Myocardial Infarction-From Atherosclerosis to Thrombosis.

Myocardial infarction (MI) is a leading cause of death and disability in the developed world and a major socioeconomic burden.' It is typically the culmination of a long and complex process where the formation of an occlusive thrombus within a coronary artery leads to cardiac ischemia and infarction. Atherosclerosis-the primary underlying disease process-begins in early adulthood and is driven by lipid accumulation in the arterial wall, inflammation, and vascular injury. As it progresses, some plaques evolve to take on a more unstable phenotype with greater degrees of inflammation. Eventually, plaque rupture can occur, and contact of blood with the exposed subendothelial matrix and plaque content causes the formation of occlusive thrombi. This cascade of events leads to the clinical manifestation of MI with angina pectoris, myocyte death, and ultimately, impaired cardiac function. Other coronary artery pathologies such as plaque erosion or spontaneous coronary artery dissection can also cause MI, although their frequency compared with plaque rupture is unclear and controversial, mainly based on a surprisingly low number of autopsy studies available. Preventing and treating MI faces several challenges, and there is the need for thorough research and hopefully breakthroughs in several areas. This includes research on the mechanisms driving plaque instability and causing MI, identification of the patient at risk of MI, identification of plaques that are vulnerable, developing approaches for plaque stabilization, and finally if MI occurs, the treatment/prevention of thrombotic occlusions, as well as preventing ischemia/reperfusion (I/R) injury. This highlight article shines light on recent high-quality articles published in Arteriosclerosis, Thrombosis, and Vascular Biology and illustrates the groundbreaking work taking place in these areas of research and the promise it holds for patients in preventing or treating MI.