Abstract 5864: Differential Proteomic Profiling of Coronary Stent Thrombosis versus Atherothrombosis
Purpose: Coronary stent implantation is reducing the risk of major adverse cardiac events. However, the occurrence of stent thrombosis (ST) remains a severe complication that results in abrupt coronary artery closure and acute myocardial infarction (AMI). The underlying molecular and cellular mechanisms of ST are not fully understood.
Methods: We compared thrombus aspirated from the site of plaque rupture of 34 patients with ST and 39 patients with AMI due to atherosclerotic occlusion within a native coronary artery (time from first medical contact to balloon inflation 89±12 versus 81±16 minutes) by proteomic profiling.
Results: While leukocytes were low at the culprit site in ST (−0.48±2.45 G/L), they accumulated at the site of atherosclerotic plaque rupture (1.71±4.41 G/L, p=0.019). In contrast to native thrombus, stent thrombus was characterized by high levels of von Willebrand factor, and platelet specific proteins e.g., Platelet glycoprotein I beta and Platelet glycoprotein IX and Platelet factor IV. Local complement activation was not detected in ST, with low levels of C-reactive protein, serum amyloid P, cell adhesion molecules, and low levels of other mediators of inflammation.
Conclusion: Our results demonstrate different proteomic patterns in stent thrombus compared with native coronary artery thrombus, displaying proteins involved in platelet aggregation rather than inflammation.