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Published on: April 6, 2017
Thrombopoietin and platelet aggregation in patients with stable coronary artery disease
Sanne Bøjet Larsen1, Erik Lerkevang Grove1,2, Søs Neergaard-Petersen1
1a Department of Cardiology , Aarhus University Hospital , Aarhus , Denmark.
Insights
Thrombopoietin (TPO) did not significantly impact platelet aggregation or activation in patients with stable coronary artery disease (CAD). This study found only weak associations between TPO levels and platelet aggregation in this patient group.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Platelet Biology
Background:
- Thrombopoietin (TPO) is implicated in platelet activation and aggregation.
- Limited data exist on TPO's role in platelet function among patients with stable coronary artery disease (CAD).
Purpose of the Study:
- To investigate the association between serum TPO levels and platelet aggregation and activation in patients with stable CAD.
- To identify factors influencing platelet aggregation and TPO levels in this cohort.
Main Methods:
- Serum TPO levels were measured using ELISA in 900 stable CAD patients.
- Platelet aggregation was assessed via Multiplate Analyzer (arachidonic acid and collagen agonists) and VerifyNow Aspirin Assay.
- Platelet activation (sP-selectin) and cyclooxygenase-1 inhibition (serum TXB2) were also evaluated.
Main Results:
- TPO showed weak correlations with platelet aggregation (Multiplate AA: r = -0.09, p = 0.01; VerifyNow: r = 0.07, p = 0.03) but not with collagen-induced aggregation (r = -0.03, p = 0.43).
- No significant correlation was observed between TPO and sP-selectin (platelet activation).
- Independent predictors of platelet aggregation included sP-selectin, serum TXB2, platelet count, age, BMI, female sex, and smoking. Predictors of TPO included low platelet aggregation, hs-CRP, smoking, and high VerifyNow results.
Conclusions:
- Serum TPO levels demonstrated no substantial association with platelet activation in stable CAD patients.
- Weak correlations between TPO and platelet aggregation suggest TPO plays a limited role in facilitating platelet aggregation in this population.
Abstract:
Thrombopoietin (TPO) may facilitate platelet activation and aggregation. However, data on the impact of TPO on platelet aggregation in patients with stable coronary artery disease (CAD) are scarce. We aimed to investigate associations between TPO and platelet aggregation and activation in patients with stable coronary artery disease (CAD). We studied 900 stable CAD patients. Serum TPO was assessed by ELISA. Platelet aggregation was evaluated using the Multiplate Analyzer (agonists: arachidonic acid [AA] and collagen) and the VerifyNow Aspirin Assay. Platelet activation was evaluated by soluble (s)P-selectin. Cyclooxygenase-1 inhibition was evaluated by serum thromboxane B2 (TXB2). We found that TPO correlated weakly with platelet aggregation evaluated by Multiplate using AA (r = -0.09, p = 0.01) and collagen as agonists (r = -0.03, p = 0.43) and by VerifyNow (r = 0.07, p = 0.03). We found no correlation between TPO and sP-selectin (r = -0.01, p = 0.70). Independent predictors of AA-induced platelet aggregation by Multiplate included high levels of sP-selectin and serum TXB2, high platelet count, increasing age and body mass index, female sex, and active smoking. Independent predictors of TPO included low AA-induced platelet aggregation by Multiplate, high levels of hs-CRP, active smoking, and high platelet aggregation evaluated by VerifyNow. In conclusion, TPO levels did not correlate with platelet activation and only weak associations were found between TPO and platelet aggregation, suggesting that TPO did not substantially facilitate platelet aggregation in stable CAD patients.
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