Platelet-fibrin clot strength and platelet reactivity predicting cardiovascular events after percutaneous coronary interventions

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).

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 (PFCS_High) 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)-PFCS_Normal (31.8%), (ii) HPR-PFCS_Normal (29.0%), (iii) NPR-PFCS_High (18.1%), and (iv) HPR-PFCS_High (21.1%). Major adverse cardiovascular event (all-cause death, myocardial infarction, or stroke) and major bleeding were followed up to 4 years.

High platelet reactivity and PFCS_High showed an additive effect for clinical outcomes (log-rank test, P < .001). Individuals with NPR-PFCS_Normal, NPR-PFCS_High, HPR-PFCS_Normal, and HPR-PFCS_High demonstrated MACE incidences of 7.5%, 12.6%, 13.4%, and 19.3%, respectively. The HPR-PFCS_High group showed significantly higher risks of MACE compared with the NPR-PFCS_Normal group [adjusted hazard ratio (HR_adj) 1.89; 95% confidence interval (CI) 1.23–2.91; P = .004] and the HPR-PFCS_Normal group (HR_adj 1.60; 95% CI 1.12–2.27; P = .009). Similar results were observed for all-cause death. Compared with HPR-PFCS_Normal phenotype, NPR-PFCS_Normal phenotype was associated with a higher risk of major bleeding (HR_adj 3.12; 95% CI 1.30–7.69; P = .010).

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.