Abstract Background The neutrophil-to-lymphocyte ratio (NLR) is a well-known risk marker in acute coronary syndrome (ACS). Its pathophysiological basis relies on the assumption that this index, which reflects the behavior of both innate and adaptive cellular immune responses, represents both inflammation and stress. However, to date, we lack solid evidence demonstrating the correlation of this index with stress markers in the context of ACS. Methods Single-center, prospective, observational study. Patients admitted to the coronary care unit with a diagnosis of ACS were included. On admission, peripheral blood samples were obtained to measure blood cell counts (neutrophil and lymphocytes), levels of high-sensitivity troponin I (hsTnI), high-sensitivity C-reactive protein (hsCRP) and serum cortisol. Clinical variables were obtained from electronic medical records. Statistical analysis was performed using R version 4.3.3. Statistical significance was set at p 0.05. Results We included 91 patients. The mean age was 65 (IQR 57 - 72) years, 61 (67%) were male, 51 (56%) had hypertension and 21 (23%) were diabetics. A total of 78 (86%) patients had positive hsTnI, 53 (59%) had ST elevation acute coronary syndrome (STE-ACS), 16 (17%) had Killip-Kimball class 1, the mean GRACE value was 118 (IQR 98 - 140), 81 (89%) patients had at least one vessel disease, 77 (84%) were revascularized, and 7 (7.9%) patients died. Basal characteristics can be observed in the table. Higher levels of neutrophil to lymphocyte ratio were associated with STE-ACS (3.01 vs 4.56, p0,01), positive troponin (2.21 vs 4.78, p0.01), correlated with fewer ejection fraction (r=-0.26, p=0.01) and were associated with higher mortality (7.54 vs 3.24, p=0,03). Patients who died had higher cortisol levels (32.36 ± 19.74 mg/dL vs. 15.48 ± 11.41 mg/dL, p = 0.0009). The same was observed for hsCRP (206.3 ± 142.7 mg/dL vs. 131.8 ± 60.8 mg/dL, p = 0.03). When observing the behavior of NLR in relation to inflammation and stress responses, we found a significant correlation with both hsCRP (r=0.43, p0,01) and cortisol (r=0.25, p=0.03), as can be seen in the figure. When analyzing the behavior of each component of the NLR, we observed that cortisol did not significantly correlate with the neutrophil count (r=0.12, p=NS) but did correlate with the decrease in lymphocytes (r=-0.26, p0.05). Meanwhile, hsCRP correlated with the increase in neutrophil count (r=0.40, p0.01) but not with the lymphocyte count (r=-0.21, p=NS). Conclusion This work demonstrates the correlation of NLR with inflammation and stress markers in ACS. Additionally, analyzing the behavior of each determinant of NLR in relation to hsCRP and cortisol allows us to gain a deeper understanding of the immune response in ACS and its relationship with stress and inflammation.Table.Basal characteristics. NLR, cortisol and hsCRP correlations
Aladio et al. (Sat,) studied this question.