Inflammatory cell content of coronary thrombi is dependent on thrombus age in patients with ST-elevation myocardial infarction.
ST-elevation myocardial infarction (STEMI) is typically caused by an occlusive coronary thrombus. The process of intracoronary thrombus formation is poorly understood. It is known that inflammatory cells play a role in the formation and resolution of venous thrombi, however their role in coronary thrombosis is not clear. We therefore analyzed inflammatory cells in thrombi derived from patients with STEMI in relation to histologically classified thrombus age.



Thrombus aspirates of 113 patients treated with primary percutaneous coronary intervention were prospectively collected and classified (fresh, lytic, or organized) based on hematoxylin and eosin staining. The density of inflammatory cells neutrophils (MPO), monocytes/macrophages (CD68), lymphocytes (CD45), and the platelet area (CD31), were visualized using immunohistochemistry. Patients' history, medication, and laboratory data were registered.



Fresh thrombi (76.1%) were the most abundant as compared to lytic (16.8%) and organized (7.1%) thrombi. Neutrophils were significantly less present in organized (169cells/mm2) compared to fresh (327 cells/mm2) and lytic thrombi (311 cells/mm2). Monocytes/macrophages were significantly more present in lytic (471 cells/mm2) than in fresh (312 cells/mm2) thrombi. We additionally found that thrombi from patients aged <50 years as compared to >50 years old contained significantly more neutrophils and monocytes/macrophages irrespective of thrombus age. Furthermore platelet area was smaller in patients on aspirin again irrespective of thrombus age. No gender differences were found.



The composition of inflammatory cells differs with thrombus age in thrombosuction material of STEMI patients that in part depends on patient age and medication.
Department of Internal Medicine, VU University Medical Center, Amsterdam, the Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, the Netherlands; Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands. Electronic address: w.fuijkschot@vumc.nl.
Wessel W
WW
Fuijkschot
Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands.
Wouter E
WE
Groothuizen
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, the Netherlands; Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands.
Yolande
Y
Appelman
Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands.
Teodora
T
Radonic
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, the Netherlands; Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands.
Niels
N
van Royen
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, the Netherlands; Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands.
Maarten A H
MA
van Leeuwen
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, the Netherlands; Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands.
Paul A J
PA
Krijnen
Department of Pathology, Academic Medical Center, Amsterdam, the Netherlands.
Allard C
AC
van der Wal
Department of Internal Medicine, VU University Medical Center, Amsterdam, the Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, the Netherlands.
Yvo M
YM
Smulders
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, the Netherlands; Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands; Department of Cardiac Surgery, VU University Medical Center, Amsterdam, the Netherlands.
Hans W M
HW
Niessen
D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001792:Blood Platelets / Q000473:pathology; D003328:Coronary Thrombosis / Q000150:complications / Q000473:pathology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D017493:Leukocyte Common Antigens / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D062645:Percutaneous Coronary Intervention; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D011446:Prospective Studies; D000072657:ST Elevation Myocardial Infarction / Q000209:etiology / Q000473:pathology*; D013997:Time Factors; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D018836:Inflammation Mediators; D017493:Leukocyte Common Antigens; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C516769:PTPRC protein, human
Cardiovascular; Immunohistochemistry; Inflammation; Myocardial ischemia; Thrombosis