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A shift in the platelet lipidome affects platelet differentiation into distinct subfractions in patients with acute pulmonary embolism

https://doi.org/10.1007/s00392-025-02625-4

Jessica Henes (Tübingen)1, M. Friedel (Tübingen)1, R. Stübenrath (Tübingen)1, Z. Laspa (Tübingen)1, V. Dicenta-Baunach (Tübingen)1, A.-K. Rohlfing (Tübingen)2, T. Harm (Tübingen)1, Z. Xu (Tübingen)1, X. Fu (Tübingen)1, M. Droppa (Tübingen)1, K. A. L. Müller (Tübingen)2, T. Geisler (Tübingen)2, M. Laemmerhofer (Tübingen)1, M. Gawaz (Tübingen)2, D. Rath (Tübingen)1

1Universitätsklinikum Tübingen Innere Medizin III, Kardiologie und Angiologie Tübingen, Deutschland; 2Universitätsklinikum Tübingen Innere Medizin III, Kardiologie und Kreislauferkrankungen Tübingen, Deutschland

 

Introduction: Acute pulmonary embolism (PE) is a life-threatening condition with high morbidity and mortality. Severity of PE is significantly driven by right ventricular (RV) failure and thrombus composition possible alters susceptibility towards therapy including anticoagulation and lysis. Following platelet activation, platelets differentiate into different phenotypes, including a procoagulant and an aggregatory phenotype. Differentiation into these phenotypes may be orchestrated by changes in the platelet lipidome. Hence, the purpose of the present study was to investigate platelet subfractions and the platelet lipidome in patients with acute PE and concomitant vs. absent RV distress.

Methods: We examined isolated platelets from 56 patients that were diagnosed with acute PE. PE and RV distress were diagnosed with CT scan and transthoracic echocardiography, respectively. We identified platelet subpopulations based on platelet surface expression of CD42b, phosphatidylserine and GPIIb/IIIa using flow cytometry. Additionally, platelet lipidome was characterized via HPLC-ESI-QTOF-MS/MS. We thus compared patients with signs of RV dysfunction on echocardiography echocardiography or CTPA (n=38) to patients without (n=18).

Results: In patients with RV distress (n=38), we found a higher proportion of aggregatory platelets while in patients without RV dysfunction (n=18), the procoagulant platelet subfraction was up-regulated.  Moreover, we found an up-regulation of distinct lipids, especially cholesteryl esters, in patients with RV dysfunction. Finally, the afore mentioned lipids correlated significantly with percentage of aggregatory platelets in the overall cohort of patients.

Conclusion: Alterations in the platelet lipidome may affect differentiation of platelets into distinct subfractions in PE. These subfractions possibly affect thrombus composition and efficacy of therapy thus influencing RV distress. Consequently, distribution of platelet subfractions may help to individualize antithrombotic therapy and thus improve RV function in PE patients.

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