## 4 Discussion  
The results of this study showed that there are specific changes in the homeostasis of polyamines and isoamylamine in the blood cells and plasma of patients suffering from AMI and CHF, and these changes correlate differently with the tissue damage markers and haemodynamic clinical parameters of the patients. This is the first study to provide data on the association of the remarkably lower levels of polyamines and isoamylamine in blood cells and plasma related to ventricular function in CHF patients. Polyamine homeostasis is tightly regulated within cells and is modified in pathological situations. In cardiac disease, alterations in polyamine metabolism have been described in experimental heart models and human cardiac tissue in association with anatomical and functional parameters of the heart. These changes may be biological markers in the pathophysiology of cardiac disease. However, there are limitations, as obtaining human cardiac tissue is not feasible. In this study, we focused on analysing data on readily available cells from patients to determine whether potential changes in their polyamine metabolism can be linked to cardiac damage or function in AMI or CHF, which may have clinical implications. Peripheral blood is one of the most accessible sources for obtaining cells, which are broadly categorised into two distinct types: erythrocytes and mononuclear cells. In addition, blood cells may be subjected to stimulatory stress mediators that account for the cardiac pathologies studied. Using the control group as a reference, the determination of polyamine levels in blood cells and the analysis of the data reveal physiological correlations between polyamine synthesis (putrescine, spermidine, and spermine) and catabolism (N-acetyl putrescine and N-acetyl spermine). Based on these two processes, there are variations in the correlations between different polyamines in the blood cells of patients with AMI and CHF. A discriminant function analysis revealed three well-differentiated groups: the control group, patients with AMI, and patients with CHF. This finding highlights specific alterations in polyamine and isoamylamine metabolism associated with different cardiac conditions. Our analysis encompassed the following: isoamylamine levels in mononuclear cells, erythrocytes, and plasma; spermidine levels in erythrocytes; and N-acetyl putrescine levels in plasma. When comparing the control and patient groups, significant differences in median polyamine levels and isoamylamine levels were observed across blood cells and plasma. Patients with AMI, with no differences between NSTEMI and STEMI, exhibited low putrescine levels in mononuclear cells and elevated isoamylamine levels in erythrocytes and plasma. In contrast, in CHF patients, all the polyamines analysed in erythrocytes and plasma were diminished, with elevated isoamylamine levels in erythrocytes. Patients with CHF were older than participants in the other groups; notably, it has been reported that there is typically a significant decrease in putrescine levels in erythrocytes and plasma during the sixth decade of life [29]. An age effect was invalidated by comparing the amines in the different samples with a control group of the same age range, which revealed equally significant decreases in all samples. Therefore, alterations in the homeostasis of polyamines accompany underlying AMI and CHF. The findings of variations in the blood and plasma isoamylamine levels--isoamylamine is a primary amine--are interesting and novel. Isoamylamine has been discovered in human cardiac tissue from patients with CHF [17], and as seen in our study, it is equally present in human peripheral blood cells and plasma. Therefore, it may play a role. In addition to observing varying intracellular and plasma levels between the different groups, establishing potential clinical significance was also explored.