Percutaneous Transluminal Coronary Angioplasty Essay -- Anatomy, Coron

Introduction In 1977, percutaneous transluminal coronary angioplasty (PTCA) was introduced to dilate narrow coronary arteries. Over the years, the development of the procedure knocked down major anatomical obstacles. Typically the procedure involves a small incision into the leg, a catheter is inserted through the groin vein and is then steered to the blocked coronary vessel via a guide wire. On the tip of the catheter is a deflated balloon. Once at the congested region of the artery the balloon is inflated, causing plaque to compress against the artery wall, dilating the artery and restoring blood to flow [1]. The initial success was demoted by the occurrence of elastic recoil. Nevertheless, scientist over came these drawbacks (well so they thought), by mounting a bare-metal stent (BMS) on the balloon of the catheter [2]. Jacques Puel and Ulrich Sigwart inserted the first stent into a human coronary artery in 1986. The inflation of the balloon caused the minute expandable metal to implant into t he vessel, causing the vessel to expand and remain expanded. The hindrance of elastic recoil was believed to be defeated, therefore in 1994 the U.S Food and Drug Administration approved the use of the first Palmaz-Schatz stent [3]. The insertion of BMS did initially improve results, mainly by reducing the risk of abrupt closure and improving long-term results. However, a new barrier was exposed in the form of In-Stent Restenosis (ISR). The new problem included negative remodelling and neointimal formation. One way to combat ISR was the concept of â€Å"coating† the metallic stent with an anti-proliferative pharmacological agent. The drug coated stents, referred to as drug eluting stents (DES), delivered the drug locally from the surface of the... ...st generation SES. The second generation EES showed superior clinical and safety over PES in the SPIRT trails. Highly significant data in TLF, MACE, stent thrombosis and target lesion revascularization was demonstrated in favour of EES. However, second generation DES may not be the â€Å"be all† of what they are made out to be. A number of clinical trail’s report negative information for ZES. ENDEAVOR I and III trails and Kandazri et al. observed significantly higher rates of in-stent late lumen loss ZES verses SES. Furthermore, SORT-OUT III trails also observed negative results for ZES, reporting considerable increases in stent thrombosis, myocardial infarction and target lesion revascularisation. On comparing both of the second generation DES together, mixed results were obtained. ESTROFA-2 reported low rates of thrombosis in both ZES and ESS. Explain difference....