Purpose of review
Thrombus formation, usually on a ruptured atherosclerotic plaque, is pivotal in the pathogenesis of ST segment elevation myocardial infarction (STEMI). This thrombus formation provides the milieu for re-occlusion of the infarct-related artery, the main location of re-infarction post-STEMI. Although rates of re-infarction are lower after reperfusion by primary percutaneous coronary intervention (PCI) than after fibrinolytic therapy, re-infarction remains a major cause of morbidity and mortality.
The predominant cause of re-infarction after primary PCI is stent thrombosis. Two recent trials [A Prospective, Randomized Trial of Ambulance Initiation of Bivalirudin vs. Heparin ± Glycoprotein IIb/IIIa Inhibitors in Patients with STEMI Undergoing Primary PCI (EUROMAX) and Unfractionated heparin versus bivalirudin in primary percutaneous coronary intervention (HEAT-PPCI)] have each reported higher rates of stent thrombosis in the first 24 h after primary PCI in patients assigned to receive bivalirudin, which affects the balance of risks and benefit of bivalirudin post-STEMI. Also, in a subanalysis of the Platelet Inhibition And Patient Outcomes trial, ticagrelor reduces re-infarction compared with clopidogrel in patients with STEMI after primary PCI. Other nonpharmacological or mechanical interventions during primary PCI, with the exception of newer-generation drug-eluting stents in the Swedish Coronary Angiography and Angioplasty Registry, have not affected rates of re-infarction.
Re-infarction remains a major cause of morbidity and mortality. Re-infarction rates are altered by pharmacological strategy and stent selection in primary PCI. The design of future trials to detect possible treatment differences in relatively low event rates will provide challenges, and may require more novel strategies such as administrative data collection for patient characteristics and key outcomes.