## 4 Discussion
\begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Dependent Variable** & **r Squared** & **Independent Variable** & **Coefficient** & \(p\)**Value** \\ \hline Grace score & 0.006 & MPV & 4.7371 & 0.44 \\ \hline Grace score & 0.002 & MCV & 0.4741 & 0.679 \\ \hline Grace score & 0.007 & PDW & 3.8644 & 0.54 \\ \hline Grace score & 0.001 & RDW & 1.6079 & 0.774 \\ \hline \hline \end{tabular} The table is an original contribution by the authors.  
\end{table} 
Table 15: Relationship between GRACE score and MCV, MPV, RDW, and PDW derived from logistic regression. These analyzers employ different techniques but yield a consistent measure known as the RDW [21]. Research conducted in the past has shown a link between MCV, RDW, and an elevated risk of long-term unfavorable outcomes in patients with ACS. Despite being a basic and often overlooked laboratory test, routine blood examinations hold valuable insights [22]. Our findings suggest that MCV is a standalone risk factor in predicting the prognosis of patients with NSTEMI. Specifically, higher MCV levels are associated with an increased risk of developing Killip class III-IV and serve as a substantial indicator of in-hospital death. Using a threshold value of \(>\)104 fl, we identified NSTEMI patients who are at risk of developing Killip class III-IV, while a cut-off value of \(>\)108 fl was indicative of in-hospital mortality. Although Killip classification provides valuable clinical information, it alone may not offer a comprehensive understanding of the underlying pathophysiology and prognosis. By identifying biological predictors like MCV, we can gain further insights into the disease mechanisms. Moreover, this information can potentially enhance risk stratification, inform personalized treatment decisions, and guide the development of targeted therapies. In addition to MCV, our dataset also revealed RDW as an independent predictor of NSTEMI prognosis. Elevated RDW levels were associated with triple vessel disease, the need for surgical revascularization, and longer hospital stays. The cut-off values for RDW to predict the necessity of surgical revascularization and triple vessel disease were 16% and 17%, respectively. Furthermore, our study demonstrated a correlation between high RDW levels and elevated creatinine values, consistent with previous research suggesting an increased risk of renal dysfunction associated with RDW [23; 24]. [PERSON] et al. proposed that the connection between elevated RDW and kidney injury could be attributed to inflammation and resulting oxidative stress [25]. Further investigation is warranted to determine whether high RDW levels simply reflect underlying inflammation caused by kidney disease or if they pose a substantial risk for progressive renal damage. Our data align with the findings of [PERSON] et al., who demonstrated an association between RDW, ineffective erythropoiesis, and impaired renal function [26]. Moreover, we observed a statistically relevant relationship between NT-pro BNP and RDW values. Previous studies have explained this association by the presence of high anisocytosis and erythrocyte deformability, which can impair myocardial tissue oxygenation and contribute to heart failure [27]. Platelet activity plays a significant role in the pathophysiology ACS, which is primarily characterized by plaque rupture and thrombus formation. Research indicates that when an atherosclerotic plaque ruptures, there is an important depletion of platelets within the plaque, followed by the release of immature platelets from the bone marrow. Platelets exhibit variations in both activity and size [28; 29]. In an activated state, platelets that are overall larger in size (measured by MPV), while also exhibiting significant size variability (in terms of PDW), are more metabolically active, adhesive, and have a higher capacity for aggregation. This heightened platelet activity speeds up the formation of blood clots within the blood vessels, triggering a series of clinical events linked to ACS.