## 1 Introduction  
Polyamines are found in all living cells and play crucial roles in numerous biological functions in the organism. These biological compounds are synthesised endogenously: ornithine decarboxylase (ODC), the first enzyme in polyamine biosynthesis, convertsornithine into putrescine, which is subsequently metabolised into spermidine and spermine. Catabolic enzymes and membrane transport mechanisms regulate intracellular polyamine homeostasis [1]. Polyamines exert acute effects on the heart, modulating physiological properties such as chronotropism and intotropism via direct interaction with the rat [2] and human [3] cardiac \(\beta\)-adreno acceptor system and as mediators of cardiotonic agents [4; 5; 6], as demonstrated in experimental models and cultured human cardiomyocyte studies. Polyamines are also involved in mechanisms related to the cardioprotective effect of ischaemic preconditioning, as it is associated with an upregulation of ODC and an inhibition of spermidine/spermine acetyltransferase. Furthermore, it is abolished by inhibiting ODC activity [7]. In addition, spermine conferred cardiomyocyte protection when administered before ischaemia/reperfusion injury is induced [8; 9], and spermidine also showed cardioprotection [10]. Polyamines have been linked to more than just protective influences on the heart. An increase in polyamine synthesis [11] or a decrease in polyamine catabolism has been implicated in cardiac hypertrophy and myocardial damage in response to several hormonal and trophic stimuli in experimental models [12; 13; 14; 15; 16]; some of the effects can be pharmacologically counteracted. In patients with chronic heart failure (CHF), elevated ODC activity detected in cardiac tissue is positively associated with left atrium dilation. However, cardiac polyamine levels are not related to clinical hypertrophy parameters such as septum and left ventricular wall size; on the contrary, spermidine has been positively correlated with cardiac output [17]. The positive relationship between spermidine and cardiac output aligns with the findings of epidemiological studies in which high spermidine intake has been associated with a cardioprotective effect [18; 19]. In several models, spermidine supplementation produces cardioprotection and extends the lifespan in mice [10]. Lifespan enhancement was previously reported in various experimental models [20]. The proposed mechanisms include the stimulation of autophagy, antioxidant and anti-inflammatory effects [1], and improving the contractile function of cardiomyocytes [21]. Polyamine levels in cardiac tissue may be an independent biological marker of cardiac damage and function in humans. However, this method is not feasible in clinical settings, and it is more practical to search for biomarkers in peripheral blood. In this sense, plasma levels have revealed that a decrease in ornithine is associated with the protective mechanisms of remote ischaemic preconditioning, which protects the myocardium from ischaemia-reperfusion injury [22], which has been proposed as a biomarker of ischaemic cardiomyopathy [23]. In addition, serum polyamines have shown prognostic value in patients with acute myocardial infarction (AMI) and cardiovascular events [24]. Isoamylamine has been discovered in human cardiac tissue from patients with CHF [17]. In mammals, it has been reported that mouse kidneys express a specific decarboxylase of leucine-forming isoamylamine [25; 26]. This primary amine acts as a metabolic intermediate in the degradation of leucine, is a by-product of microbial activity, and is found in fermented foods [27; 28]. However, its sources and potential biological role in mammals are poorly understood. In healthy individuals, the levels of polyamines in peripheral blood cells are more sensitive to age-related changes than measurements made in whole blood [29]. This difference may be because the polyamine level within cells is tightly regulated, while the levels in plasma or serum are more susceptible to enzymatic metabolism.