Background Elabela (ELA) was newly discovered as a novel endogenous ligand of the apelin receptor (APJ) which has demonstrated to be crucial for cardiovascular disease such as myocardial infarction, hypertension and heart failure. Previous experiments have revealed that ELA reduced arterial pressure and exerted positive inotropic effects on the heart. However, the role of plasma ELA levels in patients with acute coronary syndrome (ACS) and its relationship with severity of coronary arteries have not been investigated. Methods Two hundred and one subjects who were hospitalized for chest pain and underwent coronary angiography were recruited in this study. One hundred and seventy five patients were diagnosed with ACS and twenty-six subjects with negative coronary angiography were included in the control group. Plasma ELA levels, routine blood test, blood lipid, liver and kidney functions were measured. The number of coronary arteries and SYNTAX (Synergy Between Percutaneous Coronary Intervention With Taxus and Cardiac Surgery) score of coronary lesions were used to evaluate the extent of coronary artery stenosis. Results ELA in patients with ACS was significantly higher than that in the control group (P ＜ 0.01). There was no significant difference in plasma ELA levels among patients with single-, double- and triple-vessel diseases. However, in the generalized ad?ditive model (GAM), there was a threshold nonlinear correlation between the ELA levels and Syntax I score (P ＜ 0.001). Plasma ELA levels were positively correlated with the Syntax I score when the ELA levels ranged from 63.47 to 85.49 ng/mL. There was no significant associa?tion between the plasma ELA levels and the extent of coronary artery stenosis when the ELA levels were less than 63.47 ng/mL or higher than 85.49 ng/mL. Conclusion The present study demonstrates for the first time that plasma ELA levels are increased in patients with ACS.The rise in endogenous ELA levels was associated with severity of coronary stenosis and may be involved in the pathogenesis of ACS.