## 1 Introduction  
Despite therapeutic advances in recent decades, coronary artery disease (CAD) and its sequela acute myocardial infarction (AMI) are still a major cause of morbidity and mortality worldwide [1,2]. In AMI, early recognition and initiation of reperfusion therapy are crucial to limit myocardial ischemia and infarct size and thereby reduce mortality and post-infarct complications such as heart failure [3,4]. Up to 25% of patients with urgent need of primary percutaneous coronary intervention lack typical ST-segment elevation on a 12-lead electrocardiogram (ECG) as an indication of coronary occlusion or critical stenosis [5]. Therefore, a combination of ECG analysis and biomarker tests is the gold standard for the diagnosis of AMI [6]. Currently, elevated high-sensitivity cardiac troponins (hs-cTn) are required for the diagnosis of AMI [6]. However, the specificity of hs-cTn for acute myocardial infarction is limited [7] and they are frequently 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]. Furthermore, there is a lack of established biomarkers for ischemia reperfusion (IR) injury [10]. IR injury occurs when reinitiated blood flow through a percutaneous coronary intervention (PCI) causes additional cardiomyocyte death by activating a complex cascade of cellular myocardial and coronary microvascular reactions [10,11].  
Finding novel biomarkers for AMI and IR has therefore become an important focus of medical research.  
In recent years, platelet serotonin (5-hydroxyryptamine (5-HT)) has come into focus as an important factor in AMI [12]. The effects mediated by 5-HT are very complex, as it acts as both a peripheral hormone and a neurotransmitter. Central 5-HT is synthesized by tryptophan hydroxylase 2 in the brainstem. It is separated from the peripheral 5-HT by the blood/brain barrier and is reported to regulate mood, appetite, and circadian rhythm. Disturbances in the central serotonergic system lead to psychiatric diseases like depression [13,14]. Tryptophan hydroxylase 2 is also expressed by the enteric nervous system in the periphery [15]. However, most peripheral 5-HT is synthetized by tryptophan hydroxylase 1 in the gut, with platelets being its main circulating reservoir [13,16]. In peripheral tissues, 5-HT is involved in a broad variety of functions, including regulation of vascular tone [17], hemostasis [18], and immune responses [19,20,21].  
5-HT was reported to be an important mediator in AMI and IR: The platelet-stimulating microenvironment in AMI leads to an activation of platelets with the consecutive release of serotonin [22]. This elevation in 5-HT levels leads to a constriction of coronary smooth muscle cells, worsening myocardial damage [23]. Moreover, platelet serotonin induces neutrophil degranulation after MI, further aggravating myocardial damage by contributing to increased IR [12]. Consequently, the depletion of platelet serotonin stores improves the outcome after AMI [12,24].  
Previous animal and human studies described an elevation of 5-HT after AMI and an association with I/R injury [12,25]. In humans, elevated 5-HT levels were found in aspirates from the culprit coronary artery of patients with acute myocardial infarction [26].  
In our study, we aimed to investigate the diagnostic potential of serum 5-HT as a biomarker in AMI and to determine whether it can be used to predict IR.