Abstract

The double-stranded DNA (dsDNA) which is scaffold of neutrophil extracellular traps (NETs) has been reported to be associated with the occurrence of major adverse cardiovascular events (MACEs) in patients with coronary atherosclerosis. However, the relationship between the dsDNA and the occurrence of MACEs in patients with ST-segment elevated myocardial infarction (STEMI) remains unclear. In this study, 142 consecutive STEMI patients were admitted to medical institutions. Blood from the infarct-related coronary artery (ICA) and peripheral artery (PA) were obtained during percutaneous coronary intervention. Clinical follow-up was performed to analyze the occurrence of MACEs. Patients were divided into low ds-DNA group and high dsDNA group according to the cut-off value of ICA dsDNA. Mean follow-up time was 24.52 months in low dsDNA group and 25.71 months in high dsDNA group. dsDNA in the ICA was significantly higher than in the PA (p = 0.038) and Spearman's correlation analysis showed that they were positively correlated (r = 0.758; p < 0.01). ICA dsDNA correlated negatively with ST-segment resolution (r = −0.227; p = 0.007). The long-term MACEs rate was higher in high dsDNA group than low dsDNA group (23.7 vs. 6.7%, p = 0.015). The ICA dsDNA (OR 7.43 95% CI 1.25 to 4.07, p = 0.027), Killip class (OR 5.01 95% CI 1.11 to 4.37, p = 0.025), BMI (OR 1.36 95% CI 1.06 to 1.7, p = 0.016) and white blood cell count (OR 1.27 95% CI 1.03 to 1.57, p = 0.024) were independent predictors of the occurrence of MACEs.

Highlights

  • Acute ST segment elevation myocardial infarction (STEMI) is the leading cause of death in patients with coronary heart disease[1]

  • The principal findings of this observational prospective clinical study are as follows: a) double-stranded DNA (dsDNA) is significantly increased in infarct-related coronary artery (ICA) compared to peripheral artery (PA); b) patients with a higher dsDNA level shows an increased long-term adverse cardiac event rate; c) Higher ICA dsDNA level is a predictor of long-term clinical outcomes in patients with segment elevated myocardial infarction (STEMI) undergoing PCI

  • In the past decades years, inflammatory response had been found to be associated with the increased risk of atherosclerosis and that could turn into acute myocardial infarction, neutrophils played a key role in this process[6]

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Summary

Introduction

Acute ST segment elevation myocardial infarction (STEMI) is the leading cause of death in patients with coronary heart disease[1]. Increasing evidences demonstrated that neutrophil extracellular traps (NETs), which contain chromatin, histones and neutrophil granular, offered a novel role in atherothrombosis[2]. Neutrophils released NETs as signals to promote thrombosis during atherothrombosis[3]. The circulating double-DNA which is scaffold of NETs has been reported to be an independent predictor of occurrence of adverse cardiac event and associated with prothrombotic state in coronary atherosclerosis patients[3]. It has been shown that coronary NETs burden and deoxyribonuclease activity are independently associated with myocardial infarct size and ST-segment resolution[4]. We compared the double-stranded DNA (dsDNA) in infarct-related coronary artery (ICA) and peripheral artery (PA) in STEMI patients undergoing primary percutaneous coronary intervention (pPCI) and looked for a threshold of ICA dsDNA predicting occurrence of MACEs

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