CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 5, November/December 2023 274 AFRICA blood (5 ml) was drawn from each patient in the other groups in the morning, the day after admission. The blood samples were collected into separation gel coagulation-promoting tubes, gently turned upside down five to six times, and stood vertically for 30 minutes, followed by centrifugation at 3 000 r/min for 15 minutes. Then 15 μl of upper-layer serum was aspirated and stored at 4°C for tests within 48 hours. Serum Lp-PLA2 concentration was measured by enhanced immunoturbidimetry using the Norman scattering turbidimetric analyser. In detail, reagent R1 [240 μl; 200 mmol/l pH 6.5 phosphate-buffered saline (PBS) and 1.30% PEG6000] and serum (12 μl) were well mixed. Then the mixture was added to reagent R2 (60 μl; 200 mmol/l pH 8.0 PBS and 0.2 g/l sensitised latex particles of mouse anti-human Lp-PLA2 monoclonal antibody) and immediately tested. According to the American Heart Association, the severity of coronary artery stenosis was assessed using the Gensini scoring system.6 The coronary artery consists of left main coronary artery (LM), left anterior descending branch (LAD), left circumflex branch (LCX) and right coronary artery (RCA). There were no abnormal findings, and stenosis of ≤ 25, 26–50, 51–75, 76–90, 91–99 and 100% were recorded as 0, 1, 2, 4, 8, 16 and 32 points, respectively. The diseased coronary artery was multiplied by the corresponding coefficient value: LM × 5, proximal LAD × 2.5, mid LAD × 1.5, distal LAD × 1, first diagonal branch × 1, second diagonal branch × 0.5, proximal LCX × 2.5, distal LCX and posterior descending branch × 1, posterior lateral branch × 0.5, proximal/mid/distal RCA and posterior descending branch × l. The score was calculated as follows: weight coefficient of coronary artery stenosis × weight coefficient of each diseased vessel, and the score of each branch was added up to obtain the total score. Statistical analysis SPSS21.0 software (IBM Inc, USA) was used for statistical analysis. Measurement data are described as mean ± standard deviation, and count data are described as rate (%). The homogeneity test of variance was first conducted onmeasurement data, and the data were compared by the t-test among groups in the case of homogeneity of variance and by the rank sum test among groups in the case of heterogeneity of variance. Count data were compared by the χ2 test or Fisher’s exact probability test. Linear correlation analysis was performed for variables. A value of p < 0.05 was considered statistically significant. Results No statistically significant differences were found in height, weight, BMI, and levels of TG, LDL-C and HDL-C in the UA, AMI and control groups (p > 0.05) (Table 1). The serum Lp-PLA2 concentrations significantly increased in both the AMI (313.81 ± 133.41 ng/ml) and UA groups (259.11 ± 121.45 ng/ml) compared with those in the control group (227.56 ± 118.84 ng/ml) (p < 0.05). There were no significant differences in the serum Lp-PLA2 concentrations between the UA and AMI groups (p > 0.05) (Fig. 1). Compared with the UA group, the AMI group had significantly increased levels of hs-CRP (3.80, 2.50–15.35 vs 1.75, 1.10–3.32 mg/l) and TNI (1.94, 0.09–8.94 vs 0, 0 ng/ml), and increased Gensini score (46.00, 36.00–78.00 vs 18.00, 8.00– 36.50) (p = 0.00, 0.00, 0.00). The UA group had increased levels of hs-CRP (3.00–4.53 mg/l) and higher Gensini score (27.81– 33.81) compared with those of the control group (p = 0.04, 0.00), while the TNI level had no significant difference between the two groups (p > 0.05) (Table 2). With serum Lp-PLA2 concentration as a dependent variable, and hs-CRP, TG, LDL-C, HDL-C, TNI and Gensini score as independent variables, the analysis results showed that Lp-PLA2 concentration was positively correlated with BMI and hs-CRP, LDL-C and TNI levels (p < 0.05) (Table 3, Figs 2–5). Discussion As the most common cardiovascular disease in China currently, coronary heart disease, characterised by high mortality and disability rates, has brought great economic and psychological burdentofamiliesandsociety.ACS, oneof themost commontypes of coronary heart disease in the clinic, has become the primary Table 1. General data (mean ± SD) Item UA group (n = 72) AMI group (n = 21) Control group (n = 72) Height (m) 1.65 ± 0.75 1.68 ± 0.83 1.63 ± 0.73 Body weight (kg) 68.80 ± 10.21 71.14 ± 8.38 68.61 ± 9.57 BMI (kg/m2) 24.98 ± 3.09 25.19 ± 2.80 25.56 ± 3.16 TG (mmol/l) 1.71 ± 0.94 1.65 ± 0.74 1.66 ± 0.89 LDL-C (mmol/l) 2.67 ± 0.76 2.78 ± 0.89 2.68 ± 0.62 HDL-C (mmol/l) 1.04 ± 0.22 1.04 ± 0.22 1.14 ± 0.22 AMI: acute myocardial infarction; BMI: body mass index; HDL-C: high-density lipoprotein cholesterol; LDL-C: low-density lipoprotein cholesterol; TG: triglyceride; UA: unstable angina. 600.00 400.00 200.00 0.00 UA AMI Control Lp-PLA2 (ng/ml) Fig. 1. Serum Lp-PLA2 levels. AMI: acute myocardial infarction; Lp-PLA2: lipoprotein-associated phospholipase A2; UA: unstable angina. Table 2. Biochemical indices and Gensini scores Item UA group (n = 72) AMI group (n = 21) Control group (n = 72) hs-CRP (mg/l) 1.75 (1.10–3.32) 3.80 (2.50–15.35) 2.70 (1.40–4.65) TNI (ng/ml) 0 1.94 (0.09–8.94) 0 Gensini score 18.00 (8.00–36.50) 46.00 (36.00–78.00) 0 AMI: acute myocardial infarction; hs-CRP: high-sensitivity C-reactive protein; TNI: troponin I; UA: unstable angina.
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