Abstract

BackgroundRecent studies have indicated that monocyte chemoattractant protein-1 (MCP-1) plays an important role in the initiation and progression of ischaemic heart disease. However, no previous research has investigated the correlation between serum MCP-1 levels and early changes in myocardial function in patients with ST-segmental elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI).MethodsA total of 87 STEMI patients who had undergone a successful primary PCI were consecutively recruited. All the patients included in this study were grouped into two subgroups according to the median value of MCP-1 upon admission. An early change in left ventricular ejection fraction (LVEF) was defined as (LVEF at 3 months post-STEMI)-(LVEF at 2 days post-STEMI).ResultsSerum MCP-1 levels increased gradually over time during the first 72 h after the onset of STEMI. The concentration of hypersensitive cardiac troponin I (hs-cTnI) upon admission as well as at 24 h and 72 h after primary PCI, especially the peak hs-cTnI concentration, declined significantly in the low admission MCP-1 group. As continuous variable, admission MCP-1 also correlated positively with admission hs-cTnI, hs-cTnI at 24 h after primary PCI, and peak hs-cTnI. Additionally, the absolute early change in LVEF improved markedly in the low admission MCP-1 group (3.77% ± 6.05% vs − 0.18% ± 7.69%, p = 0.009) compared to that in the high admission MCP-1 group. Most importantly, the global LVEF in the low admission MCP-1 group also improved significantly at 3 months compared to baseline LVEF (55.79% ± 7.05% vs 59.60% ± 6.51%, p = 0.011), while an improvement in global LVEF was not observed in the high admission MCP-1 group. Furthermore, as a continuous variable, the MCP-1 level up admission also correlated negatively with early changes in LVEF (r = − 0.391, p = 0.001). After assessment by multiple linear regression analysis, the MCP-1 level upon admission remained correlated with early changes in LVEF [beta = − 0.089, 95% CI (− 0.163 to − 0.015), p = 0.020].ConclusionMCP-1 upon admission not only correlated positively with hs-cTnI at different time points and peak hs-cTnI, but also associated inversely with early improvements in myocardial function in patients with first STEMI. So we speculated that suppression the expression of MCP-1 via various ways may be a promising therapeutic target in myocardial I/R injury in the future.

Highlights

  • Recent studies have indicated that monocyte chemoattractant protein-1 (MCP-1) plays an important role in the initiation and progression of ischaemic heart disease

  • The inflammatory response is more complicated in regard to ST-element elevation myocardial infarction (STEMI), which involves the coordinated activation of a series of inflammatory cytokines and has a profound influence on myocardial ischaemia/reperfusion (I/R) injury, leading to subsequent negative remodelling [3, 4]

  • We found that the MCP-1 level upon admission had a positive correlation with the hypersensitive cardiac troponin I (hs-cTnI) level upon admission (r = 0.268, p = 0.012), as well as at 24 h (r = 0.253, p = 0.018) after primary percutaneous coronary intervention (PCI), and it had a trend with hs-cTnI at 72 h (r = 0.155, p = 0.151) after primary PCI

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Summary

Introduction

Recent studies have indicated that monocyte chemoattractant protein-1 (MCP-1) plays an important role in the initiation and progression of ischaemic heart disease. No previous research has investigated the correlation between serum MCP-1 levels and early changes in myocardial function in patients with ST-segmental elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI). Multiple clinical and experimental evidence have supported inflammation as a critical regulatory process that links multiple traditional risk factors such as hypertension, obesity and insulin resistance with the initiation and progression of coronary artery disease (CAD) [1, 2]. In this research, we investigated the serial change in serum MCP-1 in patients with STEMI and determined the association between the time course of serum MCP-1 and early changes in myocardial function

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