Thrombus extraction in the contemporary management of ST-segment elevation myocardial infarction

Abstract

ST-segment elevation myocardial infarction (STEMI) is primarily caused by an acute thrombotic event resulting in total occlusion of a coronary artery. The precipitating factor for acute thrombosis is generally the rupture of a coronary atherosclerotic plaque, responsible for approximately 75% of all coronary thrombi leading to myocardial infarction (MI) or death. After rupture of the atherosclerotic plaque, fragments of its lipid-rich core are exposed to the arterial lumen. This highly thrombogenic material induces local platelet aggregation, resulting in an early mural thrombus that partially occludes the artery. In time, the formation of a fibrin network causes consolidation of the thrombus. This can be followed by stabilization of the plaque without clinical sequelae, but additional thrombus formation may progress until eventually the whole lumen can be occluded. If occlusion continues for several hours, the ischaemic myocardium becomes irreversibly damaged. The longer this coronary occlusion persists, the worse the clinical outcomes are.