Abstract
The percutaneous coronary intervention (PCI) has undergone rapid evolution over the last 40 years and has become one of the most widely performed medical procedures. The introduction of intracoronary stents has improved the safety and efficacy of PCI. However, with the advent of stenting, a new potentially fatal enemy has emerged: stent thrombosis. Ever since, adjunct pharmacological therapy, stent technique, and technology have been adjusted to reduce the risk of stent thrombosis. The aim of the present article is to provide an overview of the past, present, and future aspects of PCI in relation to stent thrombosis.
Highlights
Permanent scaffolding of the coronary vessel overcame the risk of abrupt vessel closure by dissection, acute closure of the stent by oth er mechanisms was recognized as an important complication
Definition of stent thrombosis In order to be able to compare the results of different clinical trials, the Ac ademic Research Consortium defined ST according to various levels of certainty (TABLE 1).[4]
Besides these procedural factors, stenting in acute coro nary artery disease with high levels of thrombin is associated with high risk of ST.[8]
Summary
In the 1980s, the bare‐metal coro nary artery stent (BMS) was introduced, which has dramatically improved the safety and efficacy of percutaneous coronary intervention (PCI).[1,2] permanent scaffolding of the coronary vessel overcame the risk of abrupt vessel closure by dissection, acute closure of the stent by oth er mechanisms was recognized as an important complication. Within 30 days after PCI, procedural factors are most likely responsi ble for ST, such as underexpansion, stent malap position, residual dissection, tissue prolapse, and medial fracture.[6,7] Since the cause of early ST is mostly procedure related, the pathological find ings are similar between various stents Besides these procedural factors, stenting in acute coro nary artery disease with high levels of thrombin is associated with high risk of ST.[8] In the early phase, platelets are exposed to nonendothelial ized stent struts, optimal inhibition of plate let activation is the key factor of preventing early ST.[7] Clopidogrel resistance and discontinuation of dual antiplatelet therapy (DAPT) are essential risk factors of early ST.[9]. The delayed arterial heal ing in DES is likely responsible for the higher rates of late ST in early‐generation DES.[10,11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
