Excercise Promotes Restenosis?

[Ken289]

Just curious if anyone has a point of view on the subject? The model would be that vigorous exercise creates turbulent flow, which may promote platlet aggregation. I think I have asked this before at least indirectly, but the subject is pretty nebulous. My cardio thought about it for a minute and said to "not worry about it" (classic answer when the doc does not know and does not want to say---"I don't know") and to enjoy the benefits of the exercise.

[started04]

Originally Posted by Ken289

Just curious if anyone has a point of view on the subject? The model would be that vigorous exercise creates turbulent flow, which may promote platlet aggregation.

I believe rigorous exercise produces a defensive and compensating factors. The blood vessels constrict defensively and the heart rate increases . The heart rate increases as demand for oxygen to repair damaged skeletal muscles increases and respiratory function increases as more CO2 is produced from exercised muscle damage and needs to be dispelled, and there is an increase demand for oxygen.

Constricted of vessels causes a rise in BP as one's system is in defensive mode recongnizing there is muscular damage.

The proposition that rigorous exercise creates turbulent flow (turbulent flow?) may promote platelet aggregation...I don't recognize the connection to restenosis as I can't associate turbulent blood flow to producing platelet aggregation!

[Ken289]

KenKeith Said: "The proposition that rigorous exercise creates turbulent flow (turbulent flow?) may promote platelet aggregation...I don't recognize the connection to restenosis as I can't associate turbulent blood flow to producing platelet aggregation!"

Yes, well...after almost 8 hours of internet searching, I found numerous articles, research papers, and even a doctoral thesis which explored this area. My takeaway from all the reading is that shear stress at the wall is one of the predominant factors (and shear stress is higher with turbulent flow) in promoting a variety of chemical and cellular changes, most bad, one good. The one I think is most applicable to my hypothesis is the promotion of neointimal cell proliferation (it is amazing the number of medical jargon/terms that are used). Nonetheless, the higher shear stresses stimulate unwanted cell growth--which is just what you do not want in the fragile period right after stent implantaion. (I realize the drug coating on the stent is supposed to inhibit this cell growth, but I do not think it logical to do things to promote on the one hand while you want it surpressed on the other,)

As semi-corroborating evidence, several papers talked about the specific mechanical design features of stents and how these factors need to be selected to promote as much laminar flow and minimize turbulent flow as possible. Even the surface smoothness of the metal used to make the stents was evaluated as a factor (smoother is better).

I could find no clinical studies, but have become convinced that this is an area about which not much is really known. Based on this, plus a swell summay PDF of cardiac rehab research, today I discontinued my hospital supervised rehab program in favor of a self administered, home exercise program which will emphasize low effect exercise. The research showed same endpoint criteria for vigorous vs "mild" exercise programs. Here, "mild" exercise is defined as not exceeding 20 bpm above resting heart rate. Same death rates, MI occurance, and interestingly, same MET achievement, except the mild exercise program took several weeks longer to achieve. The mild approach will minimize blood velocity and hence turbulence thru my stent, I will achieve similar end point goals, I will save the costs. This is my plan.

For your information......

PS: direct to your question, turbulent flow almost always has eddy currents and "dead flow" spots near and around the flow disruption features, and these "dead spots" could be a spot in which platlets aggregate. Just my theory however, nothing I read spoke directly to this.

[Lenin]

Hey guys,

I have experience with fluid flow and I DO know how difficult it is to quantify in a pipe with meters. To do so in the intima of 2 mm. artery inside a living beating heart seems as close to impossible as I can imagine.
Then to correlate any difference in clotting and muscle cell proliferation to the difference in the situation measured with completely laminar flow adds another level of frightening complexity.

Ken,
I really think you are searching too hard for a reason to hate your stent. You seem determine to believe that your artery is spasming at the leading edge of the stent. What evidence do you have for this? Do you have any significant chest discomfort, when?


An aside,
I think that hard exercise is nearly always good for the heart and I doubt the proposition that the body, when confronted with an extreme workload would cut down on the size of the coronary arteries...OTHER arteries maybe but evolutionary consequences would quickly remove the genes of those whose arteries clamped down when the largest blood flow was needed.
My thinking would be somewhat supported by the fact that arterial spasm and unstable angina is most likely to hit when one is sleeping.

[Ken289]

Lenin: I certainly respect your experience, knowledge and opinions. I think you are missing some aspects of what I am describing, plus it is hard to give every detail about why I am concerned in this area.

As background, we previously discussed unstable angina and also, separately, spasms, especially at leading edges. I have data and literature to support both issues. Not the least was my cardio expressing his concern about the spasms and prescribing isosorbide to counteract same.

The concern about the turbulent flow issue derived from my first time around where I was exercising vigoously 5 weeks post stent and then suddenly went into angina followed by cath showing 85% blockage. The blockage had not been there before so what do you think caused the blockage in 5 weeks?

Secondly, this time around, while I started slow (and had several bouts of angina which I attributed to spasm, an unrelated issue), I increased exercise rate and each time (twice) afterwards felt "bad". Bad meaning chest discomfort and arm/finger pains. Thus my search for evidence on this "theory".

Just because it is virtually impossible to MEASURE turbulence in an artery does not mean the phenomenon does not exist. Plus, why are stent manufacturers concerned with laminar vs turbulent flow thru their products if it is not, indeed, an issue?

Finally, while it appears (even to me) that this might be a bit obsessive, I also intend to push every factor that might remotely be involved in a direction that is in my favor. If, down the road, research indeed does support this theory more substantially, but I have already blocked up again and been forced into bypass when I did not need to, then I will be the poorer for it. If I can adjust my approach to exercise to get the same benefits yet avoid negative effects, then I think it is prudent to do so.

All I was looking for was a discussion of the technical factors and merits, not an evaluation of whether it appears I am crazy. Other than mentioning that you can not visualize measuring the velocity or turbulence in an artery, I did not hear any technical factors or logic refuting or supporting the theory I suggested. This is what I have admired from your posts in the past. Got any on this issue?

Edit: in rereading your post, you postulate that the body could not "close down" arteries when the body in under load. In fact, the arteries vasodilate under exercise, so they indeed do not "close down". The turbulence theory is based, instead, on cellular reaction to increased shear stress at the wall (the cellular surface)---a totaly different phenomenon.