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Plasma calprotectin was associated with platelet activation and no-reflow phenomenon in acute coronary syndrome
Nian-Peng Song1,2, Xiao-Wen Zhen3, Liu-Dong Li2
1Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Insights
Plasma calprotectin shows promise as an early predictive biomarker for no-reflow during percutaneous coronary interventions in acute coronary syndrome patients. Higher calprotectin levels correlate with platelet activation and increased no-reflow prevalence.
Area of Science:
- Cardiology
- Biomarker Discovery
- Interventional Cardiology
Background:
- No-reflow phenomenon complicates 3-4% of percutaneous coronary interventions (PCIs), negatively impacting acute coronary syndrome (ACS) outcomes.
- Identifying early predictive biomarkers for no-reflow is clinically significant.
- Calprotectin, a known biomarker for plaque instability and cardiovascular diseases, has an unclear association with platelet activation and no-reflow in ACS.
Purpose of the Study:
- To investigate the association between plasma calprotectin levels and platelet activation.
- To evaluate plasma calprotectin as a predictive biomarker for the no-reflow phenomenon in patients with ACS undergoing PCI.
Main Methods:
- Prospective study of 176 Chinese ACS patients undergoing PCI (2017-2018).
- No-reflow defined as Thrombolysis In Myocardial Infarction (TIMI) grade < 3.
- Measured plasma calprotectin and platelet-monocyte aggregates (PMA) upon admission.
Main Results:
- No-reflow occurred in 12.5% of patients (22/176).
- Higher plasma calprotectin correlated with increased PMA and no-reflow prevalence (p < 0.001).
- Plasma calprotectin independently predicted no-reflow (AUC 0.898, cut-off 4748.77 ng/mL, sensitivity 0.95, specificity 0.77).
Conclusions:
- Plasma calprotectin is associated with platelet activation in ACS patients.
- Plasma calprotectin may serve as an early predictive biomarker for no-reflow post-PCI in ACS.
Background:
No-reflow occurs in 3-4% of all percutaneous coronary interventions (PCIs) and has a strong negative impact on clinical outcomes of acute coronary syndrome (ACS). Therefore, the discovery of a biomarker that can early predict the occurrence of no-reflow has great clinical significance. Multiple factors including platelet activation are relevant to no-reflow. Calprotectin is found to be a biomarker of plaque instability and is identified to be a novel diagnostic and prognostic biomarker of cardiovascular diseases. The association of plasma calprotectin with platelet activation and no-reflow phenomenon in ACS is not clear.
Methods:
In this prospective study performed at Yantai Yuhuangding Hospital from 2017 to 2018, a total of 176 Chinese patients with ACS who had undergone PCIs were recruited consecutively, aged from 30 to 88 years. Angiographic no-reflow was defined as thrombolysis in myocardial infarction grade less than 3. Blood samples were collected immediately at admission for the detection of plasma calprotectin and platelet-monocyte aggregates formation. Statistical analysis was performed for the variable's comparisons between groups and the prediction value of plasma calprotectin for no-reflow.
Results:
The mean age of the 176 included ACS patients were 64(±11) years and acute ST-segment elevation myocardial infarction (STEMI) was present in 41.5% of patients. Twenty-two patients had no-reflow during the PCI procedures and the prevalence was 12.5%. Patients with higher plasma calprotectin had a higher level of platelet-monocyte aggregates (PMA) and a higher prevalence of no-reflow (p < 0.001). The multivariate regression showed that plasma calprotectin and admission hs-cTnI were independently associated with PMA, while plasma calprotectin and serum LDL-c were independent predictors of no-reflow (p < 0.001 and p = 0.017). AUC of calprotectin for predicting no-reflow were 0.898. The cut-off value of plasma calprotectin for no-reflow was 4748.77 ng/mL with a sensitivity of 0.95 and a specificity of 0.77.
Conclusion:
Plasma calprotectin was associated with platelet activation and may act as an early predictive biomarker of no-reflow in patients with acute coronary syndrome.
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