Abstract Background The prompt achievement of LDL cholesterol (LDLc) targets is a crucial objective in the secondary prevention of cardiovascular events among very high-risk patients. However, a significant number of patients who have experienced ST elevation myocardial infarction (STEMI) fail to reach their LDLc goals within one month of receiving maximum-dose statin therapy. Identifying predictors of statin response may facilitate the timely intensification of lipid-lowering treatments for individuals who do not achieve their LDLc targets. Purpose The objective of this study was to assess whether the neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and/or platelet-to-lymphocyte ratio (PLR) could serve as predictors of response to high-dose statin therapy one month following a STEMI. Methods The study included 267 consecutive patients admitted with STEMI who underwent percutaneous coronary intervention. All patients, statin-naïve before admission, received statin treatment at the maximum dose (rosuvastatin 40 mg). Patients were divided into two groups based on how they responded to lipid-lowering treatment at one month: group 1 (n = 211)—LDLc levels at one month ≥ 55 mg/dL, and group 2 (n = 156)—LDLc levels 55 mg/dL. For all patients, the inflammatory markers NLR, MLR, and PLR were calculated upon admission. Additionally, the lipid profile was assessed at baseline and re-evaluated during the one-month follow-up. Results At baseline, no patient had LDLc lower than 55 mg/dL. There was no significant difference in lipid profile at baseline between the two groups (all p 0.05). At one month, only 41.49% of patients reached the LDLc target. Patients in group 1 exhibited significantly higher values of NLR (5.20 ± 2.18; 3.67 ± 1.79; p 0.0001), MLR (0.47 ± 0.13; 0.39 ± 0.12; p= 0.004), and PLR (141.20 ± 66.19; 110.20 ± 43.87; p 0.0001) in comparison to patients in group 2. Univariate regression analysis revealed that NLR (R2= 0.79; p 0.0001) is a strong independent predictor of response to high-dose statin therapy, whereas MLR (R2= 0.07; p 0.01) and PLR (R2= 0.17; p 0.0001) are weak predictors. In ROC analysis, a NLR 4.06 predicted that a patient will not reach the LDLc target at one month follow-up with 70.62% sensitivity and 87.18% specificity. Conclusion(s) Our findings underscore the importance of inflammatory markers in predicting statin response following STEMI. Despite maximum-dose rosuvastatin therapy, only less than a half of patients achieved LDLc targets within one month. Among the assessed markers, NLR emerged as a strong predictor of treatment response, while MLR and PLR were less, but still effective predictors. Timely identification of patients who exhibit a poor response to maximum statin therapy within one month could enable the prompt intensification of lipid-lowering treatments, thereby increasing the chances of reaching earlier LDLc targets in secondary prevention.
Halatiu et al. (Sat,) studied this question.