## 4 Discussion
These mechanisms are particularly pronounced during acute cardiovascular events due to the body's attempt to maintain adequate perfusion despite failing cardiac function or acute stress [41]. Nonetheless, it is worth noting that elevated SBP at hospital admission is associated with better clinical outcomes for both ADHF and HTU [42; 43]. RDW-SD and RDW-CV were significantly higher during ADHF than during HTU. Both SAH and HF can alter the heart's ability to pump blood, disrupting erythropoiesis and red blood cell survival due to increased systemic inflammation and oxidative stress [44; 45; 46]. However, SAH is associated with less severe systemic inflammation and oxidative stress compared to HF [44; 45; 46]. This can explain--at least partly--the significantly higher RDW size variability observed in ADHF. We also infer that the presence of multiple comorbidities (e.g., diabetes, obesity) in HF patients contributes to higher HbA1c [47; 48]. However, we cannot exclude the notion that other factors, like the long-term use of certain drugs with effects on glucose metabolism (e.g., loop diuretics, statins) in HF, might have contributed to these outcomes [49]. Significant elevation of serum creatinine at discharge vs. admission in ADHF is indicative of ongoing renal impairment. These changes may stem from renal hypoperfusion, aggressive diuretic therapy during hospitalization, neurohormonal activation, or cardiometabolic syndrome [50]. In contrast, decreased creatinine at discharge in hypertensive subjects suggests reversible renal strain and improved renal perfusion post-discharge. Nonetheless, hyperuricemia observed during both types of acute cardiac events indicates kidney dysfunction in all patients [51]. The decline in kidney function was more evident in ADHF patients, as suggested by the significantly higher serum urea at admission [52]. Although typically elevated in HF compared to SAH [53], tryglicerides are lower in certain situations, such as cachexic HF patients. These subjects require complex medical management due to associated progressive muscle wasting, weight loss, and functional impairments [54]. Accompanying these changes are significant declines in serum hemoglobin and lymphocytes [55] and increased variance in red blood cell size (as described above). In older people with HF, anemia is mainly caused by decreased red blood cell production or chronic blood loss, but may also be linked to iron or other nutritional deficits [55]. Furthermore, ALC decrease may reflect inflammatory responses or immunosuppression associated with the underlying pathophysiology of HF [56]. Overall, these data indicate that ADHF patients display worse cardiac, hematologic, and renal profiles, with longer hospital stays and cachexic phenotype. With respect to correlational analysis, the TRAIL-ADMA association emerged as a thread linking apoptosis, endothelial dysfunction, and the CVD continuum. More specifically, the significant positive associations between these variables during both HTU and ADHF indicate an intertwining pathway between endothelial dysfunction and inflammation/appoptosis processes. Indeed, inflammatory mediators (e.g., cytokines, oxidized lipoproteins) can activate pathways like NF-kB, promoting endothelial dysfunction [57]. Moreover, pathways related to Wnt signaling and PPAR-gamma are essential for connecting endothelial dysfunction to the CVD continuum [58]. In ADHF, TRAIL also displayed strong positive correlations with CRP and serum potassium at admission. The former relationship may reflect the body's attempt to manage damaged/dysfunctional cells via apoptosis exacerbated by the inflammatory milieu specific to ADHF [59]. The second association supports a complex interplay between apoptosis, inflammation, and electrolyte balance in HF [19]. For example, elevated TRAIL may disrupt cell membrane in cardiac cells via apoptosis, raising serum potassium levels [60].