The role of exogenous Fibrinogen in cardiac surgery: stop bleeding or induce cardiovascular disease
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The role of exogenous Fibrinogen in cardiac surgery: stop bleeding or induce cardiovascular disease Fatemeh Javaherforoosh Zadeh1,2 · Mohammadjavad Mohammadtaghizadeh2 · Hojatolah Bahadori1 · Najmaldin Saki3 · Hadi Rezaeeyan3,4 Received: 24 June 2020 / Accepted: 29 September 2020 © Springer Nature B.V. 2020
Abstract The surgical treatment contributes to broad variety of cardiovascular diseases (CVD). Due to many involved factors in preoperative bleeding, it is almost difficult to perform better Haemostatic approach. Fibrinogen is a major blood glycoprotein and a coagulation factor which decreases postoperative bleeding. It has a potential role in platelet activation and bleeding inhibition; it may reflect the inflammatory responses and be related to the endothelial dysfunction. Fibrinogen can act as a pro-inflammatory element via increasing some inflammatory markers including IL-6, tumor necrosis factor-α (TNF-α), monocyte chemo attractant protein (MCP-1), macrophage inflammatory protein-1 (MIP-1a and b), matrix metalloproteinase (MMP-1 and MMP-9) and Toll-like Receptors (TLRs); through activation of these factors, fibrinogen may induce some inflammatory mechanisms such as focal adhesion kinase (FAK), mitogen-activated protein kinases (MAPK) and nuclear factor κB (NF‐κB) pathways. It may cause endothelial dysfunction by increasing P and E-selection, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) levels which activate MAPK and NF-κB pathways. This factor is also associated with increased exocytosed von Willebrand factor (vWF) as well as activation of Rho-GTPase mechanism. All of these data demonstrate the dual role of fibrinogen in cardiac surgeries, bleeding inhibition and CVD. Therefore, identifying the CVD factors is helpful for designing preventive strategies and alternative drugs. Keywords Exogenous · Fibrinogen · Cardiac surgery · Bleeding · Inflammation · Endothelial dysfunction
Introduction * Hadi Rezaeeyan [email protected] Fatemeh Javaherforoosh Zadeh [email protected] Hojatolah Bahadori [email protected] Najmaldin Saki [email protected] 1
Department of Cardiac Anesthesia, Ahvaz Anesthesiology and Pain Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
2
Atherosclerosis Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
3
Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
4
High Institute for Education and Research in Transfusion Medicine, Tehran, Iran
The cardiovascular diseases (CVDs) become a burden globally; it is also the first cause of death worldwide. Currently, CVD comprises approximately half of non-communicable diseases (NCDs) and accounts for 17.3 million deaths each year. This number is assumed to increase to 23.6 million by 2030 [1, 2]. CVD is determined as a group of disorders which the cause is dysfunction of cardiovascular system, etiolog
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