Immature platelet fraction in cardiology

Abstract

Cardiovascular diseases (CVDs) remain a leading global cause of mortality, necessitating biomarkers that enhance risk stratification and therapeutic personalization. The Immature Platelet Fraction (IPF), representing young, RNA-rich platelets (also known as reticulated platelets, RP) released from bone marrow, has emerged as a dynamic biomarker linking platelet turnover to cardiovascular pathophysiology. Clinically, elevated IPF is associated with adverse outcomes in acute coronary syndromes (ACS), myocardial infarction, and post-cardiac surgery, particularly when measured 24–72 hours after the event or post-operatively. It correlates with infarct size, recurrent thrombosis, and major adverse cardiovascular events (MACE), though its predictive value is inconsistent at the initial clinical encounter. Its rise reflects compensatory thrombopoiesis in hypercoagulable states like diabetes, COVID-19, and malignancy. IPF also informs antiplatelet therapy, high IPF correlates with clopidogrel resistance but not ticagrelor, guiding agent selection and dual antiplatelet therapy (DAPT) duration. Despite standardization challenges across measurement platforms (flow cytometry vs. automated analyzers), IPF outperforms mean platelet volume (MPV) in tracking platelet activity. Future directions include point-of-care IPF devices, multi-marker panels, and novel therapies targeting thrombopoiesis. Integrating IPF into clinical practice promises refined risk assessment, personalized treatment, and improved prognostic precision in cardiology, bridging translational innovation to patient care. This review synthesizes current evidence on IPF’s role in CVDs, highlighting its molecular characteristics, elevated prothrombotic mediators (e.g., thromboxane A₂, P-selectin), heightened reactivity, and rapid response to inflammatory stimuli.