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Boston Scientific Corporation Message Board

  • rktjockey rktjockey Aug 14, 1998 11:48 AM Flag

    Remember...

    Just a few points:

    1. Nearly all stents
    placed eventually re-stenose. The most recent research
    on the subject suggests it's not the stent that
    "causes" it, but the person't own body response. Recent
    findings also show a high correlation between restenosis
    and chronic viral infection.

    2. Don't sneer at
    a "niche" product. If a company has several
    products that make just a few million a year apiece, the
    money adds up pretty quickly. And, once a product has
    been placed in the market, users' reaction to that
    product can benefit a company's entire line, especially
    if the product fits into a niche that another corp.
    thinks isn't worth their time.

    3. SciMed/BSX
    needs to keep from underestimating AVE. AVE is a
    smaller, newer, less polished company with a smaller
    product selection -- but they're also more hungry and
    more flexible than a larger company is going to be.
    SciMed and Boston Scientific both were once *just like
    that* not so long ago, and managed to acquire assets or
    steal market share from companies that used to sit
    where BSX sits now. One company I know of used to think
    SciMed sales reps were a bunch of clowns and misfits --
    and that company doesn't exist any more.

    SortNewest  |  Oldest  |  Most Replied Expand all replies
    • I believe that you may be confusing restenosis
      and atherosclerotic disease. Restenosis is a
      progressive response to angioplasty caused by the barotrauma
      of balloon dilitation and the foreign body response
      to the stent. Most occurs between one and six
      months, but there is some late response up to about nine
      months post-intervention. Most stents do not restenose,
      in fact on a per lesion basis, patency rates are
      about 80%, far better than balloon
      angioplasty.

      With that said, atherosclerosis is not treated by
      stents other that symptomatically. In other words, these
      patients, who are by definition, atherosclerotic to begin
      with, have progressive disease. Most go on to further
      intervention, more angioplasty at different sites, and later,
      CABG for multivessel disease. Only a change in life
      style, or perhaps aggressive pharmaceutical or gene
      therapy will treat the disease and not just the symptoms.

      • 1 Reply to MrStent
      • I probably should have been more complete in my
        first point.

        Restenosis is generally caused by
        cellular hyperplasia in the artery. The hyperplasia is
        triggered in part by vessel-wall trauma, which is why a
        restenotic response occurs when treatment is performed using
        any current transluminal method, whether it's a
        balloon, high speed rotational atherectomy, or stent
        placement. It usually makes itself most apparent in the
        first six months, but hyperplastic growth can continue
        for a year. It is this type of cellular proliferation
        I was addressing.

        With a stent, the
        hyperplasia often doesn't occlude the artery as quickly as
        with the other methods, though the exact reasons why
        are subject to debate. Some of the reasons I've seen
        are that the lumen is wider than after ballooning or
        atherectomy, or that the stent prevents long-term elastic
        rebound of the vessel wall, or that the stent itself
        physically blocks enough of the wall to slow cellular
        proliferation. In the long run, the vessel lumen does grow
        smaller(even if not enough to effect TIMI flow estimates or
        produce clinically significant effects), and the material
        in the lumen is largely neointima.

        Yes,
        atherosclerotic disease also reoccludes arteries after
        procedures, but generally (though not exclusively) on longer
        time scales than neointimal hyperplasia. Progressive
        disease lesions have a different structure and histology,
        but the two mechanisms can and often do work together
        to plug an artery back up. I agree, the only
        long-term hope right now for most people with the disease
        is diet and lifestyle changes. There are some
        interesting cell-receptor experiments that have been reported
        over the last couple of years that may produce
        clinically useful results, but that will take some
        time.

        The reocclusion of stents is an interesting problem;
        some physicians have re-stented, some have used
        balloons to re-expand the lumen locally, and some are
        using high speed rotational atherectomy to clear things
        out. It will be interesting to see what, if anything,
        eventually works best.

        I realize I'm pretty much
        preaching to the choir, here; none of this changes the fact
        that stents are producing good clinical results, that
        people worried about restenosis should realize that
        nearly every intervention produces some degree of
        hyperplasia (even if it doesn't significantly affect an
        angiogram), and that people with long-term disease treated by
        any transluminal method need to really work on
        lifestyle changes to avoid CABG as long as
        possible.

        Thanks for the opportunity to trade views with you.

 
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