Acute coronary syndromes are caused by plaque rupture and thrombus formation. Inflammation and oxidative stress play a pivotal role in atherosclerosis progression and plaque instability. Recruited inflammatory cells produce several cytokines, chemokines and adhesion molecules stimulating the biosynthesis of further pro-inflammatory factors. Mediators of inflammation are able to trigger several pathophysiological processes involved in plaque vulnerability such as neoangiogenesis, MMPs activity, extracellular matrix degradation, ROS production, lipid peroxidation and others. Several studies investigated the role of markers of inflammation and oxidative stress in the pathophysiology of plaque formation and progression, basis of clinical epiphenomena.
Author(s): Piergiusto Vitulli, MD, Gaetano Tanzilli, MD2, Antonino GM Marullo, MD, PhD, Mariangela Peruzzi, MD, and Giuseppe Biondi Zoccai, MD