## 1 Introduction  
Oxidative stress (OS) is defined as a disruption of the equilibrium between the generation of free radicals and the activity of antioxidant systems [1; 2]. In a pathological state, many activities of the organism are disturbed, which influences the level of antioxidants, making it difficult to detect the causes of OS. A lot of research indicates elevated free radical production in many diseases [3; 4; 5]. Advanced oxidation protein products (AOPP) are a marker of oxidative stress first detected in the plasma of chronic uremic patients [3]. AOPP originates from reactions between free radicals, chlorinated oxidants, and plasma proteins [6], mainly albumin [7]. They can either escalate the OS or reactive oxygen species (ROS) generation [7; 8; 9]. AOPP is also associated with coronary artery disease (CAD) [10], atherosclerosis [11], and comorbidities, such as diabetes mellitus (DM), hypertension, metabolic syndrome [12], and lipid disorders (hypercholesterolemia and hypertriglyceridemia) [13]. The relationship between the level of AOPP and monocyte activation markers suggests that the oxidized proteins can contribute to the inflammatory process. An increased inflammatory response also causes an increased production of free radicals, which enhance OS and stimulate the production of AOPP. However, AOPP may be a valuable tool for measuring protein oxidative damage and a general level of OS.  
Uric acid is a commonly known antioxidant detectable in human serum plasma [14; 15]; however, some conditions can provoke and escalate OS [16]. This organic compound is the end product of purine metabolism [17], mainly regulated by xanthine oxidoreductase, converting hypoxanthine to xanthine and xanthine to uric acid. Many factors could increase serum uric acid levels: diet (alcohol consumption, meat, high fructose intake) [18], uncommon genetic disorders connected with enzymatic degradation pathways [16; 18], metabolic syndrome, DM, hypertension, women after menopause, race, renal diseases, inflammatory process, diseases with high cell turnover, some drugs [19], obesity, and ischemia [16; 17; 18]. Evidence shows that the overproduction of uric acid by xanthine oxidase produces excessive free radicals, such as ROS [20; 21]. The main ROS generators are NADPH oxidase, xanthine oxidase, mitochondrial enzymes, myeloperoxidase (MPO), lipoxygenase, and uncoupled nitric oxide (NO) synthase [22]. Myocardial infarction (MI), as well as post-infarction, is one of the most urgent situations in the health system, and needs follow-up due to the possibility of developing heart failure (HF) [23]. In this context, seeking therapeutic markers and links that can prevent or help in the control and management of the patient is of great importance. The pathophysiological interaction between acute coronary syndromes (ACS), including MI, and the appearance of inflammatory cells that produce oxygen radicals, proteases, and proinflammatory cytokines leading to endothelial damage and plaque rupture was proved [24; 25]. The increase in OS likely reflects the effect of the accumulation of inflammatory cells in unstable atherosclerotic plaques. Moreover, free radicals are generated due to acidosis, decreased blood flow to heart muscle, and sodium and calcium pump dysfunction. Thus, the status of antioxidant defense systems in patients after MI could provide potentially relevant prognostic information [26]. This, however, needs to be verified. Still, there are no tests to measure OS in individual patients, nor are there effective methods to counteract these processes. The correct interpretation of markers of OS may be the basis for assessing prognosis and making appropriate treatment decisions.  
This study aimed to evaluate the interplay of uric acid and AOPP in patients after MI, and verify the correlation between uric acid and AOPP as the markers of OS in patients with MI.