old dog who loves learning new tricks.
 
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I also had every possible test under the sun prior to surgery and had 6 different surgeons review my results. Everyone said bicuspid, but only one said unicuspid, because he said combination of ascending aorta aneurysm, root dilatation + heavily regurgitant & calcified valve is very rare in my age group. He though unicuspid more likely. He ended up being right.

I suspect that interpretation of these tests probably involves a fair amount of guess work. It is like Pellicle said, not having a bicuspid valve is good news, as the probability of developing an aneurysm is much lower in that case.
 
this is good news in some ways; for now you are less likely to have the connective tissue disorder which is associated with BAV (aneurysm).

Have you had Lp(a) tested. Some cause for the stenosis exists and you should now start slowly researching and thinking about that.

Are you "pre-diabetes" (sheet, I'm sounding like @Chuck C now). But I'm an old dog who loves learning new tricks.
What is LP(a)? I am not pre-diabetes. Im would like to know what contributed to this so I could make sure no other health issues arise or at least be aware of what could.
 
This is what the pathology report stated

FINAL DIAGNOSIS:

Aortic valve leaflets, valve replacement:
• Three valve leaflets with myxoid change.
• No inflammation or calcifications identified.
 
Lp(a)
https://www.athero.org.au/fh/lipoproteina/
This is what the pathology report stated

FINAL DIAGNOSIS:

Aortic valve leaflets, valve replacement:
• Three valve leaflets with myxoid change.
• No inflammation or calcifications identified.
Interesting, I'm still trying to work out how stenosis forms without calcification

Could anyone chuck me a bone here?

https://en.wikipedia.org/wiki/Aortic_stenosis#Pathophysiology
Inflammation is thought to be involved in the earlier stages of the pathogenesis of AS and its associated risk factors are known to promote the deposition of LDL cholesterol and lipoprotein(a), a highly damaging substance, into the aortic valve, causing significant damage and stenosis over time.[6][23] Infiltration of inflammatory cells (macrophages, T lymphocytes), followed by the release of inflammatory mediators such as interleukin-1-beta and transforming growth factor beta-1 occurs. Subsequently, fibroblasts differentiate into osteoblast-like cells, which results in abnormal bone matrix deposition leading to progressive valvular calcification and stenosis.​
 
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Lp(a)
https://www.athero.org.au/fh/lipoproteina/

Interesting, I'm still trying to work out how stenosis forms without calcification

Could anyone chuck me a bone here?

https://en.wikipedia.org/wiki/Aortic_stenosis#Pathophysiology
Inflammation is thought to be involved in the earlier stages of the pathogenesis of AS and its associated risk factors are known to promote the deposition of LDL cholesterol and lipoprotein(a), a highly damaging substance, into the aortic valve, causing significant damage and stenosis over time.[6][23] Infiltration of inflammatory cells (macrophages, T lymphocytes), followed by the release of inflammatory mediators such as interleukin-1-beta and transforming growth factor beta-1 occurs. Subsequently, fibroblasts differentiate into osteoblast-like cells, which results in abnormal bone matrix deposition leading to progressive valvular calcification and stenosis.​
I could be wrong but I don’t think I had stenosis. Just severe AI with moderate to severe regurgitation.
 
I was asked this several times, but nope. I never had rheumatic fever. At least as far back as I can recall.
I believe there are other causes for this result

This 2011 paper makes the following points:

Mechanistic studies examining the contributions of true ectopic osteogenesis, nonosseous calcification, and ectopic osteoblast-like cells (that appear to function differently from skeletal osteoblasts) to valvular dysfunction have been facilitated by the development of mouse models of CAVS. Recent studies also suggest that valvular fibrosis, as well as calcification, may play an important role in restricting cusp movement, and CAVS may be more appropriately viewed as a fibrocalcific disease.​

underline mine

PS: this article puts forward something (perhaps not directly useful on myocardial tissue contribution)

1673047399830.png


lastly @preciosa1974 another causal possibility for your valve

https://pubmed.ncbi.nlm.nih.gov/19683643/
 
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oh and because the above is perhaps a little stale now, best start from here:
https://en.wikipedia.org/wiki/Cardiac_fibrosis
Cardiac fibrosis commonly refers to the excess deposition of extracellular matrix in the cardiac muscle, but the term may also refer to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts.

again, underline mine

an article in the references from that wikipedia

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC194859/
Interesting. I have never been a drug user. Tried pot a couple of times but never anything harder than that. I don’t even drink that much. I’d love to read anything else you find. I’ve tried googling, but I don’t think I know what I’m looking for.
 
Interesting. I have never been a drug user.
I think that's a drug which is classified under medical ... so like paracetamol is a drug as are other anti-migraine drugs. Not like the drugs that gang bangers sell (although they do also trad there).

I’ve tried googling, but I don’t think I know what I’m looking for.

I guess having done a degree in this area helps me a bit, even if it was a long time ago now.

https://en.wikipedia.org/wiki/Fenfluramine
Fenfluramine, sold under the brand name Fintepla, is a serotonergic medication used for the treatment of seizures associated with Dravet syndrome and Lennox–Gastaut syndrome.[3][4][1] It was formerly used as an appetite suppressant in the treatment of obesity, but was discontinued for this use due to cardiovascular toxicity before being repurposed for new indications.[5][6] Fenfluramine was used for weight loss both alone under the brand name Pondimin and in combination with phentermine under the brand name Fen-Phen among others.[5][7]

HTH
@preciosa1974 edited content
 
I think that's a drug which is classified under medical ... so like paracetamol is a drug as are other anti-migraine drugs. Not like the drugs that gang bangers sell (although they do also trad there).



I guess having done a degree in this area helps me a bit, even if it was a long time ago now.

https://en.wikipedia.org/wiki/Fenfluramine
Fenfluramine, sold under the brand name Fintepla, is a serotonergic medication used for the treatment of seizures associated with Dravet syndrome and Lennox–Gastaut syndrome.[3][4][1] It was formerly used as an appetite suppressant in the treatment of obesity, but was discontinued for this use due to cardiovascular toxicity before being repurposed for new indications.[5][6] Fenfluramine was used for weight loss both alone under the brand name Pondimin and in combination with phentermine under the brand name Fen-Phen among others.[5][7]

HTH
@preciosa1974 edited content
Yep! Remember it well. Pulled from the mkt by FDA in 1997 due to heart valve damage. Large damage awards. Big hit to AHP stock at the time. Turned out that a large part of the problem was Doctors over-prescibing (due to incentives) to people who only wanted to lose a few pounds. It was only approved for use on severely obese people. Greed over morality.
 
Yep! Remember it well. Pulled from the mkt by FDA in 1997 due to heart valve damage. Large damage awards. Big hit to AHP stock at the time. Turned out that a large part of the problem was Doctors over-prescibing (due to incentives) to people who only wanted to lose a few pounds. It was only approved for use on severely obese people. Greed over morality.
Very interesting. Thinking back I took phentermine for a very short time in the 2000’s I believe but it didn’t do anything so I stopped. I never took anything with phen phen. I specifically remember people getting really sick and having crazy side effects and it wasn’t worth it to me. The only think I remember taking at that time was Herbalife and metabolife. So late 90’s. I remember bc I tried to lose weight after my second son was born inn1996.
 
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