[Minimally Invasive Diagnosis & Treatments]

There are several classifications of stents – many of which pertain to the stents’ material and design. A more recent classification, however, relates to the presence of a pharmaceutical coating on the stents surface. Stents that are coated with such a drug are known as Drug Eluting Stents or DES, while stents that do not have such coating are known as Bare Metal Stents or BMS.

Drug Eluting Stents (DES) were developed to mitigate “in-stent stenosis” – one of the possible post-stenting complications. In-stent stenosis is the result of a gradual blockade of the stent’s lumen, forming over months or years after the stent’s placement. The stent lumen is gradually blocked by the in-growth of the cellular lining of the artery.

However, while succeeding in mitigating in-stent stenosis – the use of DES increases the occurrence of in-stent thrombosis. This phenomenon is similar to in-stent stenosis, but it is much more abrupt. In-stent thrombosis takes place immediately or shortly after the stent’s placement and is the result of a blood clot formation rather then cellular proliferation.

A few weeks after placement, the inner lumen of Bare Metal Stents is fully covered by epithelial cells which naturally coat the inner lumen of all coronary vessels. Therefore, the bare metal struts are exposed to the bloodstream only for a short period of time. During that short period, anti-aggregation therapy (such as Aspirin and Clopidogrel) must be administered in order to prevent in-stent thrombosis. A few weeks later the stent's inner lumen is coated with epithelial cells and there is no direct contact between the struts and the bloodstream. Therefore, the risk for in-stent thrombosis is significantly lower. However, in-stent stenosis may develop progressively over months and years due to migration of smooth muscle cells from artery walls, gradually blocking the stent's lumen. In-stent stenosis may require additional invasive intervention, as it may cause acute coronary syndrome or myocardial infarction.

Drug Eluting Stents were developed in an attempt to cope with the in-stent stenosis phenomenon. The drugs used on these stents (usually paclitaxel and sirolimus) suppress the cellular proliferation process of both epithelial and smooth muscle cells. Thus they mitigate the slow, progressive stenosis and help maintain stent patency over time.

However, delaying the epithelial coverage of the stent greatly lengthens the exposure of the stent itself to the bloodstream. Thus, it also increases the risk for in-stent thrombosis and sudden occlusion of the lumen. Therefore, the use of drug eluting stents necessitates prolonged, often life-long, treatment with anti-aggregation therapy, such as a combination of Aspirin & Clopidogrel.

Since both Bare Metal Stents and Drug Eluting Stents have their respective benefits and drawbacks there are no clear-cut guidelines for the situations in which one is preferable to the other. Current recommendations suggest that drug eluting stents should be used in cases of severe coronary artery disease accompanied by multiple risk factors for atherosclerosis, such as diabetes mellitus, hyperlipidemia and prior personal history of cardiovascular disease. Bare metal stents should be used in less severe cases of coronary artery disease, and in any case of possible future contraindications for anti-aggregation therapy.