Abstract :Although oxidative stress has been implicated in the pathogenesis of heart failure (HF), the precise mechanism of myocardial injury involved has been unclear. We previously identified an apoptosis-inducing humoral factor secreted from cells subjected to oxidative stresses. We named this novel post-translationally modified secreted form of eukaryotic translation initiation factor 5A (eIF5A), Oxidative stress-Responsive Apoptosis Inducing Protein (ORAIP) [1]. ORAIP is rapidly secreted from cells in response to oxidative stresses and induces apoptosis of the cells in an autocrine fashion. To investigate the role of ORAIP in the mechanism of oxidative stress-induced myocardial injury in HF, we analyzed plasma levels of ORAIP, cardiac troponin T (cTnT), and brain natriuretic peptide (BNP) in 110 patients (male/female: 83/27; age 71.67±0.98 [mean±SE] years) with HF of various etiology including atrial fibrillation, ischemic heart disease, aortic stenosis, chronic kidney disease, and diabetes mellitus.