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.
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.
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.