There are, or have been, concerns revolving around Drug Eluting Stents. However, what we have to realise is that these were developed for a very good reason. If Bare metal stents were so good, why would they invest so much money in research to develop the DES. If there are no problems with something or the problems only occurred very rarely, it is likely investment would be channeled into something more worthwhile.
Bare Metal Stents have the problems associated with restenosis more than Drug Eluting Stents, but DES can still suffer restenosis in some people. However DES makes this much rarer. The secret is the chemical coating on the Stent which inhibits scar tissue growth, allowing normal healthy artery tissue to form. Plavix is given which helps prevent clots forming along the Stent, caused by damage to the Plaque during ballooning.
I have 6 DES in my Arteries but 5 are only a few weeks old. The first one I had 2.5 years ago is doing very well indeed, the artery is still fully open and nice and smooth. Normally Plavix is taken for a period of 12-18 months because there is no real evidence to suggest it does anything after this time and new tissue should have formed over the Stent by then and be of very little risk of clotting.
We all come to our own conclusions when we research something and my personal opinion is to go for the Drug Eluting Stent every time.
I would just like to add something which you may feel important.
A DES is no stronger than a BMS, they are absolutely identicle apart from one having a chemical coating over it. So there is the same risk with an artery collapsing the Stent and the only difference is how chemical processes around the Stent are allowed to progress.
But if they don't develop clots in the first year or two, I am not sure how they can. Once new tisse forms through and around the mesh of the stent, making a smooth surface, why would a clot decide to form? It actually becomes a new lining with the stent acting as the artery wall.
The rupturing of soft plaque into the lumen causes a clot. Turbulance of irregular of blood flow over a "rough" surface or a bifurcation can cause plaque (ie circumflex and LAD bifurcation off the main. Also, blood flowing over a gradient causes turbulance on the distal side of the gradient and could present a problem. Also, rough surface, fluid stress may have a role in platelet thrombus formation.
"Yes but what about with a stent? From what I understand the risk of a thrombus forming in a stent is quite low and would normally occur quite quickly after insertion".
I'm not sure I understand your question? If there is a smooth surface over the stent after healing, it seems the likelihood of restenosis is less as a rough surface causing turbulance of cells will be decreased. If a vessel is stented and there is soft plaque within the lining above the stent placement site, it seems the likelihood of rupture is increased at the time or shortly thereafter as the vessel is remodeled. If there is hardening of the vessel it seems reasonable the probability of a rupture is increased as remodeling may be limited with a loss of some flexibility of the vessel
Yes that is my point and my question. It seems that the consensus states that restenosis of a DES is greatly reduced but it still has a high risk of clotting, virtually the same as a BMS.
As you correctly state, a sudden irregular surface is required to create a clot but that's what I can't see with a DES. The chemical coating a DES prevents scar tissue forming, something associated with BMS causing clotting and restenosis. In a DES the lumen naturally forms at a slow and steady rate, unlikely to therefore cause clotting. The fats
trapped behind any stent cannot escape, unless the stent collapses which is very rare.
So, basically I'm trying to learn why a DES is nearly as high as a BMS with regards to clotting.
Thank you for your time on this matter.
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