Not bicuspid?!?

[preciosa1974]

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.

Would these cause regurgitation/aortic insufficiency. I did not have Stenosis. Would it be a gradual change and take 25 years to begin to fail?

 

[Unicusp]

Would these cause regurgitation/aortic insufficiency. I did not have Stenosis. Would it be a gradual change and take 25 years to begin to fail?

It's possible. There's lots of data and research from the use of those drugs. You'd need to search and start reading. And maybe consult with an Attorney who specializes in that area. AHP/Wyeth is now part of Pfizer.

 

[Chuck C]

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.

If the issue was stenosis and there was no bicuspid, plus no known infection history, I would be suspicious that the cause would be having elevated Lp(a). It appears that the issue is not calcification, however.
It would still be a good idea for all to be tested for Lp(a). It is believed to be responsible for as many as 1 out of 7 cases of aortic stenosis, yet it is often overlooked.
The EU guidelines now call for everyone to be tested at least once in their lifetime for Lp(a). If your levels are normal, you generally never need to test again, as it remains at almost the same level all of your life for the vast majority, and it is almost completely unaffected by diet and exercise.

"Conclusions Lp(a) is robustly associated with presence of AVC in a wide age range of individuals. These results provide further rationale to assess the effect of Lp(a) lowering interventions in individuals with early AVC to prevent end-stage aortic valve stenosis."

https://heart.bmj.com/content/107/17/1422
"Conclusion: High plasma lp(a) levels (≥50 mg/dL) are significantly associated with increased risk of CAVD"

https://www.frontiersin.org/articles/10.3389/fcvm.2022.877140/full

 

[preciosa1974]

If the issue was stenosis and there was no bicuspid, plus no known infection history, I would be suspicious that the cause would be having elevated Lp(a). It appears that the issue is not calcification, however.
It would still be a good idea for all to be tested for Lp(a). It is believed to be responsible for as many as 1 out of 7 cases of aortic stenosis, yet it is often overlooked.
The EU guidelines now call for everyone to be tested at least once in their lifetime for Lp(a). If your levels are normal, you generally never need to test again, as it remains at almost the same level all of your life for the vast majority, and it is almost completely unaffected by diet and exercise.

"Conclusions Lp(a) is robustly associated with presence of AVC in a wide age range of individuals. These results provide further rationale to assess the effect of Lp(a) lowering interventions in individuals with early AVC to prevent end-stage aortic valve stenosis."

https://heart.bmj.com/content/107/17/1422
"Conclusion: High plasma lp(a) levels (≥50 mg/dL) are significantly associated with increased risk of CAVD"

https://www.frontiersin.org/articles/10.3389/fcvm.2022.877140/full

I did not have stenosis.

 

[Unicusp]

Would these cause regurgitation/aortic insufficiency. I did not have Stenosis. Would it be a gradual change and take 25 years to begin to fail?

This mentions aortic regurgitation.
https://www.drugs.com/sfx/redux-side-effects.html

 

[Chuck C]

I did not have stenosis.

I understood that. Whether or not it is stenotic, was there calcification on your valve and/or were the leaflets thickened? I would not dismiss the possibility of having elevated Lp(a) if either of these are the case.
Lp(a) is associated with aortic calcification and aortic stenosis. It could be the case that your valve had some calcificaiton, which led to regurgitation, but that it had not yet reached the point of being considered stenotic.

It is a simple and inexpensive blood test. All should get it done anyway and especially anyone who has had issues with their aortic valve.

 

[pellicle]

Three valve leaflets with myxoid change.

from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8762386/
Myxomatous degeneration is derived from the word myxoma. It is described as the “non-inflammatory progressive disarray of the valve structure caused by a defect in the mechanical integrity of the leaflet due to the altered synthesis and remodeling by type VI collagen” (2). The valve leaflets grossly appear thickened with thin and translucent regions in the longitudinal and transversal axis (2). Commonly this process affects not only the valves but also the chordae tendineae. The pathophysiology is not fully understood, but it is thought to be due to an imbalance in the synthesis and degradation of the extracellular matrix (2). This non-inflammatory process most often affects the mitral valve and rarely affects the aortic valve. A common complication of myxomatous degeneration of the aortic valve is the rupture of the chordae tendineae, which leads to acute valvular regurgitation and congestive heart failure. Few cases with variable patient presentations have been reported in the literature. However, no previous literature review has been completed to highlight the various manifestations, diagnostic modalities, and treatment options of myxomatous aortic valve degeneration. Herein, we presented a case of a 64-year-old Caucasian woman with aortic valve insufficiency due to myxomatous degeneration of the aortic valve, which is very uncommon.

just in case you were as interested in this as me ;-)

 

[pellicle]

This mentions aortic regurgitation.
https://www.drugs.com/sfx/redux-side-effects.html

quite interesting, thanks

Early cases of valvular heart disease were primarily reported in patients taking the combination fenfluramine and phentermine ("fen-phen") for an average duration of 10 months (range 1 to 16 months) prior to presentation. All were American women between the ages of 35 to 72 years, with an average of 43.3 years, and none had a history of cardiac problems. The disease was usually multivalvular, involving the mitral, aortic, and/or tricuspid valves. Approximately half of these women also presented with concomitant pulmonary hypertension. Some have required surgery to replace the diseased valves. The histopathology observed during surgery resembled that in carcinoid syndrome or ergotamine toxicity, indicating that a serotonergic mechanism may be involved. Later cases, however, have also included patients taking the combination dexfenfluramine (the active ingredient contained in Redux) and phentermine ("dexfen-phen"), as well as patients on either fenfluramine or dexfenfluramine alone. Analysis of available data suggests that fenfluramine and dexfenfluramine are the causal agents. Consequently, both drugs were withdrawn from the market on September 15, 1997. It is not known at the present time if the valvulopathies associated with fenfluramine and dexfenfluramine are reversible following drug discontinuation. Symptomatic disease has not been noted to resolve after stopping treatment, although symptoms of heart failure have been controlled with medications in several patients. Deterioration from no detectable murmur to a need for valve replacement has been reported in a couple of patients.​

seems related to my earlier post here mentioning fenfluramine:

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/

what I remain curious about is why this doesn't classify as stenosis (see link)
https://www.mayoclinic.org/diseases-conditions/aortic-stenosis/symptoms-causes/syc-20353139

 

[Survived03]

from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8762386/
Myxomatous degeneration is derived from the word myxoma. It is described as the “non-inflammatory progressive disarray of the valve structure caused by a defect in the mechanical integrity of the leaflet due to the altered synthesis and remodeling by type VI collagen” (2). The valve leaflets grossly appear thickened with thin and translucent regions in the longitudinal and transversal axis (2). Commonly this process affects not only the valves but also the chordae tendineae. The pathophysiology is not fully understood, but it is thought to be due to an imbalance in the synthesis and degradation of the extracellular matrix (2). This non-inflammatory process most often affects the mitral valve and rarely affects the aortic valve. A common complication of myxomatous degeneration of the aortic valve is the rupture of the chordae tendineae, which leads to acute valvular regurgitation and congestive heart failure. Few cases with variable patient presentations have been reported in the literature. However, no previous literature review has been completed to highlight the various manifestations, diagnostic modalities, and treatment options of myxomatous aortic valve degeneration. Herein, we presented a case of a 64-year-old Caucasian woman with aortic valve insufficiency due to myxomatous degeneration of the aortic valve, which is very uncommon.

just in case you were as interested in this as me ;-)

My aorta was positive for myxoid degeneration via lab pathology testing post surgery. No surprise to me or the surgeon.

 

[pellicle]

My aorta was positive for myxoid degeneration via lab pathology testing post surgery. No surprise to me or the surgeon.

Interesting. I've probably missed it because my focus was elsewhere, but why was this no surprise? Is it more common than I thought?

PS: re reading your citation (here) I missed aortic because it strangely put mitral before aortic (odd alphabetic order) and had other sentences like : In myxomatous valve degeneration (MXD), the mitral valve is also damaged due to non-inflammatory mechanisms ... even though it later puts aortic and mitral together ... perhaps it was written for mitral and then after review required to add aortic.

either way, interesting

 

[preciosa1974]

from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8762386/
Myxomatous degeneration is derived from the word myxoma. It is described as the “non-inflammatory progressive disarray of the valve structure caused by a defect in the mechanical integrity of the leaflet due to the altered synthesis and remodeling by type VI collagen” (2). The valve leaflets grossly appear thickened with thin and translucent regions in the longitudinal and transversal axis (2). Commonly this process affects not only the valves but also the chordae tendineae. The pathophysiology is not fully understood, but it is thought to be due to an imbalance in the synthesis and degradation of the extracellular matrix (2). This non-inflammatory process most often affects the mitral valve and rarely affects the aortic valve. A common complication of myxomatous degeneration of the aortic valve is the rupture of the chordae tendineae, which leads to acute valvular regurgitation and congestive heart failure. Few cases with variable patient presentations have been reported in the literature. However, no previous literature review has been completed to highlight the various manifestations, diagnostic modalities, and treatment options of myxomatous aortic valve degeneration. Herein, we presented a case of a 64-year-old Caucasian woman with aortic valve insufficiency due to myxomatous degeneration of the aortic valve, which is very uncommon.

just in case you were as interested in this as me ;-)

Very much so!! I couldn’t find very much googling. It seems it was a rare occurrence for me. Especially being so young.

 

[pellicle]

Very much so!! I couldn’t find very much googling. It seems it was a rare occurrence for me. Especially being so young.

rare things happen ... but I assmed your birth year was 1974 so you're only ten years younger than me and I had my first OHS at 10, second at 28 so I have a different view of "young"

;-)

 

[preciosa1974]

Very much so!! I couldn’t find very much googling. It seems it was a rare occurrence for me. Especially being so young.

I’m glad it hadn’t progressed to anything worse. My heart was in a great shape with no CAD. My biggest symptom at the time was extreme hypertension when standing and palpitations. I had other symptoms previously but this was what started the whole ordeal of a 911 call, etc. i believe I had had off and on symptoms when running long distance. But former cardiologist never did any tests or anything.

 

[preciosa1974]

rare things happen ... but I assmed your birth year was 1974 so you're only ten years younger than me and I had my first OHS at 10, second at 28 so I have a different view of "young"

;-)

I guess compared to what everyone says the age of typical valve failure. This is all so interesting to me. I do wish there was a concrete answer.

 

[pellicle]

Hi

I guess compared to what everyone says the age of typical valve failure.

well part of the problem is that most surgeons see old people (because most operations are on old people).

This is all so interesting to me. I do wish there was a concrete answer.

me too, because I'm always interested in learning more about this issue.

Sometimes its just a fact of life that the "why of it" can be lost ... although I think we're getting closer in the discussion on this thread.

 

[preciosa1974]

Hi


well part of the problem is that most surgeons see old people (because most operations are on old people).


me too, because I'm always interested in learning more about this issue.

Sometimes its just a fact of life that the "why of it" can be lost ... although I think we're getting closer in the discussion on this thread.

I don’t understand some of the technical terms in the link you sent. But I’m trying!

 

[pellicle]

I don’t understand some of the technical terms in the link you sent

google helps, but shoot any questions ...
PS I was looking for this before, took a minute

 

[Survived03]

Interesting. I've probably missed it because my focus was elsewhere, but why was this no surprise? Is it more common than I thought?

At the time, I was familiar with aortic aneurysms via my workplace. SNP mutation studies. In fact, my anonymous DNA is floating around in some study results.

Also, I am non-Marfans. Phenotypically far from it

 

[Survived03]

You may find this article easier to read and all encompassing when it comes to aortic aneurysms, calssifications and causes.

https://emedicine.medscape.com/article/1612552-overview

 

[preciosa1974]

I understood that. Whether or not it is stenotic, was there calcification on your valve and/or were the leaflets thickened? I would not dismiss the possibility of having elevated Lp(a) if either of these are the case.
Lp(a) is associated with aortic calcification and aortic stenosis. It could be the case that your valve had some calcificaiton, which led to regurgitation, but that it had not yet reached the point of being considered stenotic.

It is a simple and inexpensive blood test. All should get it done anyway and especially anyone who has had issues with their aortic valve.

No calcification either, but I’ll definitely look into the test!