CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 84 AFRICA divided by the absolute number of lymphocytes, and the PLR as the absolute number of platelets by the absolute number of lymphocytes. SII was calculated using the following formula: SII = NLR × total platelet count in the peripheral blood (per mm3). In hospital and 50-month follow-up events were compared with SII, NLR and PLR levels. Statistical analysis Statistical analyses of collected data were conducted using IBM SPSS Statistics for Windows 20.0 (IBM Corp, Armonk, NY, USA). Determination of the normally distributed data was conducted using the Kolmogorov–Smirnov test. Numerical variables that had normal distribution are expressed as mean ± standard deviation, while those with non-normal distribution are expressed as median (minimum–maximum). The categorical variables are expressed as numbers and percentages. Multivariable Cox logistic regression analyses were conducted to establish any possible independent predictors of MACE. Age, gender, smoking, co-morbid conditions and laboratory parameters were included in the multivariable Cox regression model. The threshold value of SII in predicting MACE was determined by the Youden index method in receiver operating characteristic (ROC) curve analysis. Survival plots according to the threshold values of SII were done with Kaplan–Meier analysis. A p-value < 0.05 was taken as statistically significant. Results The study population consisted of 1 103 patients (mean age: 68.2 ± 12.3 years) with 759 male (68.8%) and 344 female (31.2%) patients. Of the patients, 700 (63.5%) were diagnosed with NSTEMI and 403 (36.5%) with STEMI. The patients were divided into a MACE and a non-MACE group based on the in-hospital and 50-month follow-up results. MACEwasobservedin195patients(17.7%), includingall-cause mortality in 183 patients (16.6%), myocardial re-infarction in 14 patients (1.3%) and target-vessel revascularisations in 13 patients (1.2%) during the 50-month follow-up period. The demographic and clinical characteristics of the patients are shown in Table 1. In both patients groups, age, white blood cell (WBC) count, haemoglobin, neutrophil, lymphocyte, platelet, LDL-C, CRP, NLR, PLRand SII levels were determined as potential risk factors for MACE (Table 1). The data were also evaluated separately in NSTEMI and STEMI patients. In STEMI patients, age, WBC, haemoglobin, neutrophil, lymphocyte, platelet, LDL-C, CRP, NLR, PLR and SII levels were found to be potential risk factors associated with MACE (Table 2). In NSTEMI patients, age, WBC, haemoglobin, neutrophil, lymphocyte, platelet, LDL-C, CRP, NLR, PLR and SII levels were found to be potential risk factors associated with MACE (Table 3). The independent predictors of risk of MACE in the whole population and myocardial infarction subtypes in multivariate regression models, including potential risk factors, are shown in Table 4. Based on these data, age, WBC, CRP and SII Table 2. Demographic and clinical findings associated with MACE in the STEMI patients Variables Total STEMI (n = 403) MACE Univariate regression No (n = 327) Yes (n = 76) HR 95% CI p-value Gender, n (%) Men 304 (75.4) 257 (78.6) 47 (61.8) ref Women 99 (24.6) 70 (21.4) 29 (38.2) 2.00 1.25–3.18 0.004* Age, years 67.7 ± 12.6 65.9 ± 12.1 75.7 ± 11.5 1.06 1.04–1.08 < 0.001* Smoker, n (%) 109 (27.0) 94 (28.7) 15 (19.7) 0.65 0.37–1.14 0.132 Hypertension, n (%) 192 (47.6) 160 (48.9) 32 (42.1) 0.74 0.46–1.17 0.192 Diabetes mellitus, n (%) 97 (24.1) 76 (23.2) 21 (27.6) 1.22 0.74–2.03 0.430 CHD, n (%) 36 (8.9) 29 (8.9) 7 (9.2) 1.10 0.51–2.40 0.809 Hyperlipidaemia, n (%) 239 (59.3) 210 (64.2) 29 (38.2) 0.42 0.26–0.66 < 0.001* CHF, n (%) 2 (0.5) 1 (0.3) 1 (1.3) 2.84 0.39–20.41 0.301 CRF, n (%) 9 (2.2) 4 (1.2) 5 (6.6) 2.55 0.93–6.99 0.068 WBC (×10³ cells/µl) 10 (8.2–12.2) 9.6 (8–11.4) 13.2 (10.9–16) 1.24 1.18–1.3 < 0.001* Haemoglobin (g/dl) 14 ± 1.8 14.1 ± 1.7 13.5 ± 1.9 0.87 0.76–0.98 0.025* Neutrophils (×10³ cells/µl) 6.7 (5.2–8.5) 6.2 (4.9–7.5) 10.6 (9–13.4) 1.02 1.01–1.03 0.019* Lymphocytes (×10³ cells/µl) 2.3 (1.6–3) 2.4 (1.7–3.2) 1.7 (1.3–2.3) 0.46 0.34–0.62 < 0.001* Platelets (×10³ cells/µl) 217 (184–261) 212 (181–258) 240 (209–277) 1.03 1.01–1.05 0.002* LDL-C (mg/dl) 115 (90–139) 116.5 (92–142) 106.5 (80–131) 0.97 0.95–0.99 0.013* (mmol/l) 2.98 (2.38–3.60) 3.02 (2.38–3.68) 2.76 (2.07–3.39) Creatinine (mg/dl) 1 (0.8–1.2) 1 (0.8–1.2) 1.1 (0.9–1.4) 1.92 1.38–2.68 < 0.001* CRP (mg/dl) 5.7 (2.4–13.8) 4.9 (2.2–11.7) 10.7 (4.5–43.9) 1.01 1.01–1.02 < 0.001* NLR 2.9 (1.9–4.8) 2.5 (1.8–3.6) 6.4 (4.7–8.6) 1.23 1.18–1.28 < 0.001* PLR 99.6 (71.2–137.5) 92.2 (67.4–127.7) 146.3 (106.1–210.8) 1.01 1.01–1.01 < 0.001* SII 635.3 (407.3–1024) 556.7 (381–783.1) 1592.3 (1026.6–2333.8) 1.08 1.07–1.10 < 0.001* Follow-up events (MACE) Mortality, n (%) 72 (17.9) – 72 (94.7) – – – TVR, n (%) 6 (1.5) – 6 (7.9) – – – RMI, n (%) 6 (1.5) – 6 (7.9) – – – CHD: chronic heart disease, CHF: chronic heart failure, CRF: chronic renal failure, WBC: white blood cell, TVR: target-vessel revascularisation, RMI: re-myocardial infarction, LDL-C: low-density lipoprotein cholesterol, CRP: C-reactive protein, NLR: neutrophil–lymphocyte ratio, PLR: platelet–lymphocyte ratio, SII: serum immune–inflammation index, HR: hazard ratio, CI: confidence interval. Numerical variables are shown as mean ± standard deviation or median (min–max) and categorical variables as numbers (%). Levels of SII are divided into 100. *p < 0.05 indicates statistical significance.
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