Antiplatelet Therapy, Pretreatment, and Primary PCI

ST-segment elevation myocardial infarction (STEMI) is generally caused by atherosclerotic plaque rupture or erosion triggering thrombin activation and platelet-rich thrombus formation. The dissolution of this platelet-r ich thrombus is an achievable goal if treated immediately with potent antiplatelet therapy: over time, the untreated plat elet-rich thrombus transforms into a stabilized clot composed of a dense network of thick fibrin fibers insensitive to both antithrombotic and fibrinolytic therapy.1 Despite the progress of STEMI networks worldwide, shortening ischemic time rema ins an unmet challenge even in countries with a well-organized emergency health care system, as shown in the latest publication from the Get With The Guidelines U.S. registry: eg, STEMI patients requiring transfer from a nonpercutaneous coronary intervention (PCI) capable center to a PCI center continue to have markedly prolonged ischemic times (median delay ranging from 195-240 minutes) with great potential for thrombus stabilization and risk of stent thrombosis and recurrent myocardial infarction, but upstream use may be of limited value