## 4 Discussion  
Although several recent studies have linked TRAIL and its receptors to a variety of cardiovascular diseases, the understanding of their role in the heart is still in its early stages [13; 19]. The pioneering data from our study provide the first critical insights into the dynamics of serum TRAIL across different stages of the CVD continuum. Importantly, this study systematically measured TRAIL (and other health indicators) in a uniform cohort of patients at a single facility. This controlled and reliable framework for data accuracy is critical for differentiating between SAH and HF, thereby contributing to a better understanding of role of apoptosis along the CVD continuum. Notably, our findings showed significantly higher TRAIL concentrations during ADHF than in HTU, providing evidence that serum  
Figure 2: The measured values for (**a**) serum creatinine, (**b**) serum sodium, and (**c**) serum potassium. Data are given as median (box) with lower and upper quartiles (error bars), and measurements were made at both admission (brown box) and discharge (green tint). Marked boxes (*) indicate significant differences at discharge compared to the time of admission (Wilcoxon signed-rank test, ***--\(p\) < 0.001, **--\(p\) < 0.01, **--\(p\) < 0.05). TRAIL increases as CVD progresses. This is consistent with literature data, although these findings derive from different cohorts of patients and clinical settings [16; 17; 18; 36; 37]. The role of elevated TRAIL in HF is still under debate; however, it is hypothesized to serve as a compensatory mechanism. Thus, elevated serum TRAIL appears to be protective in both preserved EF and reduced EF, highlighting its potential as a beneficial biomarker in HF management [16; 17]. In contrast, low levels are associated with an increased risk of rehospitalization and mortality among HF patients over a five-year follow-up period [18; 36]. On the other hand, reduced plasma TRAIL concentrations measured 20 weeks prior to gestation have been associated with an elevated risk of developing hypertensive disorders during pregnancy [37]. Given these observations, the role of TRAIL in CVD may derive from its dual functions in cellular cleanup and as part of the body's adaptive responses to ongoing heart and vascular stress [19]. The effective matching methodology; the homogeneity of the study population; and the common prevalence of certain risk factors and comorbidities, such as diabetes and smoking, among patients with heart-related issues may account for the lack of significant inter-group differences in sociodemographic and most clinical characteristics. However, the significant differences in the incidence of renal dysfunction underscores its potential importance in distinguishing between these ADHF and HTU patients. Shorter hospital stays with HTU may originate from different disease pathophysiology, treatment requirements, and patient management strategies. SAH is a less severe condition than HF, although it can lead to HF development over time [28]. In addition, HTU is associated with fewer complications and can be rapidly controlled with antihypertensive medications, leading to quicker stabilization and discharge [28; 38]  
The significantly elevated HR and significantly lower EF seen in ADHF (versus HTU) are in line with clinical data [28; 39; 40]. Associated with altered cardiac output and increased sympathetic activation, HF often prompts compensatory mechanisms such as elevated HR to maintain perfusion to vital organs [39]. Reduced EF implies perturbed contractile function of the heart muscle [40]. As a result, the weakened heart in HF struggles to pump blood efficiently through the body, which attempts to compensate by increasing HR to maintain circulation and overcome the reduced cardiac output. Elevated SBP in these acute cardiac conditions reflects the increase in systemic vascular resistance derived from the activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) in response to neurohormonal stimuli [41].