Abstract 13781: Megakaryocytes Participating in Thrombosis Under Inflammatory Stress and Sepsis: Direct Pathological Evidence in Two Cases

Abstract

Introduction: Megakarycytes (MKs) produce platelets (PLTs) which enter the circulation and play its roles in hemostasis and thrombosis. However, direct pathological evidence that MKs participate in thrombosis has not been reported in clinical practice. We describe here direct observations in two cases where MKs were found in thrombosis in coronary artery and in the right atrium under open-heart surgery. Hypothesis: MKs might be mobilized into circulation and directly participate in and magnify thrombosis under sepsis, inflammatory stress and full heparinization. Methods: Case one was a 51-year-old male with ischemic cardiomyopathy, coronary stenoses and severe mitral insufficiency who underwent coronary artery bypass grafting (CABG) and mitral annuloplasty under cardiopulmonary bypass (CPB). A thrombus was pulled out from the right atrium when an atrial cannula was removed under full heparinization. Case two was a 53-year-old male with known mitral endocarditis and acute anterior myocardial infarction. Acute coronary angiogram after admission showed thrombosis in the left anterior descending (LAD) branch. The patient underwent emergency thrombectomy, CABG and mitral valve replacement with CPB. The thrombus was completely removed from the LAD through a small incision. Both thrombi, valve tissue and vegetation were sent for pathological examination with HE and CD41-IHC staining on paraffin sections. Results: Large number of giant polyploidy MKs surrounded by PLTs were seen in different areas in the thrombi of MKs-PLTs-fibrin networks from the right atrium and LAD. The coronary thrombus was consisted of MKs, PLTs and red cells in fibrin networks while the infected vegetation was consisted dominantly of inflammatory cells, bacterial legions and fibrin. Conclusions: MKs may enter both venous and arterial circulation, actively participate in thrombosis under inflammatory stress and sepsis, and be capable of escaping from inhibition of full heparinization.