Key markers and detection methods for evaluating platelet dysfunction in mechanical circulatory support devices.

Mechanical circulatory support devices (MCSDs) have emerged as life-saving interventions for patients with end-stage heart failure. However, the non-physiological shear stress (NPSS) generated by MCSDs is a known precipitant of platelet dysfunction, augmenting risks of thrombotic and bleeding complications. Addressing this issue necessitates innovative approaches to attenuate platelet dysfunction, thereby enhancing the safety of MCSDs. This review synthesizes knowledge pertaining to the normal hemostatic process, the implications of NPSS on platelet function, the array of markers extensively employed to assess platelet dysfunction, and relevant detection assays, within the scope of MCSDs-related hemocompatibility. NPSS can induce platelet activation and receptor shedding, causing both thrombosis and bleeding. The use of fluorescence-activated cell sorting (FACS) to monitor changes in markers, including platelet surface receptors, P-selectin, platelet monocyte aggregation (PMA), platelet-derived microparticles (PDMPs), and phosphatidylserine (PS), Enzyme-Linked Immunosorbent Assay (ELISA) for platelet secretion analysis, and the modified prothrombinase platelet activity state (PAS) for thrombin assessment, are central to investigating these consequences. PS and thrombin, particularly, present unique responses to NPSS, underscoring their potential as targeted markers for platelet dysfunction research. Additionally, assessments of morphological shifts and platelet aggregation, through scanning electron microscopy (SEM) and fluorescence microscopy provide a more visualized evaluation of NPSS-mediated platelet dysfunction. Combining distinct markers and assays is essential to understanding and potentially mitigating NPSS-induced complications in MCSD therapy. Future research should focus on validating NPSS-specific biomarkers, standardizing detection methodologies, and elucidating interactions with MCSD-induced hemolysis and coagulopathy, ultimately improving safety and efficacy.