Introduction
Dual antiplatelet therapy (DAPT), pairing aspirin with a P2Y12 receptor antagonist, is a cornerstone after percutaneous coronary intervention (PCI) with drug-eluting stents. While effective at reducing stent thrombosis and major adverse cardiac events (MACE), patient responses to clopidogrel and aspirin vary. High residual platelet reactivity (HRPR) after clopidogrel treatment correlates with worse outcomes, underscoring the need for regular platelet function monitoring. The VerifyNow P2Y12 assay is a common tool to gauge platelet reactivity, though results can be influenced by blood cell counts and hematologic variables.
To enhance risk prediction, researchers evaluated a composite COP-INH score, which merges P2Y12 reaction unit (PRU) with the percentage of platelet inhibition (%INH). This approach aims to identify ACS patients at higher risk of adverse events after PCI and to support early, individualized therapy adjustments.
Study Overview
The study analyzed 337 ACS patients undergoing PCI at Ji’an Central People’s Hospital (November 2017 to December 2023). After applying exclusion criteria, 226 participants were followed for 12 months. All patients received clopidogrel and aspirin around the procedure, with maintenance therapy thereafter. Twenty-eight days post-PCI, VerifyNow P2Y12 testing measured PRU, BASE, and %INH. The COP-INH score was assigned as follows: 2 points for both high PRU and low %INH, 1 point if only one parameter worsened, and 0 points if neither parameter indicated poor response.
Key Metrics and Outcomes
Poor clopidogrel responsiveness was defined as PRU ≥ 230 or %INH < 40%. The primary outcome was MACE, including cardiovascular death, non-fatal myocardial infarction, and target vessel revascularization, tracked for 12 months. Notably, although PRU ≥ 230 or %INH < 40% were individually associated with risk in preliminary analyses, the COP-INH score emerged as a stronger predictor of MACE on multivariate analysis. Patients with COP-INH score 2 had a notably higher MACE rate (23.08%) compared with those with scores of 1 or 0 (5.88%).
Long-Term Implications
Kaplan–Meier analysis showed significantly different survival curves, with COP-INH score 2 linked to poorer outcomes over the year following PCI. Regression analyses identified diabetes, a history of MI, and COP-INH score = 2 as significant predictors of MACE after adjustment for age and sex. These findings suggest COP-INH captures risk signals that PRU or %INH alone may miss, reflecting a combined view of platelet reactivity and inhibition dynamics over time.
Clinical Significance
This study supports using COP-INH as a practical biomarker to stratify risk after PCI in ACS patients. By integrating PRU with %INH, clinicians can better identify individuals who may benefit from tailored antithrombotic strategies, potentially adjusting therapy intensity or duration to mitigate late adverse events. The results align with the broader shift toward personalized medicine in cardiology, where molecular biomarkers guide therapy beyond one-size-fits-all approaches.
Limitations and Future Directions
Limitations include a single-center design and a modest sample size, which may constrain generalizability. External validation across diverse populations is needed. Future studies should explore whether COP-INH-guided treatment adjustments—such as alternative P2Y12 inhibitors or extended monitoring—improve long-term outcomes in ACS patients post-PCI.
Conclusion
The COP-INH score represents a promising, integrated measure of P2Y12 reactivity and platelet inhibition. By predicting MACE more accurately than PRU or %INH alone, COP-INH can inform personalized antiplatelet strategies after PCI in ACS patients, with the potential to improve prognosis and reduce adverse cardiovascular events.
