## 4 Discussion  
In this pilot study, we investigated for the first time if 5-HT serum levels are altered in patients with STEMI and if they are associated with the severity of myocardial damage, in order to evaluate it as a potentially novel biomarker for AMI and I/R injury. Immediate restoration of blood flow by coronary angiography improves survival and outcome in patients with STEMI [3,4]. The death of cardiomyocytes during STEMI results from both necrosis and apoptosis. Troponins and CK-MB are routinely used in clinical practice and are validated biomarkers of cell lysis, necrosis, and overall myocardial damage to estimate infarct size [6,35,36]. However, the specificity of these markers is limited [7] and they can be elevated in acute myocardial injury of non-ischemic origin [6,8,9]. Moreover, troponins can be chronically raised in patients with congestive heart failure or chronic kidney disease [6,7] and CK and myoglobin can be altered in patients with rhabdomyolysis [37]. Therefore, there is need for additional, more specific, and more precise biomarkers. In this pilot study, we assessed if serum 5-HT correlates with clinical variables and markers of cell lysis (e.g., CK, myoglobin, and cTNT) and further investigated whether it could predict I/R injury in STEMI patients after PCI. The hypothesis that 5-HT serum levels might be associated with the extent of myocardial damage after AMI was, on the one hand, based on previous studies reporting altered serotonin levels after myocardial infarction and, on the other hand, based on recent findings that that 5-HT aggravates I/R injury [12,22]. 5-HT plays a crucial role in AMI. Ninety to ninety-five percent of 5-HT is stored in the dense granules of platelets, and released upon activation [13]. In AMI, the platelet-stimulating microenvironment \begin{table}
\begin{tabular}{c c c} \hline \hline  & **r** & \(\mathbf{p}\)**-Value** \\ \hline \multicolumn{3}{c}{**Overall Characteristics**} \\ \hline age & \(-0.4258\) & \(0.0086\) \\ sex & \(-0.025\) & \(0.880\) \\ \hline \multicolumn{3}{c}{**Cardiovascular Risk Factors**} \\ \hline diabetes & \(-0.071\) & \(0.673\) \\ HbA1c & \(-0.06591\) & \(0.7025\) \\ hypercholesterolemiaemia & \(0.006\) & \(0.972\) \\ total cholesterol & \(-0.03373\) & \(0.8452\) \\ LDL cholesterol & \(-0.01326\) & \(0.9388\) \\ overweight & \(0.095\) & \(0.572\) \\ BMI & \(0.1458\) & \(0.4034\) \\ arterial hypertension & \(-0.248\) & \(0.133\) \\ positive family history & \(0.278\) & \(0.092\) \\ smoking & \(0.007\) & \(0.965\) \\ \hline \multicolumn{3}{c}{**CAD Characteristics**} \\ \hline number of coronaries affected & \(-0.235\) & \(0.156\) \\ CK peak & \(0.180\) & \(0.279\) \\ CK-MB peak & \(0.065\) & \(0.703\) \\ myoglobin peak & \(0.099\) & \(0.578\) \\ troponin peak & \(-0.116\) & \(0.542\) \\ proBNP peak & \(-0.300\) & \(0.071\) \\ LVEF & \(0.421\) & \(0.009\) \\ \hline \multicolumn{3}{c}{**Other Laboratory Findings**} \\ \hline platelet count & \(-0.1124\) & \(0.5403\) \\ creatinine & \(0.1662\) & \(0.3326\) \\ BUN & \(-0.1773\) & \(0.2938\) \\ CRP & \(-0.3023\) & \(0.0926\) \\ \hline \hline \end{tabular}
\end{table} 
Table 3: Correlation analysis. and the thrombus formation in the coronaries lead to an activation of platelets with the subsequent local release of 5-HT [22]. The increased local 5-HT levels contribute, on the one hand, to enhanced recruitment and aggregation of platelets [13]. On the other hand, 5-HT, as a vasoactive substance, leads to the constriction of coronary smooth muscle cells, further worsening myocardial damage [23]. Consistent with this are findings from rat experiments revealing an increase in 5-HT concentrations in the heart tissue after myocardial infarction [23], representing enhanced platelet activation and aggregation. As a consequence of the release of platelet 5-HT in the coronary arteries, plasma 5-HT levels markedly increase after AMI in mice and humans [12; 25]. [PERSON] et al. reported a significant increase in plasma 5-HT in mice within the first 24 h after LAD ligation [12].