Which Stent is Best?
Angioplasty (inflating a balloon inside an artery to open a blockage) often results in the artery closing due to a blood clot forming (thrombosis) or thickening of the artery’s wall (restenosis).
Since the 1990s, the vast majority of angioplasties have been followed with stenting, significantly decreasing the incidence of thrombosis and restenosis. Stents are tiny metal coils loosely resembling the springs inside a clickable pen. They are used to prop open a coronary artery at the site of a blockage. In this way, blood can flow through the coronary artery and deliver oxygen to heart muscle.
Restenosis is an overgrowth of a lining, neointima, on the stent. This growth can narrow the diameter of the coronary artery. A coronary artery with restenosis can cause angina, or heart attack. Smaller diameter coronary arteries tend to be at greater risk of restenosis. As noted above, when angioplasty is done without stenting, the risk of restenosis is very high. Bare-metal stents (without a drug coating) are a significant improvement on this problem. Drug-coated stents reduced restenosis even more.
The drug-coated (or drug-eluting) stent is a development in stent technology. The “drug” on a drug-coated stent is one of several approved compounds which prevent the cell growth of the neointima. Interestingly, these same drugs are used to prevent cancer growth. The drug-coated stents do a much better job of preventing restenosis than the older, non-drug-coated, bare-metal stents. It is unclear what happens once the drug coating wears off. A concern is the formation of blood clots (thrombosis) inside the stent.
Thrombosis can occur during the balloon and stent procedure, or in the days to months afterwards. Early thrombosis occurs within 6 months of the procedure, while late thrombosis occurs after 6 months. The inflation of a balloon inside the coronary artery (angioplasty) and the placement of a stent cause damage to the lining of the artery. The body perceives this damage as a bleeding vessel, much like when you cut your finger. The response is to quickly form a blood clot to stop the bleeding. Unfortunately, this clot forms inside the vessel and blocks blood flow.
Early thrombosis can occur with both the bare-metal stent and drug-coated stent. Aspirin and Plavix (see below) are effective in reducing the risk for both kinds of stents. Late thrombosis is a bigger problem with drug coated stents than for bare metal stents. It’s possible that the risk of thrombosis in the drug-coated stents persists forever.
Preventing blood clot formation includes the use of medications such as aspirin and clopidogrel (Plavix). These two pills help prevent platelets from sticking together and forming blood clots. It is not clear how long one must take the medications after stenting. The medical literature recommends from three months to one year, depending on the specific type of stent. For my patients with bare-metal stents, I advise taking aspirin for life and Plavix for at least three months. Those with drug-coated stents should take both drugs for life.
Taking two powerful medications such as aspirin and Plavix for life is no small matter. For example, many surgeons are hesitant, or simply refuse, to operate on patients taking this combination. They are concerned about bleeding occurring during the surgery. Those on aspirin and Plavix have less effective platelets, and hence, prolonged bleeding time. I’ve heard many frustrated patients caught between a surgeon requiring them to stop Plavix for a procedure and a cardiologist telling them they can never stop it. Additionally, the bleeding risk from trauma, such as a car accident, is much high if you are taking both aspirin and Plavix. Moderate trauma can be converted into a life-threatening condition.
Before committing my patients to long-term Plavix use, I consider the above consequences. It’s important for doctors to communicate the benefits and risks of Plavix use. Patients need to understand, in advance, the risks of stopping Plavix for a future medical procedure. Only when patients understand this risk should Plavix be recommended.
The drug-coated stents have decreased the problem of neointimal growth and restenosis but may increase the risk of later thrombosis. Patients who prematurely stop aspirin and Plavix have been known to have very sudden blockage of their stents, with blood clots leading to heart attacks and sometimes death.
I suspect that more research will shed light on when one or the other of these two stent types is preferred. For example, the size of the coronary artery, length of the blocked area, presence of diabetes, and the long-term use of aspirin and Plavix may affect which stent is better for a patient.
In an emergency, the decision as to which stent to use rests with the cardiologist performing the procedure. However, if a balloon and stent procedure is done electively, a discussion between cardiologist and patient should occur ahead of time. This should include the risks, benefits, and alternatives of each procedure and specifically, the need for Plavix.
Regardless of the type of stent, you can help prevent the catastrophic consequences of stent blockage by following the instructions of the cardiologist and the rest of your medical team, and by taking medications for appropriate periods of time.