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Coronary artery disease

Changes in fractalkine in patients with ST-elevation myocardial infarction.


PMID 26049921

Abstract

Fractalkine (FKN) was recently shown to play an important role in atherosclerotic plaque rupture and cardiac remodeling and dysfunction. We evaluated the changes in serum FKN (sFKN) in patients with acute ST-elevation myocardial infarction (STEMI) and the influence of a percutaneous coronary intervention (PCI) on the levels of sFKN. The study population included 40 patients with acute STEMI [acute myocardial infarction (AMI)+PCI: 20 underwent primary PCI; AMI: 20 without PCI] and 40 patients with symptomatic stable angina pectoris (SAP+PCI: 20 underwent PCI; SAP: 20 without PCI). sFKN were measured at different time points by ELIZA. The gene expression of heart FKN was assessed by real-time reverse transcription-PCR in a model of myocardial infarction mice. We found that the baseline level of sFKN in patients with acute STEMI was significantly higher than that of patients with SAP. Primary PCI in STEMI resulted in a rapid decrease within 24 h and to a similar level after 48 h as in the SAP and SAP+PCI patients, whereas in the AMI group, the sFKN level showed a slight decrease from 6 to 24 h (from 1307.6±368.9 to 1092.7±258.1 pg/ml, P=0.036) and remained significantly higher at all later time points (P<0.001 for all). The sFKN level at 30 days was correlated positively with the NT-proBNP level (r=0.490, P=0.014). The time course of myocardial FKN gene expression in mice has a pattern similar to sFKN change in AMI patients. Our study suggested that STEMI had a higher sFKN level and correlated positively with the NT-proBNP level at 1 month. PCI could lead to a rapid decrease in the sFKN level.