## 4 Discussion
The mortality rate of male patients with serum uric acid concentrations of more than 7 mg/dL was 3.76 times higher than those with serum uric acid concentrations below 7 mg/dL during the 30 days after admission. Results of this study indicate that serum uric acid levels might have a prognostic role in in-hospital and short-term mortality. In another study, [PERSON] et al. [52] included 5124 patients with ACS who underwent PCI (1629 with acute STEMI, 1332 with NSTEMI, and 2163 with unstable angina). All patients were divided into quartiles according to serum uric acid concentration. The primary endpoint was 1 year of mortality. Table 3 presents data on this study. This study showed that elevated serum uric acid levels are an independent predictor of 1 year of mortality across the whole spectrum of patients with ACS. [PERSON] et al. [53] obtained similar results from their study, which created a database cohort study with high-risk CVD patients (n = 3098). All patients were divided into quartiles according to serum uric acid concentration (Table 3). In this study, the mortality rates were also the highest in quartile 4. Moreover, they estimated that for every 1 mg/dL elevation in the serum uric acid level, the risk of death from all causes increased by 39%. Recently, there were established cut-off values for the optimal prediction of fatal MI and all-cause mortality of 5.7 mg/dL and 4.7 mg/dL, respectively. As previously mentioned, a J-curve showing the relationship between uric acid and AOPP was observed in individuals after an MI. This observation may have significant clinical implications, enabling the determination of a desirable value for uric acid in this context. However, it is also necessary to consider other explanations. This part of the curve may be associated with an effect of the increase in uric acid and AOPP, directly resulting from severe MI. The intricate mechanisms involved in MI are not limited to direct cardiac tissue damage, but also encompass a series of biochemical and cellular responses. MI, commonly known as a heart attack, is characterized by the death of cardiac muscle cells, primarily due to the occlusion of coronary arteries [54]. This blockage initiates a cascade of events at the cellular level, central to the release of intracellular components from necrotic cardiac cells [55]. A key component among these is extracellular mitochondrial DNA (mtDNA), which is released significantly during cell death [56; 57; 58; 59]. Due to its structural similarity to bacterial DNA, mtDNA is adeply recognized by the immune system as a damage-associated molecular pattern (DAMP) [56; 60]. This recognition triggers immune responses designed to mitigate the injury, a vital process in the body's attempt \begin{table}
\begin{tabular}{c c c c c c c c c} \hline \hline \multirow{2}{*}{**Variable**} & \multicolumn{6}{c}{**[PERSON] et al. [52]**} & \multicolumn{6}{c}{**[PERSON] et al. [53]**} \\ \cline{2-9}  & **Q 1** & **Q 2** & **Q 3** & **Q 4** & **Q 1** & **Q 2** & **Q 3** & **Q 4** \\ \hline Number of patients & 1271 & 1261 & 1300 & 1292 & 755 & 802 & 751 & 790 \\ UA level, [mg/dL] & 1.3–5.3 & 5.3–6.3 & 6.3–7.5 & 7.5–18.4 & 0.4–4.9 & 5.0–5.9 & 6.0–7.0 & 7.1–13.9 \\ Primary endpoint, [1 year mortality] & 80 deaths & 77 deaths & 72 deaths & 221 deaths & 20 deaths & 28 deaths & 36 deaths & 71 deaths \\ \hline \hline \end{tabular}
\end{table} 
Table 3: Summary of the studies: [PERSON] et al. [52] and [PERSON] et al. [53] (own preparation of statistical data). to cope with the damage. Neutroph play a noteworthy role in the immune response as early responders to damaged cardiac tissue in MI. Upon encountering extracellular DNA, including mtDNA, neutrophils undergo NETosis, releasing neutrophil extracellular traps (NETs) [61; 62]. However, this also leads to the release of multiple cellular components, including DNA and several enzymes. In this context, myeloperoxidase (MPO) is a heme-containing enzyme abundantly found in the azurophilic granules of neutrophils [63].