Coronary Stents

Coronary stents (CS) are expandable tubular metallic devices which are introduced into the coronary arteries that demonstrate stenosis due to an underlying atherosclerosis disease. This revascularization procedure is termed as a percutaneous coronary intervention (PCI) or coronary angioplasty with stent placement. The coronary stent was first developed in the 1980s and has continued to evolve in terms of shape, structure, and the material used within them. In a pre-stent era, balloon angioplasty was the mainstay of coronary revascularization in which an inflatable balloon-tipped catheter was inserted percutaneously through an arterial entry site in the extremity and advanced into the coronary arteries. On reaching the coronaries, the balloon was inflated to compress the atherosclerotic plaque against the vascular wall and restore blood flow to the myocardium. The balloon was withdrawn after deflating. This procedure had major drawbacks such as acute vessel closure due to arterial recoil, coronary artery dissection, acute arterial thrombosis, and restenosis due to neointimal hyperplasia. With the introduction of coronary stents, coronary dissection and vascular recoil were eliminated due to the expandable, metallic meshwork of the stent, which prevents negative remodeling.

Types of Coronary Stents

1. Bare metal stents (BMS)

2. Drug-eluting stents (DES)

3. Bioresorbable scaffold system (BRS)

4. Drug-eluting balloons (DEB)

DES consists of three components: a metallic stent platform, an active pharmacological drug agent, and a carrier vehicle. Stainless steel or cobalt-chromium is the most common metal and gives long-term mechanical stability to counteract vascular recoil. Commonly used drugs act to block signal transduction and cell cycle progression in different phases, thereby blocking smooth muscle cell (SMC) proliferation or intimal hyperplasia in the stented arterial site. Rapamycin agents bind to the intracellular protein, FKBP-12, that inhibits the protein kinase mammalian target of rapamycin (mTOR). This intracellular complex increases the expression of p27 and blocks the progression of the cell cycle from the G1 phase to the S phase (DNA synthesis). Another drug category is taxanes, which interfere with microtubule function, which is necessary for the M phase (mitosis). So cells get arrested in the G2 phase of the cell cycle. To increase surface area, a carrier vehicle matrix or a polymer coating is used to enable sufficient drug loading and release for a long time. Polymer coating consists of repeating units of biodegradable poly-L-lactide, poly–D, and L-lactic-co-glycolic acid in a regular pattern, which are degraded into lactic acid and glycolic acid that ultimately get converted into water and carbon dioxide. First-generation DES has sirolimus or paclitaxel coating on a stainless steel base. In contrast, second-generation DES has zotarolimus or everolimus coating on top of biocompatible cobalt-chromium or platinum-chromium platform. The drug release is carried out by diffusion through pores in the polymeric coating.

While DEB has only antiproliferative drug coating without an underlying metallic structure of the stent, BRS is also devoid of metallic structure and is entirely resorbed in a few months after serving their purpose. Other stents like bifurcation stents and covered stents are designed for special circumstances such as lesion over vascular bifurcation or coronary artery perforation, respectively.