A Pad 4 Plaque Erosion

Abstract

Despite the development of new intervention strategies, acute coronary syndromes (ACS) are among the leading cause of global mortality. ACS is predominantly caused by plaque rupture, which is the consequence of inflammatory processes within the atherosclerotic plaque that contribute to expansion of the necrotic core and thinning of the fibrous cap. However, with current therapeutic strategies targeting traditional risk factors such as plasma LDL-C (low-density lipoprotein cholesterol) levels and hypertension, the relative contribution of plaque erosion to ACS is on the rise. Plaque erosion is characterized by endothelial cell desquamation and small intraluminal thrombi, and now accounts for ≈25% to 30% of all ACS.1 Article, see p 33 Neutrophils are the most abundant white blood cells and form the first line of defense against microbes and bacteria. In addition to their key role in host defense, studies over the past decade have revealed that neutrophils are of major importance to cardiovascular pathologies, including atherosclerosis, neointima formation, and myocardial infarction.2–4 Neutrophils mainly act through their granule proteins which can be released directly or when bound to neutrophil extracellular traps (NETs), a network consisting of neutrophil-derived DNA, and proteins of nuclear, granular, and cytosolic origin. Markers of NETs have been associated with coronary stenosis and plaque erosion in humans5,6 and NET formation (NETosis) has been suggested to promote atherogenesis in mice.7,8 In addition, recent studies have shown that NETs play a key role in regulating processes …