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Published on: January 28, 2020
Calprotectin and platelet aggregation in patients with stable coronary artery disease
Sanne Bøjet Larsen1, Erik Lerkevang Grove1, Manan Pareek1
1Department of Cardiology, Aarhus University Hospital, DK-8200, Aarhus N, Denmark.
Insights
Inflammation marker calprotectin showed a weak positive correlation with platelet aggregation in coronary artery disease (CAD) patients on aspirin. This study also identified independent predictors of elevated calprotectin levels in these high-risk individuals.
Area of Science:
- Cardiology
- Inflammation research
- Platelet biology
Background:
- Calprotectin, an inflammation-associated protein, is increasingly linked to coronary artery disease (CAD) pathogenesis.
- The specific relationship between calprotectin levels and platelet aggregation in CAD patients remains unexplored.
Purpose of the Study:
- To investigate the association between calprotectin levels and platelet aggregation in stable, high-risk CAD patients on aspirin monotherapy.
- To identify independent clinical and laboratory factors associated with calprotectin levels in this patient cohort.
Main Methods:
- A cross-sectional study of 581 stable, high-risk CAD patients on daily aspirin (75 mg).
- Platelet aggregation assessed using impedance aggregometry (Multiplate Analyzer) with arachidonic acid and collagen, and the VerifyNow Aspirin Assay.
- Inflammation markers (calprotectin, hs-CRP, IL-6), platelet activation (soluble P-selectin), and COX-1 inhibition (serum thromboxane B2) were measured.
Main Results:
- Calprotectin levels positively correlated with platelet aggregation (r=0.12, p=0.01) and activation markers.
- Calprotectin also showed positive associations with leukocytes, hs-CRP, IL-6, and serum thromboxane B2.
- Type 2 diabetes mellitus was an independent predictor of higher calprotectin levels; BMI and smoking showed trends.
Conclusions:
- Calprotectin levels are weakly but positively associated with platelet aggregation and activation in high-risk CAD patients treated with aspirin.
- These findings suggest a potential role for calprotectin in modulating platelet function in the context of CAD and inflammation.
Background:
Recent studies suggest that the inflammation-associated protein calprotectin may be implicated in the pathogenesis of coronary artery disease (CAD). However, the impact of calprotectin levels on platelet aggregation in CAD patients has never been investigated.
Objectives:
We investigated the association between calprotectin levels and platelet aggregation in stable, high-risk CAD patients receiving aspirin as mono antiplatelet therapy. Furthermore, we aimed to investigate independent clinical and laboratory determinants of calprotectin levels.
Methods:
We performed a cross-sectional study including 581 stable, high-risk CAD patients. All patients received 75 mg aspirin daily as mono antiplatelet therapy. Platelet aggregation was assessed by 1) impedance aggregometry (Multiplate Analyzer) using arachidonic acid (AA) and collagen as agonists and by 2) the VerifyNow Aspirin Assay. Low-grade inflammation was evaluated by calprotectin, high-sensitive C-reactive-protein (hs-CRP) and interleukin-6. Platelet activation was assessed by soluble P-selectin, and cyclooxygenase-1 inhibition was evaluated by serum thromboxane B2, both measured by ELISA.
Results:
Calprotectin levels correlated positively with platelet aggregation according to Multiplate Analyzer (r=0.12, p=0.01). Additionally, calprotectin was positively associated with leukocytes (r=0.33, p<0.0001), hs-CRP (r=0.31, p<0.0001), interleukin-6 (r=0.28, p<0.0001), soluble P-selectin (r=0.10, p=0.02) and serum thromboxane B2 (r=0.10, p=0.02). Type 2 diabetes mellitus was an independent predictor of increased calprotectin levels (p=0.004), and trends were seen for body mass index (p=0.06) and smoking (p=0.07). Compliance with aspirin was confirmed by low serum thromboxane B2 levels in all patients (median [25%;75%]: 1.07 [0.52;1.87] ng/mL).
Conclusion:
Calprotectin levels correlated positively, though weakly, with platelet aggregation and activation as well as serum thromboxane B2 in high-risk, stable CAD patients treated with aspirin.
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