Coronary arteries Like all invasive medical procedures, implanting stents in the coronary arteries carries risk. For the newer<unk> s, very-long-term results are not yet available; however, five years after implantation, sirolimus-eluting stents remained superior to bare-metal stents. Risks associated with cardiac catheterization procedures include bleeding, allergic reaction to the X-ray contrast agents used to visualize the coronary arteries, and myocardial infarction. With PCI, the requirement for emergency CABG has markedly decreased since the days of balloon angioplasty, such that in some communities, coronary stenting is permitted in hospitals without on-site cardiac surgery facilities. This remains highly controversial in the United States because of the rare but largely unpredictable risk of coronary artery perforation. Rarely, a type of allergic reaction to the<unk>  may occur; episodes of fatality have been reported. Stent thrombosis Although<unk> s continue to represent a major medical advance for angioplasty, evidence has always shown new clot thrombosis formation with stents to be a problem, thus clotting suppressant agents are routinely given during placement, and anticlotting agents should be continued. Coronary arterial healing occurs after the placement of a<unk> , but complete healing of the vessel takes time. For<unk> s, the time course of complete healing in humans is unknown. A stent is a foreign object in the body, and the body responds to the stent’s presence in a variety of ways. Macrophages accumulate around the stent, and nearby smooth muscle cells proliferate. These physiological changes, which can cause restenosis, are limited by the<unk> s released by the stent, but these<unk> s also limit the formation of a new endothelial layer over the new stent to inhibit clot formation. Endothelialization is a hallmark of vascular healing and is important for the prevention of thrombus formation. Lack of healing caused by antiproliferative<unk> s can make the stent an exposed surface on which a clot, sometimes life-threatening, can form. For<unk> s (which delay the formation of a new endothelium cover over the stent), the incidence of clot formation within the stent may persist for a longer period of time, perhaps as long as five years after treatment.<unk> s have been associated with delayed arterial healing and the prevalence of latent thrombus after five years, suggesting patients may continue to be at risk for stent thrombosis for an extended period of time. Though less frequent with<unk> s, neointimal proliferation can still occur in<unk>  and cause restenosis. Stent occlusion because of thrombosis may occur during the procedure, in the following days, or later. The presence of thrombi around the stent may, in turn, affect the<unk><unk>  performance of the stent. Treatment with the antiplatelet<unk> s aspirin and clopidogrel appears to be the most important factor reducing this risk of thrombosis, and early cessation of one or both of these<unk> s after<unk> ing markedly increases the risk of stent thrombosis and myocardial infarction. A recent histopathology study showed very late<unk>  thrombosis is associated with histopathological signs of inflammation and intravascular ultrasound evidence of vessel remodeling. Compared with other causes of myocardial infarction, eosinophilic infiltrates are more common in thrombi harvested from very late<unk>  thrombosis and correlate with the extent of stent malapposition. Whether or not<unk> s are at higher risk than bare-metal stents for late thrombosis is intensely debated. In meta-analyses of the sirolimus- and paclitaxel-eluting stent trials, a small but statistically higher risk of thrombosis was shown after the first year, compared to bare-metal stents. Late stent thrombosis often causes myocardial infarction and sometimes death. In other analyses, the late thrombosis risk is offset by<unk> s' markedly reduced risk of restenosis and its complications including myocardial infarction. A meta-analysis concluded the mortality risk associated with<unk><unk>  and bare-metal stents is similar.<unk> ign==<unk><unk>  out of the stent.<unk> s generally consist of three parts - the stent platform, a polymer coating that binds the<unk>  to the stent and releases<unk> , and the<unk> . Stents have been tested that work without the coating layer. The stent platform itself is an expandable framework, generally with an elaborate mesh-like<unk> ign to allow expansion, flexibility, and in some cases the ability to make or enlarge side openings for side vessels. The first<unk>  were stainless steel alloys composed of iron, nickel, and chromium and were based on existing bare metal stents. These stents were hard to visualize with medical imaging, posed a risk of causing allergic responses, and were difficult to deliver. Subsequent new alloys were used, namely cobalt-chrome and platinum chrome, with improved performance. Recently, bioresorbable stents have been developed in which the stent itself dissolves over time. As of 2009, materials that had been explored for use included magnesium, polylactic acid, polycarbonate polymers, and salicylic acid polymers. Resorbable stents have held the promise of providing an acute treatment that would eventually allow the vessel to function normally, without leaving a permanent device behind. One to three or more layers of polymer can be used in the coating, e.g., a base layer for adhesion, a main layer that holds and elutes (releases) the<unk>  into the arterial wall by contact transfer, and sometimes a top coat to slow down the release of the<unk>  and extend its effect. The first few<unk> s to be licensed used durable coatings. The first generation of coatings appear to have caused immunological reactions at times, and some possibly led to thrombosis. This has driven experimentation and development of new coating approaches. The<unk>  is mainly used to inhibit neointimal growth due to the proliferation of smooth muscle cells that would cause restenosis. Much of the neointimal hyperplasia seems to be caused by inflammation. Hence, immunosuppressive and antiproliferative<unk> s are used. Sirolimus, paclitaxel, and everolimus were previously used for other medical applications and have been included in licensed<unk> . Vascular stents are Class III medical devices that are intended for use as a mechanical radial support to enhance vessel patency over the intended<unk> ign life of the device. Device properties and the intended use are dependent on results from extensive testing that involve mechanical tests on universal testing machines. Types of mechanical test include bend testing, fatigue testing, radial loading, tensile testing, and torsion testing. Depending on the type of vascular stent, its location and intended use, other tests may include crush resistance, kink resistance, corrosion, coating integrity, and more.
Drug-eluting stent
Cypher stent
Dual therapy stent
Coronary stent
Hybrid coronary revascularization
Bare-metal stent
Transmyocardial revascularization
Valvulotomy