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.

Quote from Ken289:

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?

What you describe is a very common situation of a stent that failed by excessive "furring," clotting, or scarring. The progression can very VERY fast, yes, 5 weeks; for the clot, 5 seconds!

Don't get defensive; we are both trying to help and if we both happen to believe in Occam's razor, or the medical version of it: "When you hear hoofbeats, don't look for zebras" we are expressing the normal and expected response to your hypothesis.
Your doctor is prescribing isosorbide to dilate your coronary arteries in exactly the same way that he would prescribe it for someone with stable angina caused by any common, stable, coronary blockage. There is nothing special about nitrates and spasm.
You've mentioned your pain several times WHEN EXERCISING...again, that's classic ischemic angina brought on by increased workload.

There is no intention to impugn your sanity, in fact if I told you what I sometimes envision to be the state of my stent it would curl your hair. Trying to blend facts, hopes, fears, pain, and medical research into the creation of a logical picture is difficult when we are faced with life and death issues. It doesn't help that we can never SEE the condition of our stents, in fact that mystery only fuels our imaginations.

It is always important when researching the literature to remember that just because something CAN happen, it doesn't mean it HAS happened.

If all you wanted was a terse answer to your question:
[QUOTE]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.
Yes, I have a view on the subject and a background in fluid flow mechanics: vigorous exercise creates a MORE turbulent flow, which MAY increase the likelihood of platelet aggregation but insignificantly in the presence of adequate aspirin. The turbulant flow is also created to a huge degree in the chaos of a beating heart and passed into the aorta...completely laminar flow is rare in nature. If you want to imagine truly chaotic turbulent flow imagine the pulse of blood exiting the heart into the aorta and than making abrupt right angle high speed turns into the much smaller RCA and LAD...if turbulent flow indeed caused many clots, the we'd all be dead after the first few heartbeats from clots initiated at those junctions and passed into coronary blood system.
Yes, I agree with your cardio's estimate of the situation.

On the title question:
"Exercise Promotes Restenosis?"
My answer is an emphatic, no.