CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 AFRICA 83 Methods We included 1 103 patients with a diagnosis of acute myocardial infarction who underwent coronary angiography between January 2017 andDecember 2021. The inclusion criteria were as follows: 403 patients with ST-elevation myocardial infarction (STEMI) and 700 with non-ST-elevation myocardial infarction (NSTEMI) who were diagnosed based on the European Society of Cardiology guidelines on the fourth universal definition of myocardial infarction.10 The hospital angiographic records were screened retrospectively. We excluded patients with cardiogenic shock, severe infection, major surgery, bleeding, aortic dissection, myocarditis, endocarditis, hypertrophic cardiomyopathy, acute pulmonary embolism, stroke and tumour over the previous three months. We also excluded patients with no complete clinical data or on drug therapy potentially affecting coagulation, as well as those on whom coronary angiography was not performed and medically followed up. All patients were followed up by a cardiovascular physician at an out-patient visit, and national medical records for all subjects were obtained. Long-termmajor adverse cardiac events (MACE) were defined as all-cause mortality, non-fatal re-infarction and repeat target-vessel revascularisation. The patients were divided into a MACE and a non-MACE group based on 50-month follow-up results. This study was approved by the local ethics committee (ethics committee date: 13.01.2022. number: 2022265) and complied with the Declaration of Helsinki. Current practice guidelines were followed for coronary interventions and the data were recorded in digital storage for quantitative analysis. The access site for coronary angiography was the femoral artery with the Judkins technique. Two experienced interventional cardiologists estimated the degree of coronary stenosis visually. Significant stenosis was defined as a luminal narrowing of > 50% in a major sub-epicardial vessel (left anterior descending, left circumflex or right coronary artery). After stent placement, prasugrel, ticagrelor or clopidogrel were used for at least one year, and aspirin was used indefinitely. All treatments were given following the European Society of Cardiology guidelines. The patient’s adherence to medical therapy was standardised. According to coronary angiography results, PCI, coronary artery bypass surgery or medical treatment was performed. The hospital electronic database was used for the results of laboratory parameters. All blood samples were collected within the first hour of admission and analysed in the central laboratory with an automatic blood counter, Beckman Coulter AU 2700 Plus (Beckman Coulter, Tokyo, Japan). Together with the complete blood cell count, creatinine, low-density lipoprotein cholesterol (LDL-C) and C-reactive protein (CRP) levels were measured. The NLR was defined as the absolute number of neutrophils Table 1. Baseline clinic and demographic characteristics of patients in the MACE and non-MACE groups Variables Total (n = 1 103) MACE Univariate regression No (n = 908) Yes (n = 195) HR 95% CI p-value Gender, n (%) Men 759 (68.8) 636 (70.0) 123 (63.1) ref Women 344 (31.2) 272 (30.0) 72 (36.9) 1.30 0.97–1.74 0.081 Age, years, median (range) 68.2 ± 12.3 66.3 ± 11.8 77.3 ± 10.6 1.07 1.06–1.09 < 0.001* Smoking, n (%) 212 (19.2) 189 (20.8) 23 (11.8) 0.53 0.34–0.82 0.004* Hypertension, n (%) 592 (53.7) 495 (54.5) 97 (49.7) 0.79 0.60–1.05 0.104 Diabetes mellitus, n (%) 307 (27.8) 250 (27.5) 57 (29.2) 1.13 0.83–1.54 0.445 CHD, n (%) 178 (16.1) 143 (15.7) 35 (17.9) 1.17 0.81–1.68 0.413 Hyperlipidaemia, n (%) 625 (56.7) 539 (59.4) 86 (44.1) 0.61 0.46–0.81 < 0.001* CHF, n ( %) 8 (0.7) 3 (0.3) 5 (2.6) 4.42 1.82–10.76 < 0.001* CRF, n (%) 18 (1.6) 10 (1.1) 8 (4.1) 2.11 1.01–4.42 0.048* MI type, n (%) STEMI 403 (36.5) 327 (36.0) 76 (39.0) ref NSTEMI 700 (63.5) 581 (64.0) 119 (61.0) 0.94 0.71–1.26 0.694 WBC (×10³ cells/µl) 9.5 (7.7-11.4) 9.1 (7.4–10.7) 12.5 (10.1–14.7) 1.24 1.21–1.28 < 0.001* Haemoglobin (g/dl) 13.8 ± 1.8 14 ± 1.8 13.2 ± 1.8 0.79 0.73–0.86 < 0.001* Neutrophil (×10³ cells/µl) 6.2 (4.6–7.8) 5.8 (4.4–7.1) 9.8 (7.6–12) 1.02 1.01–1.03 < 0.001* Lymphocyte (×10³ cells/µl) 2.3 (1.6–3) 2.4 (1.8–3.1) 1.6 (1.1–2.3) 0.39 0.33–0.48 < 0.001* Platelets (×10³ cells/µl) 218 (183–264) 217 (183–261) 233 (187–276) 1.03 1.01–1.06 0.007* LDL-C (mg/dl) 114 (89–140) 116 (92–142) 103.5 (78.5–132) 0.98 0.97–0.99 < 0.001* (mmol/l) 2.95 (2.31–3.63) 3.00 (2.38–3.68) 2.68 (2.03–3.42) Creatinin (mg/dl) 0.9 (0.8–1.1) 0.9 (0.8–1.1) 1.1 (0.9–1.4) 1.00 0.97–1.03 0.931 CRP (mg/dl) 5 (2.2–12) 4.3 (2.1–10) 10 (4.2–30.6) 1.01 1.01–1.01 < 0.001* NLR 2.6 (1.8–4.2) 2.2 (1.7–3.3) 6.4 (4.2–9.1) 1.02 1.01–1.03 < 0.001* PLR 98.5 (73–135.3) 91.8 (69.7–124.1) 148.6 (108.2–211.3) 1.02 1.01–1.03 < 0.001* SII 564 (382.4–941.4) 501.8 (355.9–734.1) 1403.2 (1020–2195.5) 1.03 1.01–1.05 < 0.001* Follow-up events (MACE) Mortality, n (%) 183 (16.6) 0 (0.0) 183 (93.8) – – – TVR, n (%) 13 (1.2) 0 (0.0) 13 (6.7) – – – RMI, n (%) 14 (1.3) 0 (0.0) 14 (7.2) – – – 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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