Relationship between platelet aggregation and stroke risk after percutaneous coronary intervention: a PENDULUM

Yuji Matsumaru1, Takanari Kitazono2, Kazushige Kadota3

  • 1Division of Stroke Prevention and Treatment, Department of Neurosurgery, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. yujimatsumaru@md.tsukuba.ac.jp.

Heart and Vessels
|January 1, 2022
PubMed

Insights

High on-treatment platelet reactivity, measured by P2Y12 reaction units (PRU), is linked to increased ischemic stroke risk after percutaneous coronary intervention (PCI). Monitoring PRU levels post-PCI may help identify patients at higher risk for stroke.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Pharmacology

Background:

  • High on-treatment platelet reactivity (HPR) after percutaneous coronary intervention (PCI) with stenting is a potential risk factor for thrombotic events, including stroke.
  • P2Y12 reaction unit (PRU) is a common assay for assessing platelet reactivity in patients treated with P2Y12 inhibitors.
  • Understanding the relationship between PRU levels and stroke risk post-PCI is crucial for optimizing antiplatelet therapy.

Purpose of the Study:

  • To investigate the association between on-treatment platelet reactivity, quantified by PRU values, and the risk of non-fatal stroke following PCI.
  • To compare the incidence of ischemic and non-ischemic stroke across different categories of PRU levels (high, optimal, low).

Main Methods:

  • A post hoc analysis of the PENDULUM registry involving patients aged ≥20 years who underwent PCI.
  • Patients were stratified into high (HPR, PRU > 208), optimal (OPR, PRU > 85 to ≤ 208), and low (LPR, PRU ≤ 85) on-treatment platelet reactivity groups.
  • Incidences of non-fatal ischemic and non-ischemic stroke were recorded up to 12 months post-PCI, with PRU measured at 12 and 48 hours.

Main Results:

  • A total of 5906 patients had PRU data. The cumulative incidence of non-fatal ischemic stroke was 0.68% and non-ischemic stroke was 0.18%.
  • Patients experiencing a non-fatal ischemic stroke had significantly higher post-PCI PRU values compared to those without stroke (P=0.037).
  • A significant difference in the cumulative incidence of non-fatal stroke at 12 months was observed when stratifying by PRU ≤ 153 versus > 153 at 12-48 hours post-PCI (P=0.044).

Conclusions:

  • Higher on-treatment platelet reactivity, indicated by elevated PRU values 12-48 hours post-PCI, is associated with an increased risk of ischemic stroke.
  • The incidence of non-ischemic stroke was not found to be related to PRU values.
  • These findings suggest that PRU monitoring may aid in identifying patients at higher risk of ischemic stroke after PCI, potentially guiding therapeutic adjustments.

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