## 4 Discussion
Platelet activity can be measured by some indices obtained by blood count tests, such as PDW and MPV [10; 11]. Analyzing the data gathered from our patient cohort, we concluded that the cut-off value for PDW to predict 30-day mortality was 19%, while the cut-off value for MPV to predict Killip class III-IV in NSTEMI patients was 11.7%. Our results are in accordance with other studies from the literature that also found the MPV and PDW as strong independent prognostic factors in ACS [13]. Regarding the association between MPV and creatinine levels, our study supports previous research showing a positive correlation [30]. Elevated MPV is considered a marker of ongoing inflammation and oxidative stress, both of which can contribute to kidney dysfunction. The pro-inflammatory and pro-thrombotic effects of larger platelets are believed to play a role in the progression of kidney disease [31]. Further research is necessary to fully understand the relationship between increased MPV and kidney function and to determine if targeting MPV could be a potential therapeutic approach for managing kidney function. However, our study did not find a correlation between infarct size and the parameters we proposed. This unexpected result contradicts the expectation that a higher level of proinflammatory status during a myocardial infarction would directly correlate with infarct size and these parameters. We hypothesize that the small sample size of our study may have limited our power to effectively determine this association. Conversely, antiplatelet therapy has been extensively studied and proven effective in reducing mortality and morbidity in cardiovascular diseases. Interestingly, our data suggest that this therapy does not have a significant effect on MPV and PDW. This could explain why patients with high PDW and MPV, even if they receive antiplatelet therapy, have a more unfavorable prognosis with a higher death rate [31; 32]. We speculate that antiplatelet therapy primarily targets platelet aggregation and activation and, while it can affect various aspects of platelet function, it typically does not directly impact PDW and MPV levels. Several studies have consistently shown no significant relation between MPV, PDW, and the use of antiplatelet medications [33; 34]. Considering all the information above, our study suggests that measuring MCV, MPV, RDW, and PDW (which are useful low-cost markers) is a straightforward way of stratifying cardiovascular risk, predicting the occurrence of complications, and imposing rapid management in some patients with a high risk masked by an old risk stratification score. Thus, we have demonstrated that MCV is associated with in-hospital mortality and Killip class III/IV, while RDW is correlated with kidney dysfunction, an indication for surgical intervention, and also represents a stand-in for triple vessel disease and longer duration of hospitalization. Furthermore, PDW independently predicts short-term mortality and MPV is correlated with Killip class III/IV and kidney dysfunction. However, we are not able to show a correlation between the GRACE score and MCV/MPV/PDW/RDW. The new predictive markers proposed by us are correlated with heart failure after ACS and renal dysfunction, outcomes included in the GRACE score. Nevertheless, these new markers not only anticipate in-hospital mortality, within one month, but also forecast the length of hospital stay, the likelihood of a patient requiring cardiac surgery, and the presence of triple vessel disease--all of which are endpoints not covered by the GRACE score. The predictive markers we have proposed serve as surrogate indicators of the pathophysiological processes occurring during ACS, going beyond the clinical and biological aspects encompassed by the GRACE score. These observations may elucidate the absence of a correlation between these markers and the aforementioned score.