Diminished running ability after mitral valve surgery.

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JimHewes

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Jul 7, 2023
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4
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This is my first post and I only have a mitral valve repair and not a replacement so sorry if I'm in the wrong place. I've been looking for other people who might have a similar experience to mine after surgery.

I'm now 64 and have enjoyed running off and on most of my life, including the last eight years or so continuous. I discovered I had mitral valve prolapse with moderate regurgitation about ten years ago which progressed into severe regurgitation more recently. But I had no symptoms besides occasional a-fib. I could still run pretty well and my last 10K run at 60 years old was under 47 minutes. A year ago I finally got the surgery to do the repair. It was minimally invasive surgery. Recovery was easy.

I expected that since my valve was no longer leaking I should be able to run at least as well after the surgery as I could before. Maybe even a little better. But the opposite turned out to be the case. I can only run much slower now. Roughly about 2/3 the pace and it's very difficult compared to before. Sometimes I even need to stop and walk. Not enjoyable or rewarding as it was. (If you like to run you know what I mean.) I'm currently working with my cardiologist to try to find out the problem but no clues yet. All tests so far look OK.

I'm just wondering if anyone else has had a similar experience even at any age. Have you been able to get back to your ability before surgery? Or have you seen a significant drop? I'm trying to find out what might be wrong.
 
Hi Jim... I had a minimally invasive mitral valve repair 8 years ago when I was 53. I'm not a runner, but I exercise vigorously with fast walking on an inclined treadmill. After the surgery I got back to pretty much where I had been, though not better. I'm glad your cardiologist is working with you to investigate your situation.
 
Hi


I expected that since my valve was no longer leaking I should be able to run at least as well after the surgery as I could before. Maybe even a little better. But the opposite turned out to be the case. I can only run much slower now. Roughly about 2/3 the pace and it's very difficult compared to before. Sometimes I even need to stop and walk.

recovery is different for everyone, myself I was better within a few months but then I was a lot younger (48 and it was my 3rd OHS). However I had a setback a year later and it then took another year of hard work to be where I was (say) a few months before the surgery. Another year of diligently not over training but training carefully I was probably where I was at 45.

This sort of feeds into why I tell people you don't want to make choices that plan for a redo at any age over over 65 if you can possibly avoid it.

So work with your cardio, and use the data you get from training tech like garmin to actually see what your cardio is and don't push too hard, but keep pushing gently.

Best Wishes
 
My experience has some similarities to what you are experiencing. I have a mechanical mitral valve. Lifelong runner. Afib around age 45 (ultimately corrected with an ablation). It took two surgeries about six months apart just before and after my 50th birthday. I turn 60 in a couple of weeks. Regurgitation was the primary reason for the valve replacement. I still run regularly . .. . but slower for sure. Over the course of a couple years post surgery race times from 5K to 1/2 mar got as close as 30 sec. per mile to what I had done in the preceding year. That may not sound like much to non-runners but to a runner that is dramatic. Now, psychologically I ultimately benefitted from the negative of needing two surgeries. I literally could not run after the 1st. I can assure you that I tried . . .many times. So I went through a period where I (largely!) adapted to 'just get me running again'. I ran a 5k last weekend and a 1/2 mar a couple weeks ago that were about 90 -120 sec/mile slower than a decade ago and I'm just fine with that.

I am also a (retired) hydraulics engineer by training and here's what I believe is going on:
- If you take a look at the valve area of the native mitral valve vs. the replacement, you'll see a substantial difference. The replacement area is likely 1/2 to 1/3 the size.
- This is the result of a couple different things. The replacement valve starts on the outside diameter as a rigid circle. The native valve is not circular, not planar, and the two flaps are not evenly sized.
- In our native mitral valve, the heart wall muscle pulls those flaps open wide through the chords. When a replacement valve is substituted, the chords are eliminated. (which is a key factor behind repairs leaving structure intact being preferred when possible)

It's a stretch to compare the heart to most man-made pumps but I think I can make a simple point in doing so. For a host of reasons, it is common in many pump types to have the inlet size larger than the outlet size. In a normal heart, the mitral valve (inlet to the primary pumping chamber) is meaningfully larger than the outlet aortic valve. When a replacement valve is put in the mitral position, the inlet and outlet sizes are similar, the rigid ring keeps the inlet size from changing, and heart muscles do not impact 'flap' positioning. Net of all of this is that there is going to be less flow and more pressure drop.

My opinion, is that what we end up 'feeling' or 'perceiving' at max flow rates (i.e. aerobic exercise) is whatever the difference is between the prior inefficiency/backflow of regurgitation and the new reduced inlet size.

Note: as it sounds like you had a repair I'll share a couple more details of my 'post repair':
- When I would attempt to run, I was able to push to as far a mile. I could feel the pressure steadily build in my chest and pretty quickly I'd cough up blood.
- It took some testing and a different hospital to make clear that my prior regurgitation had been solved but the effective resultant area was now stenotic.
- I still keep a DVD of a TEE that showed quite clearly how little my calcified mitral flaps were moving once they were nicely 'tightened up' with the annuloplasty ring.

Lengthy post. I hope some is useful and you don't have any trouble sorting my facts/experiences/conjectures as I have commingled them! Please just ask if I should clarify anything.
 
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Hi
pardon me but:
I am also a (retired) hydraulics engineer by training and here's what I believe is going on
agreed

Although there are other factors because the hydraulic fluid also needs a chemical exchange of Oxygen and Carbon Dioxide (and a bunch of other factors) which may have changed in efficiency too. So there's at least that other biochemical issue acting on fitness.

But I want to restate my agreement with your pump efficiency point.

https://www.ncbi.nlm.nih.gov/books/NBK538336/
Oxygen is carried in the blood in two forms. The vast majority of oxygen in the blood is bound to hemoglobin within red blood cells, while a small amount of oxygen is physically dissolved in the plasma. The regulation of unloading of oxygen from hemoglobin at target tissues is controlled by several factors, including oxygen concentration gradient, temperature, pH, and concentration of the compound 2,3-Bisphosphoglycerate. The most critical measures of adequate oxygen transportation are hemoglobin concentration and oxygen saturation; the latter is often measured clinically using pulse oximetry.
Understanding oxygen transport informs our understanding of the underlying mechanisms of tissue hypoxia, ischemia, cyanosis, and necrosis and management to improve global hypoxemia.​

Even pressure changes it (which divers will know well)

Best Wishes
 
I never thought about a mitral regurgitation repair giving someone stenosis, but I guess it makes sense that it could. Mitral stenosis was my primary issue but I didn’t know I had it till I became pregnant with twins which means more strain on the heart. I couldn’t walk up the stairs in my house without resting and I coughed up blood and was unable to sleep lying down due to the coughing. So since I was quite symptomatic I did much better after repair (and giving birth). I mention it only in case you notice any positional issues or persistent dry coughing along with shortness of breath, that could indicate mitral stenosis. Hopefully it’s nothing ominous and more just the way it is, which sucks for a runner I know but I hope you can still enjoy it.
 
After my mitral repair w anulplasty ring I felt so good. I was back to walking briskly with my dog up hill, no weird pressure on my chest. I felt back to normal. But, as a few yrs went by, I noticed the symptoms returning when I walked. My valve was leaking moderately. I was in chronic a fib 5 yrs after surgery, too. Now that it’s leaking mostly severely, I often have to stop walking and wait until I feel better to go on. It’s too bad because I remember how good I felt after recovering from repair. I’m one of the percentage that’s had their repair fail.
 
have a mitral valve repair

Have you been able to get back to your ability before surgery? Or have you seen a significant drop? I'm trying to find out what might be wrong.
I also had minimally-invasive MVr. But have not run regularly for decades, so can only infer the ability from other exercises.

For me the recovery status depends on the intensity of the exercise:
  • For moderate-intensity (fast walking), the recovery was quick. It's more complicated to say if I "got back", since there were 2 phases of stamina/endurance deterioration before the surgery. A slow phase that probably lasted about 3 years. And fast phase, that happened about 2 months before the surgery. I got better than the pre-surgery level a month after. Got to the pre-fast-phase state about 7-8 months after. Still improving, going "back in time" in terms of endurance.
  • For the high-intensity workout, it's harder to assess the status exactly. For the first few months felt a minor discomfort at pulse rates above 120, and, being mindful of a couple of aFib episodes, did not want to cause it again. It has definitely been improving, just because I can do more "stuff" of various kinds. But now (9 months out) maybe still not quite to the level before the fast-phase.
I don't want to stress about the exact ability right now. For one, the "reverse remodeling" of the heart does take a while, perhaps up to a year (after an initial fast improvement). Also, the heart, and the rest of the body systems are not quite the same anymore. Got 1st degree heart block, probably because of the scarring. The pulse at rest is a bit higher than it used to be. The blood pressure a bit lower. And, for some strange reason, I taste the food a lot more :) But the endurance and the exercise ability are still increasing.
 
- If you take a look at the valve area of the native mitral valve vs. the replacement, you'll see a substantial difference. The replacement area is likely 1/2 to 1/3 the size.
Thanks a lot for the message, lots of interesting details! The statement above surprised me. The factor of 2 or 3 in area change is huge. Could imagine a few possible reasons (fitting a smaller artificial valve if the original was enlarged, radial reduction due to the artificial valve periphery, effective area taken by the new leaflets). But do you know the cause, or have a reference for this observation?
 
But do you know the cause, or have a reference for this observation
complicated area this. I stay out of it. But a mm or so makes a big difference in area,
  • 17mm = 227
  • 18mm = 254
  • 19mm = 283.5
  • 20mm = 313.16
...but there is also outflow characteristics to consider

https://www.ahajournals.org/doi/10.1161/circ.122.suppl_21.A10394
Background: Transcatheter aortic valve implantation (TAVI) has emerged as an alternative to aortic valve replacement. To calculate the effective orifice area (EOA) of TAVI valves by continuity equation, some investigators have used the LV outflow tract diameter (LVOTD) measured at insertion of prosthetic valve leaflets (Method #1), whereas others used the diameter measured immediately proximal to the prosthesis stent (Method #2) (Figure). The objective of this study was to compare the performance of these two methods for estimation of EOA in TAVI valves.
...Accordingly, incidence of severe prosthesis-patient mismatch was 2-fold lower with the use of EOA2 than EOA1 (11 vs. 22%; p<0.001). Mean transprosthetic gradient correlated better with indexed EOA2 (r=−0.71, p<0.0001) than with EOA1 (r=−0.50, p<0.0001). Inter-observer and intra-observer variability were lower with LVOTD2 compared to LVOTD1 (inter: 1.7±3.9% vs. 4.5±9.8%, p<0.001; intra: 0.4±4.0 vs. 1.6±12.2%, p=0.23) and for EOA2 compared to EOA1 (inter: 3.6±8.0 vs. 7.0±20%, p<0.001; intra: 0.5±7.9% vs. 3.9±18.7, p=0.06).

https://europe.medtronic.com/xd-en/...vidence/patient-prosthesis-mismatch/calc.html
Mismatch is bad not only because it results in you starting with the effect of "mild stenosis" but also is correlated with shorter duration of the valve life (meaning you require another surgery soon).

https://www.jacc.org/doi/10.1016/j.jacc.2022.12.023
After regression standardization, the cumulative incidence of all-cause mortality at 10 years was 43% (95% CI: 24%-44%) in the no PPM group compared with 45% (95% CI: 43%-46%) and 48% (95% CI: 44%-51%) in the moderate and severe PPM groups, respectively. The survival difference at 10 years was 4.6% (95% CI: 0.7%-8.5%) and 1.7% (95% CI: 0.1%-3.3%) in no vs severe PPM and no vs moderate PPM, respectively. The difference in heart failure hospitalization at 10 years was 6.0% (95% CI: 2.2%-9.7%) in severe vs no PPM.

All sorts of stories abound at interventional cardiologists attempting to "crack the frame" of calcified bioprosthetic valves to get that extra mm or so of space for the TAVI (Yeeee har, rye dem cow-boy).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9095411/
perhaps someone with more experience in this (@nobog ) could make some comment and let me know how much I missed the mark by.

short answer : you totally want to avoid mismatch
 
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V__ said:
But do you know the cause, or have a reference for this observation
As Pellicle notes, there's a lot to this. My 1/2 to 1/3 is a simplification from:
- normal MV area is 4-6 sq cm
- my personal MV area after MV repair (for mod/severe regurgitation) was 1.2 sq cm (1-1.5 is mod stenosis)
-I now have a 29mm St Judes which has a nominal geometric area of 4.4 sq cm

I believe that the reason the repair had such a large impact on me is that the leaflets were also severely calcified and after rigidly fixing the outside with the annuloplasty ring, they simply could not move enough. Peak gradient across the valve before repair was 4 mm HG and after repair it was 20 mm HG. (reminder: a reason those echo results have so much information on them is that rarely does one metric tell the complete story. When I am running my leg muscles do not care what my mitral area is . . .they just want oxygen!)
 
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Mitral stenosis was my primary issue but I didn’t know I had it till I became pregnant with twins which means more strain on the heart.
This reminded me of some things. In my case, my post-repair stenosis was not a problem . . . except when exercising. In your case, it was a strain that was going to steadily increase for 9 months. Commonality is that the heart has to provide more flow so pressure and/or rate must increase (most likely both). As noted above, my peak MV gradient after repair increased to 20 mm Hg. That is not good but also not terrible. I found this in an old file with some echo's and recall discussing this with my cardiologist (apologies, I do not recall the source).

Key point is that around 35 mm HG pressure, lung problems develop. What they had me do was a type of stress echo. They put the ultrasound equipment and a bed right next to the treadmill/EKG and had me run. I recall that there was only one ultrasound technician specified for this because she had to be good and quick. They increased the treadmill load until there was a problem on the EKG and then I jumped on the table where they quickly did the echo. Challenge is that with exercise as the cause, as soon as I stopped the pressures and rates drop. Occurs to me that when the load is from pregnancy, there is no break .. . . steadily increasing load.

My pressure under load was over 40 mm Hg and that was why I felt chest pressure and coughed up blood when I tried to run. When the mitral valve is too small, the atrium will increase the pressure to get the body the flow it demands. There is no valve on the atrium inlet so this 'backpressure' is felt in the lungs. A type of pulmonary hypertension.

Another way I think about this is that a desirable normal blood pressure is 120 mm HG (systolic). That increases during exercise so I'll call it 200 mm Hg for simple math. If it's taking 40 mm Hg just to cross the mitral valve and get blood into the main pump (ventricle) . . . that's a lot of loss!

1688911339434.jpeg
 
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Size is not that critical on the mitral side, it is "big" to start out with and the flow is much slower than thru the aortic valve, this is because systole/diastole is not 50/50. Not that I agree with it but an example of that is the OnX only goes to a carbon size 25mm, whereas typically an average male would have a mitral size of 27mm to 31mm.
 
pellicle, Woodcutter, nobog, thanks for the discussion!

short answer : you totally want to avoid mismatch
Would imagine so. Woodcutter's message made me realize that some changes (in terms of fluid dynamics) would still be in effect even after a perfectly matched valve.

As Pellicle notes, there's a lot to this. My 1/2 to 1/3 is a simplification from:
- normal MV area is 4-6 sq cm
- my personal MV area after MV repair (for mod/severe regurgitation) was 1.2 sq cm (1-1.5 is mod stenosis)
-I now have a 29mm St Judes which has a nominal geometric area of 4.4 sq cm
Ah! Then, it seems, the point was a possibility of a significant change after repair?

Just looked up my numbers. It seems post-repair the effective MV area indeed went down, from ~3 cm^2 to 1.86 cm^2. The peak gradient remained at 3 mm Hg though.

This reminded me of some things. In my case, my post-repair stenosis was not a problem . . . except when exercising.
...
Key point is that around 35 mm HG pressure, lung problems develop. What they had me do was a type of stress echo.
Quite useful information. Thanks!

Size is not that critical on the mitral side, it is "big" to start out with and the flow is much slower than thru the aortic valve,
Would imagine this to be the case "up to a point" ? My, perhaps naive, understanding is that in biological systems 20-30% change can usually be accommodated through different feedback loops. But the factors of few could be significant.
 
Would imagine this to be the case "up to a point" ? My, perhaps naive, understanding is that in biological systems 20-30% change can usually be accommodated through different feedback loops. But the factors of few could be significant.
my perhaps only slightly more advanced understanding is not only up to a point but you also need to factor in duration.

While the system has the capacity for accommodation to range changes it is not without cost. Even for small accommodations (like 10%). But when it moves into "chronic" then we have problems.

Consider it like posture, if you sit badly for 10 minutes its not a problem and the body can adapt. If you sit badly (like working in IT engenders) for decades it'll cause issues.

Trees are another example, you can't get a tree that's been bent to grow straight again.

1688936106299.png


This is why health is a delicate balance.
 
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I was an avid runner prior to my first aortic valve replacement at age 31, running 5:50 minute miles in a half marathon and 6:25 miles in a marathon a few months before I found out I needed surgery. I gave up racing after surgery but still never got anywhere close to those times again. Really I switched to running more for exercise than to improve my times at that point, but physically it did not feel like I could run like I used to. Part of it was definitely mental as I did not feel comfortable pushing it like I did before, but it felt like I just didn’t have the physical capacity for it anymore. I’m sure there are reasons for that, be it valve size or whatnot, but my experience was similar to yours.
 
Here's a blurb from an older Circulation article

https://www.ahajournals.org/doi/full/10.1161/circulationaha.108.778886

that supports several PPM points made above. The point about age and different aortic vs. mitral impacts resonated with me.

Clinical Impact of PPM​

Several studies have reported that aortic PPM is associated with less improvement in symptoms and functional class,30 impaired exercise capacity,31 less regression of LV hypertrophy,32 less improvement in coronary flow reserve,33 and more adverse cardiac events.30,34 Moreover, PPM has a significant impact on both short-term35,36 and long-term mortality.34,36,37 Recent studies also have reported that the impact of PPM is most significant in patients with depressed LV function with regard to heart failure and mortality after AVR.34,35 These findings reflect the fact that an increased hemodynamic burden is less well tolerated by a poorly functioning ventricle than by a normal ventricle. The impact of PPM also is more pronounced in young patients than in older patients,16 which might be related to the fact that younger patients have higher cardiac output requirements and are exposed to the risk of PPM for a longer period of time. Mitral PPM is independently associated with persisting pulmonary hypertension, increased incidence of congestive heart failure, and reduced survival after MVR.28,29


V_ . .. . yes, I consider my MV repair difficulty to be PPM. I do not know how it is/was medically categorized.

 
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Thank you! Looks interesting, but I have to delay reading until the next weekend.

FWIW, in the meantime I also found this article. From conclusions:
In RMA patients, EOA increases during exercise despite fixed annular size. Diastolic AL tethering plays a key role in this dynamic process, with increasing AL opening during exercise being associated with higher exercise EOA. EOAi at peak exercise is a strong and independent predictor of exercise capacity and is associated with clinical outcome. Our findings stress the importance of maximizing AL opening by targeting the subvalvular apparatus in future repair algorithms for secondary mitral regurgitation.

I think they are saying that the effective area is increasing during the exercise in spite of the annuloplasty ring implantation. And that the leaflet opening plays a role in that. So... predictably, the system is not quite simple. And I'm sure there may be other factors, like the leaflet flexibility, as it seems you indicated. At the same time, the ring size/area are still quite important, as they seem to modulate the effective flow, even at load.

Thanks for sharing your knowledge and experience.
 
This reminded me of some things. In my case, my post-repair stenosis was not a problem . . . except when exercising. In your case, it was a strain that was going to steadily increase for 9 months. Commonality is that the heart has to provide more flow so pressure and/or rate must increase (most likely both). As noted above, my peak MV gradient after repair increased to 20 mm Hg. That is not good but also not terrible. I found this in an old file with some echo's and recall discussing this with my cardiologist (apologies, I do not recall the source).

Key point is that around 35 mm HG pressure, lung problems develop. What they had me do was a type of stress echo. They put the ultrasound equipment and a bed right next to the treadmill/EKG and had me run. I recall that there was only one ultrasound technician specified for this because she had to be good and quick. They increased the treadmill load until there was a problem on the EKG and then I jumped on the table where they quickly did the echo. Challenge is that with exercise as the cause, as soon as I stopped the pressures and rates drop. Occurs to me that when the load is from pregnancy, there is no break .. . . steadily increasing load.

My pressure under load was over 40 mm Hg and that was why I felt chest pressure and coughed up blood when I tried to run. When the mitral valve is too small, the atrium will increase the pressure to get the body the flow it demands. There is no valve on the atrium inlet so this 'backpressure' is felt in the lungs. A type of pulmonary hypertension.

Another way I think about this is that a desirable normal blood pressure is 120 mm HG (systolic). That increases during exercise so I'll call it 200 mm Hg for simple math. If it's taking 40 mm Hg just to cross the mitral valve and get blood into the main pump (ventricle) . . . that's a lot of loss!

View attachment 889363
Thanks for this chart and info, makes sense. I definitely did have both pulmonary hypertension and pulmonary edema. I guess it was good that my blood pressure has always been lowish (not clinically low but low normal like 100/60). In fact this was a problem for me in the ICU as they said they were waiting for my blood pressure to get higher before discharging me (it was more like 96 / 56 after lying around for a few days). I said well we’ll be waiting a while then. It’s also interesting to me that any gradient over about 12 mm hg my cardiologist does not like. It’s crazy to think of it being so much worse.
 

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