A n 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 al 1 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 1810Acute 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 at the site of plaque rupture results in blood coagulation proximally and distally to the occlusion and causes red thrombus formation, consisting mainly of erythrocytes and inflammatory cells entrapped by a fibrin network. 2 Recently, adjunctive mechanical devices have been developed to retrieve thrombus from the infarct-related lesion during primary percutaneous coronary intervention (PCI) in patients with STEMI. 6 -9 Favorable results have been reported with distal protection devices including distal occlusion devices and distal embolic filters, as well as with anterograde approaches with manual thrombus aspiration catheters or technically more complex mechanical thrombectomy catheters. Currently, the inexpensive and user-friendly manual thrombus aspiration devices seem to hold most promise. 6 With these devices, thrombotic material can be obtained in 73 to 89% of patients. 8,9 Several studies have reported that thrombus aspiration improves myocardial perfusion and reduces microvascular obstruction in patie...