An acute thrombotic event resulting in total occlusion of a coronary artery is considered the principal mechanism of ST-segment elevation myocardial infarction (STEMI). De Wood et al1 were the first to show that total coronary occlusion was visible on the coronary angiogram in a large majority of patients presenting during the early hours of STEMI. Thrombus could be retrieved in 52 of 59 patients with angiographic, and in 5 of 20 patients without, features of thrombus, suggesting that thrombus formation plays a major role in the pathophysiology of total occlusion and subsequent infarction. Total coronary artery occlusion has also been described, though less frequently, in a range of nonthrombotic events such as intraplaque hemorrhage, vasospasm, spontaneous coronary artery dissection, coronary emboli, coronary arteritis, and compression by myocardial bridging.2,3 Article p 1810 Acute coronary thrombosis is caused primarily by the rupture of a coronary atherosclerotic plaque, responsible for approximately 75% of all coronary thrombi leading to myocardial infarction or death,4 or by plaque erosion or calcified nodules. After rupture of the fibrous cap covering the atherosclerotic plaque, fragments of the lipid-rich core are exposed to the arterial lumen. This highly thrombogenic material causes platelet aggregation within the lipid core and on the ruptured fibrous cap, forming a mural thrombus consisting mainly of platelets, resulting in early coronary obstruction.3 In this early stage of thrombus formation, intermittent flow is often present, because the platelet aggregates are unstable and embolize into the microcirculation.4,5 As a consequence of a balance between thrombotic and thrombolytic factors, episodic growth of thrombus may take place that results in layered thrombus material of different ages. As platelet aggregation continues, the formation of a fibrin network causes stabilization of the white platelet-rich thrombus until eventually the whole lumen is occluded. Persistent obstruction of flow …