Related Experiment Video
Updated: Jul 3, 2025

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Low on-clopidogrel ADP- and TRAP-6-induced platelet aggregation in patients with atrial fibrillation undergoing
Diona Gjermeni1, Viktoria Anfang1, Hannah Vetter1
1Department of Cardiology and Angiology, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Insights
High on-clopidogrel platelet reactivity (HPR) is rare in atrial fibrillation (AF) patients undergoing PCI. Low platelet reactivity was common, and ADP-induced aggregation may help identify bleeding risk in this population.
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis
Background:
- High on-clopidogrel platelet reactivity (HPR) is linked to ischemic events post-percutaneous coronary intervention (PCI).
- Atrial fibrillation (AF) patients undergoing PCI often require oral anticoagulation (OAC), complicating antiplatelet therapy management.
- Assessing platelet reactivity in AF patients on OAC post-PCI is crucial for managing ischemic and bleeding risks.
Purpose of the Study:
- To investigate the association between HPR, assessed by multiple electrode aggregometry (MEA), and ischemic, thromboembolic, and bleeding risks in AF patients post-PCI.
- To determine the prevalence of HPR and low platelet reactivity (LPR) in this specific patient cohort.
- To evaluate the utility of ADP-induced aggregation in predicting clinical outcomes.
Main Methods:
- Prospective cohort study including 159 AF patients 1-3 days after PCI.
- Platelet aggregation analyzed using MEA, defining HPR as ADP-induced aggregation ≥ 46 U and LPR as ≤ 18 U.
- Primary outcome: composite of all-cause death, myocardial infarction, or stroke at 6 months. Secondary outcome: bleeding events.
Main Results:
- The majority of patients (93%) exhibited low overall platelet aggregability, with only 1% showing HPR and 79% demonstrating LPR.
- ADP-induced aggregation did not significantly correlate with the primary ischemic outcome (p=0.309).
- ADP-induced aggregation showed an inverse correlation with bleeding risk (r=-0.201, p=0.011), suggesting a potential role in bleeding risk assessment.
Conclusions:
- HPR is uncommon in AF patients undergoing PCI, and overall platelet aggregability is typically low.
- Current conventional cut-off values for HPR may not be appropriate for AF patients on OAC post-PCI.
- ADP-induced aggregation levels may serve as a valuable tool for identifying patients at higher risk of bleeding.
Abstract:
High on-clopidogrel platelet reactivity (HPR) associates with ischemic risk in patients after percutaneous intervention (PCI). This study aimed to evaluate the association of HPR as assessed by multiple electrode aggregometry (MEA) with ischemic, thromboembolic, and bleeding risk in patients with atrial fibrillation (AF) undergoing PCI. Patients with AF and an indication for oral anticoagulation (OAC) were included in this prospective cohort study on day 1-3 after PCI. Platelet aggregation [U] was analyzed by MEA. HPR and low platelet reactivity (LPR) were defined as ADP-induced aggregation ≥ 46 U and ≤ 18 U, respectively. TRAP-6-induced aggregation reference was 94-156 U. The primary outcome was time to all-cause death, myocardial infarction, or stroke at 6 months. The secondary outcome was time to non-major clinically relevant bleedings or major bleedings. 159 patients were enrolled between May 2020 and May 2021. The median age was 78 years (interquartile range 72-82) and 111 (70%) were male. Median ADP- and TRAP-induced aggregation were 12 (6-17) and 49 (35-68) U, respectively. 147 (93%) patients had a low overall aggregability. HPR was detected in 2 patients (1%) and 125 (79%) had LPR. ADP-induced aggregation did not significantly associate with the primary outcome (r = 0.081, p = 0.309) but correlated inversely with bleeding risk (r = - 0.201, p = 0.011). HPR status as assessed by MEA among patients with AF after PCI was rare and overall aggregability was low. Conventional cut-off values for HPR might be inappropriate for these patients. ADP-induced aggregation might be helpful to identify patients at risk for bleeding.
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Clot Retraction and Fibrinolysis
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

