To fully understand your choices regarding stents, you must first understand the history of coronary intervention.
Prior to 1977 there was no coronary intervention. Andreas Guentzig, preformed the first angioplasty that year. His first catheter was nothing more than a hollow tube with a balloon on the end which when inflated filled with fluid. Through the 80’s this technology was improved and perfected, but the principle remained the same. Inflate a fluid filled balloon and push the plaque out of the way and hope the artery does not recoil, tear or scar. The scar was created from the pressure exerted by the balloon on the vessel wall. If the scar continues to grow it will eventually encroach on the residual vessel lumen.
The early problem with angioplasty was largely due to “restenosis”, which is the renarrowing of the treated artery through two main mechanisms; 1) Elastic recoil and 2) Neointimal hyperplasia . Through the 80‘s and early 90‘s, under the best conditions the restensosis rate remained 30%.
Stents were thought to be the cure for restenosis. Developed in the early 90‘s, they provided a metal scafolding to hold the artery open and thus prevented elastic recoil. Various metals where used; stainless steal, nickel, gold cobalt and chromium to name a few. As the thickness of the metal decreased and the metal polymer coatings improved , restenosis dropped to 15%.
Drug eluding stents (DES) were thought to be the solution. They were targeted to solve the remaining issue of scar formation or neointimal hyperplasia. The bodies normal reaction to injury, is to form a scar. During neointimal hyperplasia this single cell type continue to proliferate and will eventually encroach on the lumen and renarrow the artery. These new stents are coated with a specific type of chemotherapeutic medication which stops the intimal hyperplasia. This lead to single digit restenosis rates, approaching 5%.
Although this sounds great, the stents are foreign bodies and the body creates clots to react against them. These clots are formed primarily by your platelets which attach to the stent to form a clot. Your platelets need to be inhibited from forming clots on your newly placed stent. This is accomplished by two types of medications, known as dual antiplatelet therapy (DAPT). Aspirin and either Plavix or Effient are prescribed until the stent is fully endothellialized (covered with new lining of the vessel). Once the endothelium or inside lining of the artery has grown over the stent, the risk of clotting or thrombosis is substantially reduced. In DES this takes much longer than a Non-DES. Remember, we helped prevent restenosis by inhibiting neointimal hyperplasia. But, this means the stent is susceptable to clot formation for a longer period of time. As such, we currently recommend DAPT for 12 months for DES and only 3 to 6 weeks for Non-DES. So, if you are prone to bleeding or are taking other anticoagulants such as coumadin, it maybe better to accept a little higher restenosis rate of 15% with a Non-DES and shorter treatment time of DAPT.
Size does matter!! In addition to the above issues, neointimal hyperplasia has a greater effect on smaller diameter vessels. If you have a larger lumen it takes more tissue growth to encroach on the lumen. The benefit of DES in larger blood vessels is less significant.
So, the moral of the story is that based on your ability to take longterm dual antiplatelet therapy and your vessel size , you along with your cardiologist need to choose the right stent for you.