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Is there a desire from the medical community to not know these things?
I'd phrase it differently: there is a desire in the medical community to need to know less.

I'd balance everything you have said (much of which I outright agree with) with the following points (in no specific order):
  • the statistics on drug compliance are dreadful with something like 50% of patients getting slack within one year (perhaps till their first stroke when they get it, but may not get a second chance)
  • knowing the statistics surgeons bias towards keeping it all under their control (which they don't control with OAT)
  • the labs don't give a shlt about anything other than
    1 their bottom line
    2 not being found culpable
    So "near enough is good enough"
  • few people are really any good at DIY, being organised or being consistent and there is no qualifications or assessment criteria used to see if you're smart enough to do it

🤷‍♂️
 
I'm sure the same topics resurface once in a while. Maybe there should be a FAQ list somewhere?
so with you having my back
1692583325552.png

I'll say:
nobody would read the FAQ (except the people who lurk and don't ask questions and who then manage to educate themselves without joining for the camaraderie).

Right now we have participants (at least one comes handily to mind) who don't even read the replies to the questions that they post (quite frequently and repetitively) nor search. I've literally seen the same question asked directly within the thread of someone else asking that actual question.

I have the view that if self help books worked there wouldn't need to be so many on the same topic.



However as you've seen of me here I'm frequently unable to learn and offer actual help on specific topics, probably because I've spent a lot of time being able to have this attribute

1692583583601.png


Being a bit aligned with Zen helps too.

: -)
 
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It boggles the mind that a large study has yet to be done that shows average time to reoperation for mechanical aortic valves placed in patients under 40. It would be useful to use patients with no comorbidities. It would be useful if only patients compliant on anti coagulants were included.
Seems like a great idea. Do you think it's a matter of analyzing data that large professional organizations (like STS) already have?

Or is it a matter of actually doing a long-term follow-up survey? (In which case I could see some issues with even young assistant professors getting grants for a 40-year long study. 🤷‍♂️)


they only now realize these bio-valves are developing thrombus formation, because of wnl ( we never looked). Would an anti-coagulated toronto spv bio valve have lasted 17 years on average vs 10?
Seems like this might also be important to TAVR recipients, who were not qualified for SAVR because of age.
 
I'll say:
nobody would read the FAQ (except the people who lurk and don't ask questions and who then manage to educate themselves without joining for the camaraderie).
That's possible. It was just a thought, that the FAQ would be useful for some people. And that it may make replies simpler. But it would also be some labor to write and maintain.

Right now we have participants (at least one comes handily to mind) who don't even read the replies to the questions that they post (quite frequently and repetitively) nor search. I've literally seen the same question asked directly within the thread of someone else asking that actual question.
I guess I hope they are exceptions to the trends :)
 
It boggles the mind that a large study has yet to be done that shows average time to reoperation for mechanical aortic valves placed in patients under 40.
This may not be exactly what you are looking for, but it is a 30 year follow up study on the St Jude mechanical valve. The bold is mine to emphasize your interest pertaining to reoperation.

For aortic valve:

"Thirty-year freedom from reoperation, thromboembolism, valve thrombosis, bleeding, and endocarditis was 92% ± 2%, 79% ± 3%, 96% ± 1%, 56% ± 5%, and 92% ± 2%, respectively. "

For mitral valve:

"Thirty-year freedom from reoperation, thromboembolism, valve thrombosis, bleeding, and endocarditis was 85% ± 5%, 55% ± 6%, 99% ± 1%, 57% ± 6%, and 95% ± 2%, respectively."

https://pubmed.ncbi.nlm.nih.gov/30342758/
 
This may not be exactly what you are looking for, but it is a 30 year follow up study on the St Jude mechanical valve. The bold is mine to emphasize your interest pertaining to reoperation.

For aortic valve:

"Thirty-year freedom from reoperation, thromboembolism, valve thrombosis, bleeding, and endocarditis was 92% ± 2%, 79% ± 3%, 96% ± 1%, 56% ± 5%, and 92% ± 2%, respectively. "

For mitral valve:

"Thirty-year freedom from reoperation, thromboembolism, valve thrombosis, bleeding, and endocarditis was 85% ± 5%, 55% ± 6%, 99% ± 1%, 57% ± 6%, and 95% ± 2%, respectively."

https://pubmed.ncbi.nlm.nih.gov/30342758/
Sure, not exactly as what I want is average time to reoperation, but very close. No great way to wag from this but if 92% are alive and not having been reoperated, that would be a great thing to tell patients, instead of "it will last a lifetime." " You have a 92% chance of it lasting at least 30 years, if you have any sense whatsoever and decent luck." I find that more to my liking, but that's just me.

The 25 year study showed 90% freedom from reoperation, I just noticed. Odd but might simply mean the average is being dragged down by early problems.
 
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The 25 year study showed 90% freedom from reoperation, I just noticed. Odd but
Not really, for instance development of an aneurysm, endocarditis, obstructive thrombosis from poor adherence to ACT, panus... These things aren't common, but neither is being a part of 8%

@Superman had his 2nd ohs triggered by that IIRC
 
Not really, for instance development of an aneurysm, endocarditis, obstructive thrombosis from poor adherence to ACT, panus... These things aren't common, but neither is being a part of 8%

@Superman had his 2nd ohs triggered by that IIRC
When I reread my comment I realized it was unclear. The odd part was that the 30 year study showed better results than the 25 year. But within the margin so its meaningless. And I meant that basically if we have the same results at 25 and 30 years of around 90%, than it appears that there is probably earlier trouble bring the average down. I think you know I am well aware of the problems that are occurring that have nothing to do with the valve itself wearing out, which is not a factor at all. And I'm certain we both realize that the valve never wearing out, doesn't mean no one has another surgery even if they are great with their anti thrombosis meds. 90% no re-surgery at 30 years is a spectacular result. I still feel like we need to know for the youngest folks, but probably fully grown, is it 40 years-45 years until re-surgery? Because done properly you want to place that valve in when you are reducing the odds of another surgery after 80. If the first surgery is mechanical and at age 15, there is likely another one at perhaps perfect timing at age 50-65. But would you want the valve placed at 40? We can get through two surgeries but do want the second one past age 80?
 
Hi
But within the margin so its meaningless. And I meant that basically if we have the same results at 25 and 30 years of around 90%,

well here's the thing, from my point of view. Studies are often done (like the LOWERING IT study by On-X which had a median duration of about the time of (but a little less than) the median time for an event. Choosing such minimises the amount of events you'll see compared to if you went (say) 50% longer.

So lets look at a study to express what I'm getting at better
1692822950992.png

so up front lets say that the average lifespan of an adult is about 80, so taking the study of people who were over 75 years old when they got their valve out to 10 years would make them at least 85. Not bad, but you'll notice two studies took it out longer pericardial (which btw is the sort of tissue valve that a Resilia is)and mechanical. For whatever reason you'll see that the Mechanical actually clearly differentiated itself over the Pericardial tissue valve once you went out that extra 5 years (or about 50%)).

Indeed from the same study, even at a younger age the results were this:
1692823192304.png

so If you look at 5 years (which is what Edwards did with their internal study which they cite on their promotional material) and then simply extend that line out to 10 or 15 years you see a different result depending how you do your extending. Probably what they do (which we don't know, because they don't tell us their methods)
1692823396310.png


This is why if you don't know how to read statistics you could conclude as does the old saying of the order of things is: "Lies, bloody lies, and statistics". (discussion and references on my blog here)

... If the first surgery is mechanical and at age 15, there is likely another one at perhaps perfect timing at age 50-65

the only that is even likely is if your reason for OHS was that you didn't have BAV (and thus a connective tissue disorder) and in that case you'd probably be one and done anyway. Such a case is still common in (ouh, say) India where the lack of proper use of antibiotics causes "strep throat" to progress into full blown Scarlet Fever, which then damages the valve surfaces and leads to eventual failure and replacement (ask @dick0236 about that).

Understanding the root cause of valvular disease is also important in determining likely outcomes in the future.

Best Wishes
 
No, I believe a tissue valve in someone super active won't last as long as in someone sedentary. I'm not sure if any studies prove that, but that's what my surgeon told me is the presumption when I chose a mechanical valve.
Kind of a bummer you get "penalized" for being more active in regards to a tissue valve
 
Good summary--thanks
Sure, not exactly as what I want is average time to reoperation, but very close. No great way to wag from this but if 92% are alive and not having been reoperated, that would be a great thing to tell patients, instead of "it will last a lifetime." " You have a 92% chance of it lasting at least 30 years, if you have any sense whatsoever and decent luck." I find that more to my liking, but that's just me.

The 25 year study showed 90% freedom from reoperation, I just noticed. Odd but might simply mean the average is being dragged down by early problems.
 
Hi All,

I have a question for all. But first I´d like to state that I´m not very good with the search option on this Forum so if the question has been asnwered in another thread please point me in the right direction and accept my apologies for bothering you.

I´m a 44 years old healthy individual with an Asc. Aorta Anaurism (5.5 cm) and a fully functional bicuspid aortic valve. I´m scheduled to go under the knife in a month (aprox.). As I´m from Spain (I used to live in Scotland) and the procedure is done by the public health system is difficult to get the exact date. I have taken the decision of going for a Tissue Valve. The reason in my personal case are a history of anxiety and depression that would make really tough for me to get used to the ticking and my job and live stile. I frequentily travel to 3rd world countries for several weeks where access to healthe services may be a challenge.

I´m not posting this to get feedback regarding my decision, although if anybody wants to provide it you are more than welcome :). I´m here to ask about exercise and tissue valves. I have seen plenty of information of exercise and mechanical valves. Really inspiting stories of people doing iron-men with it (you guys are amazing!), but not so much about the tissue ones. Can any of you share some light about it? How does it feel once everything is healed to run with a tissue valve. Also, is is true that their durantion depends on how much you use it (how much exercise) or that is a fase myth?

Massive thank you in advanced for your time. You are all heroes!
Hi all
I recently found this suggesting intense exercise can cause calcification of the arteries. Could we conclude it would calcify heart values too? This is disappointing for those of us that like hard workouts. This is just one news source, there are a few out there : https://www.news-medical.net/news/2...litating coronary atherosclerosis in athletes.
 
Hi all
I recently found this suggesting intense exercise can cause calcification of the arteries. Could we conclude it would calcify heart values too? This is disappointing for those of us that like hard workouts. This is just one news source, there are a few out there : https://www.news-medical.net/news/20230105/Intense-exercise-encourages-coronary-artery-calcification.aspx#:~:text=Exercise with a very high,facilitating coronary atherosclerosis in athletes.
That is an interesting study and thanks for the link.

A couple of important take aways from the article and then some comments on calcium scores.

From the article:

"Exercise and physical activity reduce the risk of cardiovascular disease (CVD). It has been observed that an active individual is at a 30% to 40% lower risk of CVD."

"No correlation was found between exercise volume and the progression of coronary atherosclerosis during the follow-up."

Exercise has been proven better than any medication at lowering the risk of heart disease and all cause mortality, so by all means do not stop exercising out of concern that it will increase your calcium score. For one thing, correlation does not mean causation.

Calcium scores are often misunderstood. The calcifified plaque is the stabilized plaque in our arteries- sometimes referred to as hard plaque. The real danger is soft plaque which has not yet been stabilized and at risk of bursting and causing a clot.

Let's say that a 48 year old, with no baseline CAC gets gets a CAC completed and scores 900. That is very bad and would indicate that the person is at high risk. But, the risk is more due to the fact that where there is smoke there is often fire. This person would almost always have a heavy soft plaque burden as well, which is the type of plaque putting him at risk of cardio vascular events, more so than the calcified plaque. Soft plaque and calcified plaque usually go hand in hand, but not always and it depends if the individual has been on treatment to stabilize his soft plaque, such as statins, or other factors which could have led to stabilization of soft plaque, such as improved lifestyle choices.

In addition to lowering LDL, statins also stabilize soft plaques. This is one of the reasons why they significantly lower the risk of heart attacks and strokes. For example, someone I know had a heart attack in his 40s. His CAC score came back at about 100. He was put on a number of medications, including PCSK9-inhibitor and statins. The next year his CAC score went up significantly, and he got very upset. It turns out that this occured because the statin was doing its job and stabilizing the soft plaque. His soft plaque burded had decreased considerably becuase it had been calcified and stabilized.

I am not saying that having a high CAC score is good. But, there is more to the story. Generally, a CAC score does correlate with a higher risk for heart events, with increasing score correlating with increase rate of events. But, without knowing more information, it would be impossible to say whether someone at a CAC score of 200 is at greater risk than another person who has a CAC score of 50. Perhaps the person at 200 was at 75 CAC a year earlier, with a heavy soft plaque burden. His cardiologist put him on a statin and now most of the soft plan has been stabilized, and he now shows a 200 score, but imagery reveals that the his soft plaque burden is very low. At the same time, the person who scored a 50 could have a much higher soft plaque burden. Without the advanced scans being completed, it is impossible to know the true risk. All that being said, if a person presents with a very high CAC scan, there is almost certainly heart disease present and there needs to be follow up.

So, I would look at CAC as a marker which could indicate the need for more testing to see what is going on.

Perhaps there is something about doing intense exercise that is causing damage to the endothelium and increasing the plaque burden. On the other hand, perhaps there is something about the intense exercise which is causing the soft plaque to stabilize, leading to a slightly higher CAC score, but a lower CAD risk, due to the stabilization of soft plaques. Without the advanced imagery, which includes the soft plaque burden, it is impossible to say whether these athletes are truly at higher risk. Following hard outcomes, such as actual cardiac events and mortality, is always better than following biomarkers. The hard outcomes have strongly suggested for decades that increasing exercise lowers risk of CAD and mortality.

For those who are interested I'll link below info on CCTA scans, which can dedect not only calcified plaque, but also soft plaque. A friend whose family has genetic dyslipidemia just had himself and his family tested. It cost him $1,400 out of pocket for each test. Not cheap, which is why we will not likely see this done in many large studies unless they are well funded. It's much cheaper to look at markers and not pay for imagery which gives a much clearer risk perspective. Like CAC scans, one downside of CCTA scans is that there is some radiation risk. Probably neither are something that should be done with too much frequency.

CCTA scans:

"CCTA can detect 'soft' non-calcified plaque in patients who have a zero-calcium score"

"The latest European dyslipidemia guidelines have, however, adopted the use of CCTA findings and it is likely that other societies will follow suit. Data presented on the efficacy of statins, PCSK9 inhibitors and IPE to modify plaque risk markers may encourage the adoption of CCTA"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7914610/#:~:text=CCTA can detect 'soft' non,26] (Table 1).

On a personal note, since my surgery I have modified my type of exercise. I do probably about 95% of my training in zone 2, which would be considered moderate. I do this because several studies have found zone 2 training to be the zone which maximizes mitochondria health and mitochondrial health is one of the most important markers for good health in general and longevity. Once a week I push beyond zone 2 when I do my boxing sparring rounds. Where a person's zone 2 is will depend on their fitness level and their max heart rate. My zone 2 is when my heart rate is between about 105 bpm and 125 bpm.
 
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Hey @Timmay in case you miss this:
On a personal note, since my surgery I have modified my type of exercise. I do probably about 95% of my training in zone 2, which would be considered moderate. I do this because several studies have found zone 2 training to be the zone which maximizes mitochondria health and mitochondrial health is one of the most important markers for good health in general and longevity.
 
Because the study distinguished between "vigorous" and "very vigorous" I was curious about the distinction. The original Circulation article included:

The volume (metabolic equivalent of task [MET] hours/week) and intensity (moderate [3 to 6 MET hours/week]; vigorous [6 to 9 MET hours/week]; and very vigorous [≥9 MET hours/week]) of exercise training were quantified during follow-up.

I then found it interesting to delve into MET a bit as I was totally unfamiliar. Attached is a document with a lengthy listing of MET classifications.
https://www.ergotron.com/portals/0/literature/compendium-of-physical-activities.pdf
 
That is an interesting study and thanks for the link.

A couple of important take aways from the article and then some comments on calcium scores.

From the article:

"Exercise and physical activity reduce the risk of cardiovascular disease (CVD). It has been observed that an active individual is at a 30% to 40% lower risk of CVD."

"No correlation was found between exercise volume and the progression of coronary atherosclerosis during the follow-up."

Exercise has been proven better than any medication at lowering the risk of heart disease and all cause mortality, so by all means do not stop exercising out of concern that it will increase your calcium score. For one thing, correlation does not mean causation.

Calcium scores are often misunderstood. The calcifified plaque is the stabilized plaque in our arteries- sometimes referred to as hard plaque. The real danger is soft plaque which has not yet been stabilized and at risk of bursting and causing a clot.

Let's say that a 48 year old, with no baseline CAC gets gets a CAC completed and scores 900. That is very bad and would indicate that the person is at high risk. But, the risk is more due to the fact that where there is smoke there is often fire. This person would almost always have a heavy soft plaque burden as well, which is the type of plaque putting him at risk of cardio vascular events, more so than the calcified plaque. Soft plaque and calcified plaque usually go hand in hand, but not always and it depends if the individual has been on treatment to stabilize his soft plaque, such as statins, or other factors which could have led to stabilization of soft plaque, such as improved lifestyle choices.

In addition to lowering LDL, statins also stabilize soft plaques. This is one of the reasons why they significantly lower the risk of heart attacks and strokes. For example, someone I know had a heart attack in his 40s. His CAC score came back at about 100. He was put on a number of medications, including PCSK9-inhibitor and statins. The next year his CAC score went up significantly, and he got very upset. It turns out that this occured because the statin was doing its job and stabilizing the soft plaque. His soft plaque burded had decreased considerably becuase it had been calcified and stabilized.

I am not saying that having a high CAC score is good. But, there is more to the story. Generally, a CAC score does correlate with a higher risk for heart events, with increasing score correlating with increase rate of events. But, without knowing more information, it would be impossible to say whether someone at a CAC score of 200 is at greater risk than another person who has a CAC score of 50. Perhaps the person at 200 was at 75 CAC a year earlier, with a heavy soft plaque burden. His cardiologist put him on a statin and now most of the soft plan has been stabilized, and he now shows a 200 score, but imagery reveals that the his soft plaque burden is very low. At the same time, the person who scored a 50 could have a much higher soft plaque burden. Without the advanced scans being completed, it is impossible to know the true risk. All that being said, if a person presents with a very high CAC scan, there is almost certainly heart disease present and there needs to be follow up.

So, I would look at CAC as a marker which could indicate the need for more testing to see what is going on.

Perhaps there is something about doing intense exercise that is causing damage to the endothelium and increasing the plaque burden. On the other hand, perhaps there is something about the intense exercise which is causing the soft plaque to stabilize, leading to a slightly higher CAC score, but a lower CAD risk, due to the stabilization of soft plaques. Without the advanced imagery, which includes the soft plaque burden, it is impossible to say whether these athletes are truly at higher risk. Following hard outcomes, such as actual cardiac events and mortality, is always better than following biomarkers. The hard outcomes have strongly suggested for decades that increasing exercise lowers risk of CAD and mortality.

For those who are interested I'll link below info on CCTA scans, which can dedect not only calcified plaque, but also soft plaque. A friend whose family has genetic dyslipidemia just had himself and his family tested. It cost him $1,400 out of pocket for each test. Not cheap, which is why we will not likely see this done in many large studies unless they are well funded. It's much cheaper to look at markers and not pay for imagery which gives a much clearer risk perspective. Like CAC scans, one downside of CCTA scans is that there is some radiation risk. Probably neither are something that should be done with too much frequency.

CCTA scans:

"CCTA can detect 'soft' non-calcified plaque in patients who have a zero-calcium score"

"The latest European dyslipidemia guidelines have, however, adopted the use of CCTA findings and it is likely that other societies will follow suit. Data presented on the efficacy of statins, PCSK9 inhibitors and IPE to modify plaque risk markers may encourage the adoption of CCTA"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7914610/#:~:text=CCTA can detect 'soft' non,26] (Table 1).

On a personal note, since my surgery I have modified my type of exercise. I do probably about 95% of my training in zone 2, which would be considered moderate. I do this because several studies have found zone 2 training to be the zone which maximizes mitochondria health and mitochondrial health is one of the most important markers for good health in general and longevity. Once a week I push beyond zone 2 when I do my boxing sparring rounds. Where a person's zone 2 is will depend on their fitness level and their max heart rate. My zone 2 is when my heart rate is between about 105 bpm and 125 bpm.
Thanks Chuck! I too have switched from "all out, beat the clock" exercise to a focus on zone two. The mitochondrial connection is really interesting. For those interested:There are excellent videos here on zone two; https://www.youtube.com/results?search_query=zone+two+training

RE: In addition to lowering LDL, statins also stabilize soft plaques. This is one of the reasons why they significantly lower the risk of heart attacks and strokes. For example, someone I know had a heart attack in his 40s. His CAC score came back at about 100. He was put on a number of medications, including PCSK9-inhibitor and statins. The next year his CAC score went up significantly, and he got very upset. It turns out that this occured because the statin was doing its job and stabilizing the soft plaque. His soft plaque burded had decreased considerably becuase it had been calcified and stabilized.." It would be interesting to find out Statens are actually calcifing the plaque. Because that inturn makes our arteries rigid and they will not expand under pressure.
 
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