ADP-induced platelet reactivity and bleeding events in patients with acute myocardial infarction complicated by cardiogenic shock

Abstract

While previous reports showed ADP-induced platelet reactivity to be an independent predictor of bleeding after PCI in stable patients, this has never been investigated in patients with cardiogenic shock. The association of bleeding events with respect to ADP-induced platelet aggregation was investigated in patients undergoing primary PCI for acute myocardial infarction complicated by cardiogenic shock and with available on-treatment ADP-induced platelet aggregation measurements. Out of 233 patients, 74 suffered from a severe BARC3 or higher bleed. ADP-induced platelet aggregation was significantly lower in patients with BARC≥3 bleedings (p < .001). Multivariate analysis identified on-treatment ADP-induced platelet aggregation as an independent risk factor for bleeding (HR = 0.968 per AU). An optimal cutoff value of <12 AU for ADP-induced platelet aggregation to predict BARC≥3 bleedings was identified via ROC analysis. Moreover, the use of VA-ECMO (HR 1.972) or coaxial left ventricular pump (HR 2.593), first lactate (HR 1.093 per mmol/l) and thrombocyte count (HR 0.994 per G/l) were independent predictors of BARC≥3 bleedings. In conclusion, lower on-treatment ADP-induced platelet aggregation was independently associated with severe bleeding events in patients with AMI-CS. The value of platelet function testing for bleeding risk prediction and guidance of anti-thrombotic treatment in cardiogenic shock warrants further investigation.

Keywords:

• Platelet reactivity
• cardiogenic shock
• bleeding
• acute myocardial infarction
• VA-ECMO
• Impella

Acknowledgements

None.

Declaration of interest

Mathias Orban and Daniel Braun received speaker honoraria from Abbott Vascular, outside the submitted work. Jörg Hausleiter received speaker honoraria and research support from Abbott Vascular and Edwards Lifesciences, outside the submitted work. Dirk Sibbing reports grants from Roche Diagnostics, grants from Daiichi Sankyo, personal fees from Bayer AG, Daiichi Sankyo, Eli Lilly, Roche Diagnostics, MSD, Pfizer, Astra Zeneca, outside the submitted work. Martin Orban received speaker honoraria from Abbott Medical, AstraZeneca, Abiomed, Bayer vital, BIOTRONIK, Bristol–Myers Squibb, CytoSorbents, Daiichi Sankyo Deutschland, Edwards Lifesciences Services, Sedana Medical, outside the submitted work. The other authors declare no conflict of interests.

Ethical standards

All ethical standards were met in writing and submitting this correspondence.

Author contributions

Clemens Scherer, Dirk Sibbing and Martin Orban designed the study, interpreted data and wrote the manuscript. Enzo Lüsebrink, Danny Kupka, Thomas Stocker, Konstantin Stark, Mathias Orban, Tobias Petzold, Simon Deseive, Jan Kleeberger, Kathrin Krieg, Sara Würbel, Sara Kika, Mario Istrefi, Daniel Braun, Stefan Brunner collected and analyzed data and critically revised the manuscript. Christian Hagl, Jörg Hausleiter and Steffen Massberg interpreted data and critically revised the manuscript.

Supplementary material

Supplemental data for this article can be accessed on the publisher’s website.

Additional information

Funding

There was no funding for this study.