Change of paradigm in pathogenesis of non-ST segment elevation myocardial infarction (NSTEMI)

Contact address: Rodica Dan, MD – Department of Cardiology, Institute of Cardiovascular Diseases, 13A Gh. Adam st., 300310 – Timisoara, Romania INTRODUCTION Atherosclerotic vascular disease continue to represent the leading cause of death in Western countries, but not only there, and among the different manifestations or forms of presentation, the acute coronary syndrome (ACS) plays an important role. Patients with ACS present with unstable angina (UA), acute myocardial infarction (AMI) and sudden coronary death (SCD). Most of the ACS are thought to be the result of sudden luminal thrombosis, which occurs from three different pathologies: plaque rupture, plaque erosion and calcifi ed nodules. Plaque rupture is defi ned as a lesion consisting of a necrotic core with an overlying thin ruptured fi brous cap that leads to luminal thrombosis because of contact of platelets with a highly thrombogenic necrotic core. Plaque erosion shows a luminal thrombus with an underlying base rich in proteoglycans and smooth muscle cells with minimal infl ammation. Most erosion lesions are devoid of a necrotic core, but when present, the core does not communicate with the lumen because of a thick fi brous cap. The least common of all lesions is the calcifi ed nodule, that shows an underlying calcifi ed plate with superimposed bony nodules that result in discontinuity of the fi brous cap and is devoid of endothelial cells with overlying luminal thrombus1.