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Updated: Apr 1, 2026
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Changes in platelet function independent of pharmacotherapy following coronary intervention in non-ST-elevation
Phillip M Freeman1, Konstantinos E Moschonas2, Christine Hinz3
1Cardiff University School of Medicine, Institute of Molecular and Experimental Medicine, UK; Cardiothoracic Directorate, University Hospital of Wales, UK.
Insights
Assessing high on treatment platelet reactivity (HTPR) after percutaneous coronary intervention (PCI) requires careful timing. Platelet function testing reveals significant changes within 24 hours, impacting HTPR prediction.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- High on treatment platelet reactivity (HTPR) is a significant risk factor for morbidity and mortality in acute coronary syndrome (ACS) patients on clopidogrel.
- Current strategies to identify HTPR and guide potent antiplatelet therapy have shown limited success.
- The timing of platelet function testing may influence the accurate prediction of HTPR around coronary intervention.
Purpose of the Study:
- To investigate the impact of testing timing on the ability of bedside platelet function tests to predict HTPR.
- To assess changes in platelet reactivity and markers in high-risk ACS patients undergoing percutaneous coronary intervention (PCI).
Main Methods:
- Platelet function was assessed using multiple electrode aggregometry (MEA) in high-risk ACS patients at 5 days of clopidogrel, pre-PCI, post-PCI, and 24 hours post-PCI.
- Simultaneous analysis included platelet-bound and soluble p-selectin quantification.
- Eicosanoid 12-HETE levels were measured using mass spectrometry.
Main Results:
- 40.5% of patients exhibited HTPR pre-PCI.
- Platelet aggregation significantly decreased from pre-PCI to 24 hours post-PCI (p=0.0002), but not between pre- and post-PCI.
- This decrease in aggregation contrasted with sustained platelet-bound p-selectin, increased soluble p-selectin, and rising 12-HETE concentrations.
Conclusions:
- Significant ex-vivo platelet aggregation changes occur within 24 hours of PCI in high-risk NSTEMI patients.
- Bedside platelet function testing (PFT) results are highly dependent on the timing of assessment post-PCI.
- Accurate assessment of residual platelet activity requires consideration of the critical timing of PFT.
Background:
High on treatment platelet reactivity (HTPR) is common in patients receiving clopidogrel following an acute coronary syndrome (ACS); it's also associated with increased morbidity and mortality. More potent and predictable antiplatelet drugs have addressed this issue at the expense of increased bleeding. Identification of HTPR and the targeted use of more potent antiplatelet drugs has, so far, broadly failed. We investigate this approach in terms of the timing of platelet function testing and how this can impact on the ability of these bedside tests to predict HTPR around the time of coronary intervention.
Methods:
High risk ACS patients treated with 5 days of clopidogrel had platelet function assessed using the multiple electrode aggregometry system (MEA) pre, post and 24 h following percutaneous coronary intervention (PCI). Simultaneous detailed analysis of platelet status was undertaken with quantification of platelet bound and soluble p-selectin and mass spectrometry quantification of the eicosanoid 12-HETE.
Results:
As assessed by MEA 40.5% of patients had HTPR pre-PCI; mean aggregation units (AU) in response to ADP were 499.1 ± 46.3 pre-PCI, 407.6 ± 37.7 post-PCI and 269.1 ± 24.6 AU 24 h post-PCI (pre to post PCI p > 0.05, pre to 24 h post-PCI p = 0.0002). This highly significant drop in platelet reactivity was contrasted with on-going expression of platelet bound p-selectin, increased soluble p-selectin and rising 12-HETE concentrations.
Conclusions:
This study outlines significant changes in ex-vivo platelet aggregation that occur within 24 h of PCI in high risk NSTEMI patients using bedside PFT. Whilst there were no changes in antiplatelet therapy during the study period its clear that timing is crucial when assessing high on treatment residual platelet activity.
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