['Fetuin-A is an anti-inflammatory negative acute-phase glycoprotein, synthesized by the liver. In this study, we aimed to investigate the effects of admission fetuin-A levels on coronary and myocardial blood flow and short- and long-term prognosis in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention.', 'One hundred eighty consecutive patients admitted with diagnosis of STEMI and 55 healthy age- and sex-matched volunteer controls were enrolled in the study. Patients with STEMI were divided into 2 groups in respect to thrombolysis in myocardial infarction myocardial perfusion grade after primary PCI: with thrombolysis in myocardial infarction myocardial perfusion grade 0-1-2 and thrombolysis in myocardial infarction myocardial perfusion grade 3. Serum levels of fetuin-A were lower in patients with STEMI than in the healthy group subjects. In-hospital and 1-year deaths were significantly higher in patients from the abnormal perfusion group. In-hospital major adverse cardiac event (MACE) and 1-year follow-up MACE also were significantly higher in patients from the abnormal perfusion group. The receiver-operating characteristic analysis indicated an optimal cut point of less than 200 μg/mL, which detects 1-year mortality with a negative predictive value of 95%. The 1-year mortality rate and 1-year MACE were significantly higher in patients with low fetuin-A level as compared with those with high fetuin-A level.'] Does lower fetuin-A predict angiographic impaired reperfusion and mortality in ST-elevation myocardial infarction?