Inflammation is a well-known powerful effector of atherosclerosis development. Cell infiltration induces inflammatory signal increasing plaque formation as well as its destabilization, leading to cardiovascular disease including myocardial infarction. During ischemia, necrotic cardiomyocytes stimulate the inflammatory storm into the myocardium (by chemokines, vascular adhesion molecules, interleukins action) promoting cardiac repair but also remodeling. Areas covered: Herein the authors present each condition (atherosclerosis and myocardial infarction) in two separate parts. Pathophysiology is briefly presented and focused on its implication in inflammation. Non-invasive techniques are presented, which explore inflammation in vivo. Several anti-inflammatory drugs are presented (mechanism of action, already published studies and ongoing trials are summarized). Expert commentary: Whereas atherosclerosis, regarding both the step-by-step pathophysiology and the acute plaque destabilization, is widely recognized as involving inflammatory pathways, the current translations in clinical practice remain poor. However, both basic and clinical research are active in the field, and the first large trials should soon be available, corroborating or not whether modulating inflammatory processes could be of interest in clinical practice.
Keywords: Atherosclerosis; anti inflammatory drugs; cardiac imaging; colchicine; cytokines; inflammation; myocardial infarction.