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Platelet subfractions significantly differ in STEMI patients depending on angiographic findings

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)1, T. Harm (Tübingen)1, M. Droppa (Tübingen)1, K. A. L. Müller (Tübingen)2, X. Fu (Tübingen)1, Z. Xu (Tübingen)1, M. Laemmerhofer (Tübingen)1, T. Geisler (Tübingen)2, 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: Despite major advances in therapy, ST-elevation myocardial infarction (STEMI) remains a threatening disease with high mortality. While there is a standardized treatment, the collective of STEMI patients broadly differs, including the angiographic findings. While some patients evolve STEMI based on pre-existing three-vessel disease, others only show a single lesion. While some vessels are totally occluded others keep minimal residual flow which drastically affects prognosis. Concentration of platelet subtypes, including resting, procoagulant, aggregatory and apoptotic platelets, might affect thrombus composition. The aim of this study was to identify different patterns of platelet subtypes depending on angiographic findings in STEMI patients.

Methods: We examined isolated platelets from 27 STEMI patients after successful percutaneous coronary intervention (PCI). Platelet subpopulations were distinguished based on platelet surface expression of CD42b, phosphatidylserine and GPIIb/IIIa using flow cytometry. We analyzed the coronary angiogram concerning the number of diseased vessels, culprit lesion and TIMI flow prior to intervention.

Results: While there was a higher fraction of procoagulant platelets in patients with initial TIMI 1 flow, patients with initial TIMI 0 showed a higher proportion of apoptotic platelets (Figure 1). In patients with three-vessel-disease, the procoagulant platelet subfraction was up-regulated, whereas patients with one- or two-vessel-disease had an increased proportion of the apoptotic subtype (Figure 2).  Moreover, when we investigated the culprit lesion site, the left circumflex (LCX) showed a different composition compared to the right coronary (RCA) and left anterior descending artery (LAD), since there were fewer resting and apoptotic platelets, but an increased subfraction of procoagulant platelets (Figure 3).

Conclusion: Platelet subfractions significantly differed in patients with STEMI. These subfractions possibly affect thrombus composition and subsequently influence clinical presentation and response to treatment.

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