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Updated: May 20, 2026
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelet activation and microvascular injury in patients with ST-segment elevation myocardial infarction
Jarosław Zalewski1, Monika Durak, Piotr Lech
1Centre for Interventional Treatment of Cardiovascular Diseases, The John Paul II Hospital, Kraków, Poland. jzalewski@szpitaljp2.krakow.pl
Insights
Even with dual antiplatelet therapy, excessive platelet activation in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI) is linked to increased microvascular damage.
Area of Science:
- Cardiology
- Interventional Cardiology
- Hematology
Background:
- Dual antiplatelet therapy (DAPT) is standard for reducing thrombotic events post-primary percutaneous coronary intervention (PCI).
- Microvascular damage is a significant complication following ST-segment elevation myocardial infarction (STEMI).
Purpose of the Study:
- To investigate if platelet function inhibition can mitigate microvascular damage in STEMI patients.
- To explore the relationship between platelet activation markers and microvascular impairment after primary PCI.
Main Methods:
- Studied 83 STEMI patients receiving primary PCI.
- Assessed platelet aggregation, platelet-neutrophil aggregates (PNA), and platelet-monocyte aggregates (PMA) via aggregometry and flow cytometry.
- Utilized contrast-enhanced MRI to quantify microvascular obstruction and perfusion defects.
Main Results:
- Microvascular obstruction was observed in 75.9% of patients.
- Higher levels of PMA and PNA on admission correlated with perfusion defects.
- Platelet aggregation and aggregate levels (PMA, PNA) were significantly associated with the extent of microvascular obstruction.
Conclusions:
- STEMI patients can exhibit excessive platelet activation despite DAPT during the reperfusion phase.
- This heightened platelet activation is associated with more severe microvascular impairment.
Background:
Dual antiplatelet therapy reduces the risk of thrombotic complications after primary percutaneous coronary intervention (PCI).
Aim:
To assess whether inhibition of platelet function attenuates microvascular damage in patients with ST-segment elevation myocardial infarction (STEMI).
Methods:
We studied 83 STEMI patients treated with primary PCI. Platelet aggregation was measured on admission (ADM) and 4 days later (D4) by light transmission aggregometry after stimulation with 0.5 mM of arachidonic acid and after stimulation with 5 and 20 μM of adenosine diphosphate (ADP) on treatment with dual antiplatelet therapy with aspirin and clopidogrel. Platelet-neutrophil aggregate (PNA) and platelet-monocyte aggregate (PMA) were analysed by flow cytometry. Contrast-enhanced magnetic resonance imaging was performed 2-4 days after STEMI to detect the area of perfusion defect at rest and to determine the size of microvascular obstruction. Microvascular obstruction was expressed as a percentage of infarct area.
Results:
Perfusion defect at rest was found in 56 (67.5%) patients whereas microvascular obstruction in 63 (75.9%) patients. Patients with perfusion defect at rest had on admission a significantly higher level of both PMA (7.0 vs. 4.5%, p = 0.004) and PNA (4.1 vs. 2.2%, p = 0.016), however there were no significant differences at D4. Platelet aggregation after stimulation with 5 μM of ADP on ADM was correlated (r = 0.37, p = 0.004) with microvascular obstruction area. Moreover, the higher the concentration of PMA(ADM) (r = 0.31, p = 0.016), PNA(ADM) (r = 0.34, p = 0.006) and PM(AD4) (r = 0.35, p = 0.005) the larger the size of microvascular obstruction. Infarct size (β = 0.43, 95% CI 0.19 to 0.67, p 〈 0.0001), TIMI < 3 after PCI (β = -0.27, 95% CI -1.90 to -0.11, p = 0.015) and PMA(D4) (β = 0.21, 95% CI 0.13 to 1.86, p = 0.032) independently influenced the size of microvascular obstruction (R2 = 0.60, p 〈 0.0001).
Conclusions:
Excessive platelet activation during reperfusion in STEMI patients despite dual antiplatelet therapy is associated with greater microvascular impairment.
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