Pharmacotherapy During Percutaneous Coronary Interventions

Abstract

Percutaneous arterial catheterization and transluminal dilatation of stenotic vessels were first described by Charles T. Dotter and Melvin P. Judkins in their seminal paper published in 1964 (1). With the advent of contemporary coronary angioplasty and stenting techniques for patients with coronary artery disease (CAD) and acute coronary syndromes (ACS), the procedure has now been termed percutaneous coronary intervention (PCI). While PCI has done much in the modern era to improve patient outcomes in the face of acute myocardial infarction as well as in disabling cardiac angina, its benefits can still be limited by periprocedural complications such as acute vessel closure and stent thrombosis as well as conditions occurring after 30 days post-PCI, such as in-stent restenosis or late stent thrombosis. Additionally, catheter and wire associated thrombus formation can occur during PCI in the absence of adequate anticoagulation. Excess anticoagulation on the other hand carries a risk of major gastrointestinal or intracranial bleeding as well as vascular access bleeding complications. Stent thrombosis is a rare, but serious complication of PCI and usually presents as death or ST-elevation myocardial infarction. Coronary stents are generally made of stainless steel or cobalt chromium alloys rendering them thrombogenic until they are completely covered by endothelial tissue. The timing of complete endothelialization is variable and depends on whether the implanted stent is bare metal or drug-eluting, as well as which type of anti-proliferative drug the stent is coated with. Stent thrombosis can be described based on its timing relative to stent placement and is associated with a number of different risk factors (Table 1). Acute stent thrombosis occurs within 24 hours of PCI and in one pooled analysis, approximately 80 percent of all bare metal stent (BMS) thromboses occurred within this acute period (2). Subacute stent thrombosis occurs up to 30 days after PCI and this time period encompasses the majority of all thrombotic events observed in both BMS and drug-eluting stents (DES) (3). Stent thrombosis after 30 days and up to one year post-PCI is referred to as late stent thrombosis and seems to occur with equal frequency in BMS and DES, particularly in the absence or cessation of dual antiplatelet therapy with aspirin or clopidogrel (4-5). Occurring even less commonly at greater than one year post-PCI, very late stent thrombosis appears to be associated with DES more than BMS and is thought to be related to delayed neo-intimal coverage as well as ongoing vessel inflammation (6). Current ACC/AHA guidelines make a number of recommendations regarding the concurrent use of antiplatelet, antithrombotic, and