Fibrin monomer (FM) is a transient intermediate of blood coagulation that functions as both an active regulator of haemostasis and a sensitive biomarker for prothrombotic states. Clinically, FM is measured indirectly as its derivative, soluble fibrin monomer complexes (SFMC), which is also often referred to as FM throughout the clinical literature. FM participates in a complex regulatory network modulating thrombin generation and fibrinolysis, interacting with platelet receptors, including integrin αIIbβ3 and GPVI, and engaging GPIb-vWF interactions. This comprehensive review examines FM’s molecular mechanisms in haemostatic regulation and evaluates clinical evidence for FM as a biomarker. Particular focus is placed on FM’s utility for risk stratification across thrombotic conditions, including disseminated intravascular coagulation, venous thromboembolism, ischemic stroke, myocardial infarction, and COVID-19-associated coagulopathy. Current challenges, including assay standardization and universal cut-off values, are discussed. By synthesizing mechanistic insights with clinical data, this integrated perspective may accelerate the translation of FM biology into improved risk assessment tools and novel therapeutic strategies.

In this study, we investigated von Willebrand factor (VWF)-related parameters in 30 patients with stable coronary artery disease (CAD) and 50 patients without CAD. In both groups, the following were measured: the VWF antigen level (VWF:Ag); the VWF ristocetin cofactor activity (VWF:RCo); the VWF collagen-binding activity (VWF:CB); and VWF-mediated platelet adhesion. Platelet adhesion was measured in whole blood at a shear rate of 1300 s⁻¹ using a microfluidic chamber with a collagen-coated surface. VWF:Ag and VWF:RCo were found to be the same in both groups of patients. However, VWF:CB was found to be lower in patients with CAD compared with patients without CAD, with values of 106.7% (82.1; 131.6) and 160.4% (112.5; 218.1), respectively (p < 0.001). The decrease in platelet adhesion after GPIb inhibition was more pronounced in patients with CAD compared with patients of the control group, with recorded values of 76.0% (60.6; 82.1) and 29.3% (0.0; 60.4), respectively (p < 0.001). After adjusting for traditional risk factors, the odds ratio for CAD was found to be 0.98 (95% CI, 0.97–0.99; p = 0.011) per 1% increase in VWF:CB activity, and 1.06 (95% CI, 1.03–1.09; p < 0.001) per 1% decrease in GPIb-mediated platelet adhesion. The findings presented in this paper indicate a possible critical role played by complex VWF–collagen-platelet interactions in the development of CAD.

This review discusses current issues of fibrin monomer as a marker for diagnosing cardiovascular diseases. The authors analyzed available literature data on the feasibility of fibrin monomer for assessing the risks of thrombotic complications, their severity and pre-thrombotic conditions. In the context of various cardiovascular diseases, fibrin monomer concentration allows identifying early stages of DIC syndrome and assessing its severity, differentiating the type of strokes (embolic or not), assessing the risks of postoperative deep vein thrombosis and thromboembolic complications. The shortcomings of current methods for analysis of fibrin monomer (insufficient standardization and no universal threshold values) are also considered. The authors analyze the prospects for further development of more advanced methods for analysis of fibrin monomer concentrations and their subsequent introduction into clinical practice.