## 4 Discussion
Specifically, in patients with AMI, we calculated the correlation between amine levels, heart function, and biological markers of cardiac damage, and the correlation between heart function and levels of atrial natriuretic peptide (NT-proBNP) was calculated in CHF patients. In patients with AMI, putrescine levels in mononuclear cells were positively associated with arterial diastolic pressure. Regarding LVEF, a positive correlation was established between isoamylamine levels in erythrocytes and putrescine, spermine, and isoamylamine levels in mononuclear cells. The intracellular levels of these amines may be related to the stress that occurs after AMI, leading to an activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system [34]. The mediators of these systems may stimulate all types of cells, whether they have receptors for their recognition. Thus, in addition to their known effect on the cardiovascular system, they may act on mononuclear cells and erythrocytes, as these cells express adrenergic [35; 36; 37] and angiotensin receptors [38; 39]. Therefore, there may be a link between the neurohumoral system and intracellular polyamine metabolism. It has been reported that the activation of \(\beta\)-adrenooceptors [11; 40] and angiotensin II receptors [41] increases intracellular polyamines in cardiac cells, which might be involved in cardiac remodelling [11; 42]. Furthermore, additional polyamine synthesis, at least in the heart, is associated with left atria dilation in patients with CHF, which corresponds to ODC activity [17]. Conversely, polyamines may interact with rat [2] and human \(\beta\)-adrenooceptors [3] to increase cAMP, leading to putrescine inducing a chronotropic and cardiotonic effect in isolated rat atria [2]. Therefore, it seems that the pro-inflammatory and neurohumoral responses triggered in individuals with AMI simultaneously affect polyamine metabolism in blood cells and plasma; this has potential diagnostic and prognostic value. Another interesting finding is that the plasma spermine-to-spermidine ratio in patients with AMI is inversely correlated with troponin plasma levels. These data may indicate that a positive spermine balance is associated with minor cardiac damage. This hypothesis aligns with the cardioprotective effects reported in various forms of cardiac injury and dysfunction [43; 44; 45], as well as the more thoroughly researched links between spermidine [10; 45] and the immune system [46]. Plasma isoamylamine levels might also be a marker of cardiac damage, as they were inversely correlated with troponin and LDH levels. In contrast, N-acetyl putrescine is positively correlated with LDH. These findings may have predictive value, since serum LDH levels have been associated with cardiac dysfunction after AMI [47]. The study results for patients with CHF indicate a positive correlation between plasma spermidine levels and LVEF. This finding is consistent with previous studies that have reported a positive correlation between spermidine levels in human cardiac tissue and LVEF and heart rate [17]. As mentioned earlier, the spermidine plasma levels in the CHF patients in this study were lower than those in the control and AMI groups. Although the relationship observed between these variables indicates a potential functional effect, it should not be interpreted as a causal relationship. Nonetheless, it would be interesting to investigate whether increasing the polyamine levels in blood cells and plasma could, in parallel, act as a cardioprotective agent that improves ventricular function, as indicated by spermidine supplementation in experimental models [10]. A limitation here is that spermidine-rich foods do not significantly increase blood spermidine levels in humans [48; 49]; hence, it may be necessary to employ a different strategy.