Mitral stenosis in a tissue replacement valve

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kschroed

Well-known member
Joined
Aug 17, 2008
Messages
52
Location
Southern California
I just had an angiogram and am now more confused that ever. Maybe someone can direct me to a source to research this. I have a bovine mitral valve, replacing my own valve in 2008. When I was diagnosed 10 years ago, it was mitral valve regurgitation with an EF of 30. Now I have been told I must have the tissue valve replaced because of mitral stenosis. The angio gram showed the valve was "tight," according to the doctor who did the procedure. My GP said there was a "significant leak." So how does this work? A prolapsed valve is replaced with a valve that then develops stenosis? I have emailed the cardiologist, but I've heard nothing back. The surgery coordinator at the hospital was supposed to call ASAP, but it's been three days and nothing. I just want to understand. Help?
 
Thanks, pellicle, this is good information. No one has used the word "calcification" with me, so that is a great help is trying to understand this.
 
Hi

kschroed;n883063 said:
I just had an angiogram and am now more confused that ever. Maybe someone can direct me to a source to research this. I have a bovine mitral valve, replacing my own valve in 2008. When I was diagnosed 10 years ago, it was mitral valve regurgitation with an EF of 30. Now I have been told I must have the tissue valve replaced because of mitral stenosis.

sorry to hear that your valve has now has stenosis (probably calcification). I'm not sure what your age is (your bio suggests you may be over 60). However the quite well established evidence is that tissue prosthetic valves develop stenosis due to calcification and this is called SVD or Structural Valve Degredation (SVD).

I'm not entirely sure what you mean by "direct me to a soruce of research on this" as I'd need a specific topic (as research tends to be specific). I'm happy to point you at sources if you can help me out on exactly what research you are looking for.

From what I know the durability (length of functional life) of a tissue prosthetic is something like 10 - 20 years (with some obtaining durations either side of that range). There is no mystery in this and its well established in the medical field by surgeons (who then replace them). There is a quite simple and enduring rule that is a tissue prosthesis will suffer SVD

For instance: The Journal of Heart Valve Disease 2004;
Tissue valves were
introduced to avoid anticoagulation, but undergo
structural valve deterioration (SVD), with a reported
life of between six and 12 years (7-17,22)


which is of course now a little old and makers are claiming up to 50% better life.
The angio gram showed the valve was "tight," according to the doctor who did the procedure. My GP said there was a "significant leak." So how does this work? A prolapsed valve is replaced with a valve that then develops stenosis?

basically the body seems to attack the foreign matter inside it (not knowing it was put there to help). Some people calcify valves faster than others; it depends on factors like: activity levels , age, some others. Its well known. If your doctor didn't inform you of that in the first instance it was quite remiss.

There is a general guide (like in the actual surgical guidelines surgeons are supposed to follow) that for a patient under 60 a mechanical valve should be suggested (because they don't get SVD because they're made of a type of carbon) or a tissue if the patient is against warfarin therapy (and really to me what patient isn't against something different and not sold up well).

again from that article above:

Mechanical and tissue valves have equivalent rates
for thromboembolism (23,48), a probable explanation
being that as tissue valves deteriorate they become a
source for thromboembolism.
...
The literature
reports that 40-70% of mitral tissue patients and 15-
35% of aortic tissue patients receive long-term warfarin
therapy (6,7,11-17,29).
...
More efficient management of anticoagulation has
been shown to reduce the rates of thromboembolism
and bleeding. Examples include patient INR self-testing,
self-testing and dosing, and the addition of antiplatelet
agents to low-intensity INR protocols
(23-27,29-32).
...
In conclusion, a tissue valve should be implanted if a
patient has a history of bleeding or a predicted life
expectancy of less than 10 years. Mechanical valves are
durable, and should be implanted in patients who are
expected to live more than 10 years, and also in
patients already receiving anticoagulants or who are
predicted to be anticoagulated.
More efficient anticoagulation management systems
should be instituted to further reduce thromboembolism
and bleeding.



Its interesting that while that article is authored in 2004 the author is well aware of Patient Self Testing of INR bringing benefeits, yet some 14 years later somehow not many others are (well, except us who do that themselves)

I happen to think this 2009 article sums up nicely the truth:
Prosthetic Heart Valves
Selection of the Optimal Prosthesis and Long-Term Management

Philippe Pibarot, Jean G. Dumesnil

Despite the marked improvements in prosthetic valve design and surgical procedures over the past decades, valve replacement does not provide a definitive cure to the patient. Instead, native valve disease is traded for “prosthetic valve disease,” and the outcome of patients undergoing valve replacement is affected by prosthetic valve hemodynamics, durability, and thrombogenicity. Nonetheless, many of the prosthesis-related complications can be prevented or their impact minimized through optimal prosthesis selection in the individual patient and careful medical management and follow-up after implantation.
...
Structural Valve Deterioration
Incidence of SVD

Mechanical prostheses have an excellent durability, and SVD is extremely rare with contemporary valves, although mechanical failure (eg, strut fracture, leaflet escape, occluder dysfunction caused by lipid adsorption) has occurred with some models in the past (Figure 6C).

The rate of SVD in bioprosthetic valves (Figure 6D) increases over time, particularly after the initial 7 to 8 years after implantation. With conventional stented bioprostheses, the freedom from structural valve failure is 70% to 90% at 10 years and 50% to 80% at 15 years.6,43,50,62,66
Predictors of SVD

Risk factors previously found to be associated with bioprosthetic SVD include younger age, mitral valve position, renal insufficiency, and hyperparathyroidism.43,62,66 Hypertension, LV hypertrophy, poor LV function, and prosthesis size also have been reported as predictors of SVD in bioprostheses implanted in the aortic position.66
Host-Related Factors

Bioprosthetic SVD is strongly influenced by the age of the patient at the time of implantation.43,62 The rate of failure of bioprostheses is <10% at 10 years in elderly patients (>70 years of age) but is ˜20% to 30% in patients <40 years of age.43,62 Several studies also suggest that bioprosthetic structural failure is more frequent in the mitral than in the aortic position.43,66 This difference is likely related to the higher mechanical stress imposed on the valve leaflets of mitral bioprostheses during systole. Likewise, SVD of aortic bioprostheses may be accelerated by systemic hypertension, possibly as a result of a chronically increased diastolic closure stress.
Valve-Related Factors

Several studies tend to show that newer-generation bioprostheses are more durable than older ones.43,62,66 Some reports also suggest that pericardial valves might be better than porcine valves in this regard,67 but other recent studies show no appreciable difference between these 2 types of prosthesis.68
Pathogenesis of SVD
Degenerative Process

Bioprosthetic valve tissues are cross-linked in glutaraldehyde to reduce its antigenicity and to ensure chemical stabilization; however, this chemical treatment may predispose to bioprosthetic tissue degeneration (Figure 8).62 Indeed, tissue fixation with glutaraldehyde induces a calcium influx as a result of membrane damage, which provides, along with the residual phospholipids of the membranes, an environment prone to calcium crystal nucleation. Host factors and mechanical stress then contribute to calcium crystal growth. Such findings have prompted manufacturers to try different anticalcifying treatments on bioprosthetic tissue in the hope of avoiding or slowing SVD. Opposing previous beliefs, recent studies69–74 suggest that SVD may not be a purely passive degenerative process but may also involve active mechanisms such as immune rejection and atherosclerosis (Figure 8).


Figure 8. Hypothetical model for the structural deterioration of bioprosthetic valves. OxLDL indicates oxidized low-density lipoprotein.
Immune Process

Recent studies suggest that bioprosthetic valves are not in fact completely immunologically inert (Figure 8).73 Hence, residual animal antigens could elicit humoral and cellular immune responses, leading to tissue mineralization and/or disruption. A more robust immune system might also explain the more rapid SVD usually observed in younger patients.

Atherosclerotic Process

Recent studies also demonstrate an association between bioprosthetic SVD and several atherosclerotic risk factors, including hypercholesterolemia, diabetes, metabolic syndrome, and smoking.66,70,72Moreover, 1 retrospective study reported that statin therapy is associated with slower progression of SVD.71 These recent findings support the hypothesis that similar to the native aortic valve, the SVD of bioprostheses may be related, at least in part, to an atherosclerotic process (Figure 8). The infiltration of low-density lipoproteins within the bioprosthetic tissue and their oxidation may trigger an inflammatory process and the formation of foam cells.74 In turn, the inflammatory cytokines and oxidized low-density lipoproteins may induce an osteoblastic differentiation of stem/progenitor cells that have colonized the bioprosthetic tissue.75

If you have some more specific questions I'm happy to dig through my notes of my own readings and help you as I can.

Best Wishes
 
Hi

kschroed;n883071 said:
Thanks, pellicle, this is good information. No one has used the word "calcification" with me, so that is a great help is trying to understand this.

well I'm glad you read some of it before (my editing it) caused it to be deleted by the software. I added a bit more (after god knows how much effort and at least 3 "unapproved" and 2 "spam deletions" ... anyway, if there is anything else you want Iincluding my attempt at simplifying the issues please ask :)
 
also, if you happen to be in the process of deciding here are the guidelines in table form:
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and

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Hi again...
kschroed;n883071 said:
Thanks, pellicle, this is good information. No one has used the word "calcification" with me, so that is a great help is trying to understand this.

I had to infer your question, I gather at this point you're just trying to work out why you are "back again", is that right?
 
pellicle;n883077 said:
Hi again...


I had to infer your question, I gather at this point you're just trying to work out why you are "back again", is that right?

Yes. I'm just trying to figure out what the problem is, why they need to replace the valve again, and I am getting no response from the doctors to my questions.
 
Hi

kschroed;n883083 said:
Yes. I'm just trying to figure out what the problem is, why they need to replace the valve again, and I am getting no response from the doctors to my questions.

well the answer to "why you need to have the valve replaced again" is that tissue valves are by nature of limited life span, mechanical valves baring obstruction from scar tissue never wear out and can even be cleared of obstruction in some cases.

Its just the nature of the beast.

For instance if you just read every line of table 17 and 18 above and think about the meaning of that then you'll see that implied there. Which is why that last line reads: "A bioprosthesis should be considered in patients aged >70 years in mitral position, or those with a life expectancy lower than the presumed durability of the bioprosthesis"

so perhaps you weren't well informed by your surgeon in the first place?

also in Table 17 it says: "a mechanical prosthesis is recommended in patients at risk of accelerated structural valve deterioration" ... which it seems you are now clearly aware of that being a risk for you in particular.
 
pellicle;n883085 said:
Hi




so perhaps you weren't well informed by your surgeon in the first place?

That is the truth. At the time, I was 57, and the doctors strongly urged I avoid the Coumadin complications that came with a mechanical valve. My surgeon told me he would do a tissue valve himself if he were having the surgery. I was diagnosed late in the progression of the disease, my left ventricle already badly enlarged. (Another less-than-stellar doctor in that case--the problem was discovered by his PA who was checking me for possible pneumonia. I have left that practice.) It was a sudden diagnosis and an alarmingly fast call to surgery. I don't think I really understood what problems a tissue valve could develop. Now I'm determined to find out all the facts before the next surgery (which I will do as soon as I hear from the cardiologist who seems to be taking the weekend off.)
 
kschroed;n883087 said:
That is the truth. At the time, I was 57, and the doctors strongly urged I avoid the Coumadin complications that came with a mechanical valve. ... Now I'm determined to find out all the facts before the next surgery (which I will do as soon as I hear from the cardiologist who seems to be taking the weekend off.)

that is exactly the spirit!

So let me suggest a little more reading about the complications of warfarin (trade name Coumadin). Firstly there is substantial evidence that the risks are over represented. Mainly this is due to the facts that:
  1. the vast majority of warfarin users are not well managed (see the anti-coagulation threads here to see the typical struggles that even cognizant users have with their clinics, god help the sheep)
  2. the vast majority of stats are for non-valve related users (meaning people who are on it *because* they had a stroke, thus are of increased likelyhood to have a stroke)
  3. all the studies (hello LondonAndy ) show that well managed INR brings you to about "general populatoin age related risk" levels and that self managed groups do even better. My own track record is about 95% in range clinics often average 85%.
Some reading and listening for you

A detailed presentation by a Mayo Surgeon



Some links from my blog about my own experiences

http://cjeastwd.blogspot.com/2014/09...ng-my-inr.html

and managing my INR around a small procedure (which of course happens more often as we age).

http://cjeastwd.blogspot.com/2017/12...nt-of-inr.html

If you want some more readings on valve durability let me know.

Knowledge is power in decision making.

Best Wishes
 
I am one of those folks who had a stroke post surgery that was, almost certainly, due to my not taking warfarin for several days while on vacation.......I thought I'd be ok for few days without the anti-coagulant........bad idea. That was back in 1974 and only 7 years after my surgery. I learn quickly and have gone the past 44 years without issues with warfarin. At 82 I still find warfarin easy to manage. That is primarily due the current INR system (which replaced the old PT system that was in use when my stroke occurred) along with home testing and learning "not to run with scissors".

If you are looking to reasonably avoid future heart surgeries the mechanical valve, in today's world, seems the best bet......but nothing is guaranteed.
 
Bummer kschroed. I also have mitral issues. You don't necessarily have a tendency to just stenosis or just regurgitation. At age 34 I very suddenly was dx with mitral stenosis and had a balloon-based procedure (valvuloplasty) to open the valve. That procedure left me with mod-severe regurgitation. 16 years down the line there is some stenosis happening again along with the regurgitation. I still have my native valve and it is prone to calcify in an unpredictable manner. Tissue valves are too. Several factors seem to increase the chance of calcification including it being a mitral vs aortic valve, being "young" (as in under 60 and worse the younger you are), being female, and having rheumatic heart disease. I have all of those so I guess I'm pretty fortunate I've made it this long on one non-OHS procedure. I've got in my head that I'll go mechanical if I can't get another valvuloplasty to avoid this calcification issue, but then I seem to just keep getting older and doing fine each yearly echo . . . we'll see how it goes.

If your main problem is stenosis now and you do not have too bad a regurgitation, you could be a candidate for a valvuloplasty which would avoid OHS? (Not sure if they do this on tissue valves vs. native valves). It tends to increase regurgitation by 1 to 1.5 levels so you can't do it if there's too much regurg as well as stenosis. It would also be done by an interventional cardiologist as opposed to a surgeon so you'd have to ask the right person. It has its own risks but it's a good tool for the right situation.
 

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