Proteomic and Lipidomic Profiling of Coronary Thrombus in Acute Myocardial Infarction

Ischemic heart disease is the leading contributor to the worldwide burden of disease, as assessed on the basis of disability-adjusted life-years.

ST-Elevation Myocardial Infarction (STEMI) is associated with a coronary occlusive thrombosis in 90% of patients, non-ST Elevation Myocardial Infarction (NSTEMI) only in 26% of cases. In this regard, increasing attention is given to the composition of coronary thrombus. In acute STEMI, platelet and fibrin content in the occlusive thrombus is highly dependent on ischemia time, thus one can infer that this may have a substantial impact on the efficacy of drugs or devices used for coronary reperfusion.

Among several circulating cell types - platelets, erythrocytes, monocytes, and neutrophils - as well as plasma molecules, modulating the thrombosis process, platelets constitute the major cellular component of the thrombus and their activation is essential for thrombus formation. Although the role of platelets in thrombosis has been deeply characterized, the molecular mechanisms underlying platelet activation and focal adhesion within human coronary thrombi, the composition, time changes of the occluding thrombus and its interaction with the other cells have not been clearly elucidated, mainly due to the difficult accessibility to the thrombotic material. Thrombus aspiration, although having a controversial role as an adjunctive strategy in primary percutaneous coronary intervention (PCI) for STEMI and NSTEMI, relies on the extraction of occlusive thrombi by an aspiration catheter, advanced in the coronary arterial tree and constitutes a unique opportunity for obtaining coronary thrombi from patients suffering from AMI.

Defining variable molecular pathways responsible for thrombus formation according to time lapse and pathophysiology may pave the way to newer therapeutic strategies.

Hypothesis of the study Coronary thrombus undergoes significant modification according to the pathophysiology of formation (erosion, plaque rupture or metal strut exposure) and time-lapse from symptom onset.