Showing in part features of fresh, of lytic, and organized thrombus. These results support the concept of coronary artery disease as a dynamic process. Disruption of atherosclerotic plaques may act as a stimulus for repeated or ongoing thrombosis, which ultimately progresses over a period of days or even weeks to thrombotic occlusion with a secondary fresh thrombus. Systematic histopathological analyses of the atherothrombotic material obtained with thrombus aspiration during primary PCI in large patient cohorts are limited. Our findings are in line with our previous results that describe histopathological analyses of aspirated atherothrombotic material in a smaller group of 211 STEMI patients in whom we identified older thrombus in approximately 50% of patients. The insights in the mechanisms of UNC0642 coronary thrombosis mainly come from detailed analyses of underlying plaque morphologies in necropsy specimen from sudden death victims. Autopsy studies on the histopathology of the progression of coronary plaques demonstrated the occurrence of clinically silent coronary nonocclusive atherothrombotic events before the occlusive atherothrombotic event. Furthermore, multiple subclinical episodes of plaque disruption, followed by healing, are an important mechanism of atherosclerotic plaque growth. A close relationship has been demonstrated between the number of previous plaque disruptions and the mean percentages stenosis in the coronary artery. Further, Henriques de Gouveia et al. demonstrated that histopathological evidence of plaque instability for some time was present in the majority of sudden coronary death victims. They concluded that plaque disruption with superimposed thrombus formation starts days or even weeks before the time of death. Subclinical episodes of plaque disruption may have the potential to precondition the myocardium. An alternative explanation is that several subclinical plaque disruptions may results in the development of collateral vessels. Therefore, patients with successive thrombotic occlusion after several subclinical plaque disruptions may experience less acute cardiac symptoms compared with patients in whom plaque disruption immediately leads to a superimposed luminal thrombus with total occlusion. This may explain why patients with lytic or organized thrombus had a significantly longer total ischemic time compared with patients with fresh thrombus. Interestingly, distal embolization was significantly different between patients with fresh, lytic or organized thrombus, with the highest percentage in patients with thrombus with α-santonin lytic changes. Thrombus embolization may be less frequent when the thrombus is fresh and fragile or when the thrombus is organized and more solid and attached to the vessel wall. This pathological finding is compatible with the report by Kondo et al, who found an association between the no-reflow phenomenon and a longer ischemic time. These findings suggest the presence of a time window of several days after plaque disruption when distal embolization of thrombus is most likely to occur in association with mechanical reperfusion. Except for the TAPAS study, previous studies with thrombus aspiration have been neutral or negative. In some patients, thrombus aspiration was not possible depending on coronary anatomy, and in 353 patients no material was obtained.