Acute coronary syndrome (ACS) affects around 7 million individuals each year globally and refers to a group of pathologies that cause myocardial ischemia, and ultimately acute myocardial infarction (AMI) [1]. There are three types of ACS, ST-segment Elevation Myocardial Infarction (STEMI), Non-ST-segment Elevation Myocardial Infarction (NSTEMI) and unstable angina, where the presence of high-sensitive cardiac troponin (hs-cTn) in the blood distinguishes an AMI ACS [2,3]. Reperfusion is achieved via percutaneous coronary intervention (PCI), restoring blood supply to the myocardium at the respective culprit lesion i.e., right coronary artery (RCA), circumflex or left anterior descending (LAD) artery, and when performed within 2 h for STEMI ACS can improve patient outcome [1]. However, research indicates that LAD culprit lesions have a higher risk of long-term mortality compared with RCA [4]. Moreover, for NSTEMI ACS the disease may be managed for some time before the best course of intervention is decided [5]. Therefore, biomarkers that assist with diagnosis and risk stratification of ACS are warranted.

Previous research has identified a link between ACS, AMI, and oxidative stress [[6], [7], [8]]. Oxidative stress manifests when the generation of reactive oxygen species (ROS) exceeds the antioxidant capacity of the cell, causing damage to macromolecules and organelles [9]. Tissues including the myocardium produce an array of antioxidant enzymes such as peroxiredoxin (PRDX), thioredoxin (TRX) and thioredoxin reductase (TRXR), which protect against the damaging effects of ROS [10,11]. Studies illustrate a protective role for TRX and TRXR in cardiomyocytes by promoting redox homeostasis [12]. Expression of TRX is also noted in medial smooth muscle cells of the coronary arteries and plays a central role in regulating ROS and maintaining eNOS function [12,13]. Using in vitro modelling it is shown that the expression of various PRDX isoforms (notably PRDX4) are increased in cardiomyocytes following exposure to exogenous hydrogen peroxide (H2O2) [14]. Research also illustrates that alterations in the intracellular redox environment mediates the secretion of TRX and PRDX via conventional and alternative secretion mechanisms [15], where it is suggested that this secretion may play a wider antioxidant role [16]. Support for this notion comes from studies showing that secreted PRDX4 can bind to endothelial cells, which may protect these cells during periods of oxidative stress [17]. Thus, extracellular TRX and PRDX may be central components in maintaining redox homeostasis during ischemia induced ROS, where crosstalk between cardiomyocytes and endothelial cells is important [18].

Previous research shows that PRDX2, PRDX4, TRX and TRXR are released into the blood during oxidative stress and may be used as surrogate biomarkers [[19], [20], [21]]. Thus, the aim of this study was to quantify blood PRDX2, PRDX4, TRX and TRXR in patients presenting with ACS and at 1–3-month (first) and 6-month (second) follow-up and evaluate whether concentration changes of these biomarkers may be used to support diagnosis and aid ACS risk stratification.