Bare Metal Stents vs. Drug Eluting Stents

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When angioplasty alone is used to treat coronary artery disease, there is a 20% - 40% chance that restenosis will occur within the first several months, requiring further therapy.

The first stents - bare metal stents (BMS) - reduced the incidence of restenosis after angioplasty by half. Then drug eluting stents (DES) were developed, and the risk of restenosis was reduced by as much as an additional 70%.

Because they are so effective at preventing restenosis, the use of DES has become routine after angioplasty.

The drugs which coat the metal struts of a DES inhibit the tissue growth that is responsible for restenosis. Early DES used sirolimus or paclitaxel. The so-called second-generation DES use everolimus or zotarolimus.

Is There A Problem With DES?

The dark cloud hanging over DES has to do with stent thrombosis. Stent thrombosis occurs when a blood clot suddenly forms at the site of a stent. This blood clot often causes acute and complete occlusion of the coronary artery. This is a medical catastrophe, and commonly leads to extensive cardiac damage or death. Fortunately, stent thrombosis is statistically uncommon. Unfortunately, when it does occur it is usually devastating.

Stent thrombosis is most likely to occur relatively early after the placement of a stent - in the first weeks or months.

The risk of early stent thrombosis can be greatly mitigated by the use of dual anti-platelet therapy (DAPT). DAPT consist of aspirin plus one of the P2Y12 inhibitors, which are clopidogrel (Plavix), prasugrel (Effient), and ticagrelor (Brilinta). Early stent thrombosis is equally likely to occur with either BMS or DES, so the use of DAPT is critical, for at least several months, with any stent.

The real question regarding DES relates to late stent thrombosis - thrombosis that occurs a year or more after the stent is inserted.

A chief cause of stent thrombosis, it is thought, has to do with the contact of blood platelets with the metal struts of the stent (which are exposed to the flowing blood), and the subsequent activation of the platelets and the formation of a clot. With BMS, tissue growth usually covers the metal struts within a few months, reducing the risk of stent thrombosis. But with DES, tissue growth is inhibited - which indeed is the whole purpose of using DES. Inhibiting tissue growth reduces the risk of restenosis, but (it is believed) exposes the patient to a prolonged risk of thrombosis. So, late thrombosis may occur.

Because of the risk of late thrombosis, doctors in the U.S. are recommending that treatment with DAPT be continued for long periods of time after stent placement - at least 12-30 months, and perhaps forever. Because DAPT itself introduces significant risks and difficult management issues, the optimal duration of DAPT is a controversial topic among cardiologists.


The idea that late stent thrombosis is more likely with DES than with BMS is somewhat speculative, and has not been proven. However, an apparent consensus of experts believes that if a patient who needs a stent seems likely to have issues with bleeding that would make DAPT particularly dangerous (for instance, someone who has a history of gastrointestinal bleeding or hemorrhagic stroke), they should receive a BMS instead of a DES, and the duration of their DAPT should be limited to 6 months. In these patients, the reasoning goes, the higher risk of restenosis seen with BMS (which is usually a gradual, non-catastrophic process) is acceptable, in order to avoid the use of long term DAPT that would be needed with DES. This approach, obviously, relies on the belief that late stent thrombosis is inherently less likely with BMS than with DES - which, again, is unproven.

Still, if it is apparent that if a particular patient is likely to have problems with long term DAPT, most cardiologists in the U.S. will probably opt for a BMS instead of a DES in that patient.

There is at least some evidence that second-generation DES may be less prone to late stent thrombosis than first-generation DES. In fact, in Europe (where second-generation DES have been available for quite some time, thanks to differences in the regulatory environment), doctors routinely stop DAPT after 6 months in all patients. European investigators even have studies (which are relatively small and quite imperfect) suggesting this practice is safe.

The Bottom Line

The bottom line is that the use of any stent introduces the risk - a very small risk, but a very real one - of catastrophic stent thrombosis. Cardiologists like to emphasize the infrequency of the problem, as if to minimize it. But at the same time they are concerned enough about it to insist their patients take DAPT, often for a very long time and at the cost of some tough problems introduced by DAPT itself, in order to mitigate that risk.

So, managing the risk of stent thrombosis requires doctors and patients to balance several factors - the risk of clotting vs. the risk of bleeding; the risk of restenosis vs. the risk of thrombosis; the optimal duration of DAPT; and the use of BMS vs. the use of first or second generation DES. There is no one right answer. The optimal approach for each patient needs to be individualized - and achieving this optimization will always require the full participation of a fully informed patient.

Finally, it bears mentioning that one important aspect of this whole issue, which too many cardiologists brush aside too quickly, is the question (which needs to be asked in each and every case) of whether a stent is really needed at all. In many cases, it is not.


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