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Updated: Jun 25, 2025
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelet-fibrin clot strength and platelet reactivity predicting cardiovascular events after percutaneous coronary
Osung Kwon1,2, Jong-Hwa Ahn3, Jin-Sin Koh4
1Division of Cardiology, Department of Internal Medicine, Eunpyeong St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Insights
Platelet-fibrin clot strength (PFCS) and high platelet reactivity (HPR) in patients undergoing percutaneous coronary intervention (PCI) have an additive effect on major adverse cardiovascular events (MACE). Combined assessment improves risk stratification for personalized antithrombotic therapy.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Interventional Cardiology
Background:
- Platelet-fibrin clot strength (PFCS) is associated with major adverse cardiovascular event (MACE) risk.
- The prognostic implications of PFCS and platelet reactivity in percutaneous coronary intervention (PCI) patients are not fully understood.
Purpose of the Study:
- To investigate the association between PFCS, platelet reactivity, and clinical outcomes in patients undergoing PCI.
- To determine the prognostic value of combined PFCS and platelet reactivity assessment for MACE and bleeding risk.
Main Methods:
- A registry-based study of 2512 PCI patients in South Korea (2010-2018).
- PFCS measured by thromboelastography and platelet reactivity by VerifyNow.
- Patients stratified into four groups: normal/high PFCS and normal/high platelet reactivity.
Main Results:
- High PFCS and high platelet reactivity (HPR) showed an additive effect on MACE risk (P < .001).
- The HPR-PFCSHigh group had significantly higher MACE incidence (19.3%) compared to normal-normal group (7.5%).
- Normal PFCS phenotype was associated with a higher risk of major bleeding compared to HPR-PFCSNormal phenotype.
Conclusions:
- PFCS and platelet reactivity are crucial predictors of clinical prognosis in PCI patients.
- Combined assessment of PFCS and platelet reactivity enhances risk stratification for personalized antithrombotic strategies.
Background And Aims:
Platelet-fibrin clot strength (PFCS) is linked to major adverse cardiovascular event (MACE) risk. However, the association between PFCS and platelet reactivity and their prognostic implication remains uncertain in patients undergoing percutaneous coronary intervention (PCI).
Methods:
In PCI-treated patients (n = 2512) from registry data from January 2010 to November 2018 in South Korea, PFCS using thromboelastography and platelet reactivity using VerifyNow were measured. High PFCS (PFCSHigh) was defined as thromboelastography maximal amplitude ≥ 68 mm, and high platelet reactivity (HPR) was defined as >208 P2Y12 reaction units. Patients were stratified into four groups according to maximal amplitude and P2Y12 reaction unit levels: (i) normal platelet reactivity (NPR)-PFCSNormal (31.8%), (ii) HPR-PFCSNormal (29.0%), (iii) NPR-PFCSHigh (18.1%), and (iv) HPR-PFCSHigh (21.1%). Major adverse cardiovascular event (all-cause death, myocardial infarction, or stroke) and major bleeding were followed up to 4 years.
Results:
High platelet reactivity and PFCSHigh showed an additive effect for clinical outcomes (log-rank test, P < .001). Individuals with NPR-PFCSNormal, NPR-PFCSHigh, HPR-PFCSNormal, and HPR-PFCSHigh demonstrated MACE incidences of 7.5%, 12.6%, 13.4%, and 19.3%, respectively. The HPR-PFCSHigh group showed significantly higher risks of MACE compared with the NPR-PFCSNormal group [adjusted hazard ratio (HRadj) 1.89; 95% confidence interval (CI) 1.23-2.91; P = .004] and the HPR-PFCSNormal group (HRadj 1.60; 95% CI 1.12-2.27; P = .009). Similar results were observed for all-cause death. Compared with HPR-PFCSNormal phenotype, NPR-PFCSNormal phenotype was associated with a higher risk of major bleeding (HRadj 3.12; 95% CI 1.30-7.69; P = .010).
Conclusions:
In PCI patients, PFCS and platelet reactivity demonstrated important relationships in predicting clinical prognosis. Their combined assessment may enhance post-PCI risk stratification for personalized antithrombotic therapy.
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