SA JOURNAL OF DIABETES & VASCULAR DISEASE RESEARCH ARTICLE VOLUME 21 NUMBER 1 • November 2024 17 All peripheral venous blood samples were collected early in the morning after overnight fasting (eight hours minimum) and the results were collected retrospectively from the medical records. The laboratory indicators mainly included fasting blood glucose (FBG), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C). The TyG index was calculated as: ln [fasting TG (mg/dl) × FBG (mg/dl)/2].7 The unit conversion of blood glucose: 1 mmol/l = 18.0 mg/dl, unit conversion of TG: 1 mmol/l = 88.6 mg/dl. According to the tertiles of TyG index, the 300 patients were divided into a T1 group (TyG index ≤ 8.7994, n = 100), a T2 group (8.8133 < TyG index ≤ 9.4635, n = 100) and a T3 group (TyG index > 9.4635, n = 100). The results of CAG were collected, and the number of coronary artery lesions and the degree of stenosis of each vessel were recorded. The total Gensini score was calculated according to The Guide for Gensini Score Calculation.8 The Gensini score was used to evaluate the severity of PCAD. According to the median of the Gensini score, a score ≤ 24 was defined as mild CAD, and a score > 24 was defined as severe CAD. We followed up the 300 patients for 15 months. Patients who underwent planned coronary stent re-implantation were excluded from the study. All re-admitted patients presented with symptoms of cardiogenic chest pain as their primary complaints. Each re-admitted patient underwent a routine cardiology examination and CAG. For patients with multiple re-admissions, the endpoint was determined as the hospitalisation time at which MACE occurred during the follow up. The primary end point of our study was the occurrence of MACE, which included re-admission with chest pain, coronary artery revascularisation, in-stent restenosis, heart failure, arrhythmias and haemorrhagic events. According to the presence or absence of MACE, the 300 patients were divided into a MACE group (n = 80) and a non-MACE group (n = 220). Statistical analysis IBM SPSS version 26.0 software was used for statistical analysis. The Shapiro–Wilk and Kolmogorov–Smirnov tests were performed to determine whether the research data had conformed to a normal distribution. Continuous variables are expressed as mean ± standard deviation (SD) or median interval and interquartile (IQR) values, and compared using the Student’s t-test or ANOVA test in the case of normal distribution, or the Mann–Whitney U-test or Kruskal–Wallis H-test in the case of non-normal distribution. Categorical variables are expressed as counts and percentages and were compared using the chi-squared or Fisher exact test. The relationship between the TyG index and the severity and MACE of PCAD were analysed through multivariable logistic regression analysis, and the predictive value was detected using receiver operating characteristic (ROC) curves. A p-value of less than 0.05 was considered to be statistically significant. Results The variables were compared between the three groups (T1, T2 and T3). The results showed that among the three groups, the patients’ proportion of smoking, drinking, hypertension, diabetes, body mass index (BMI), and levels of FBG, TC, TG, HDL-C, LDL-C and Gensini score showed significant differences (all p < 0.05), but age, male gender and family history of CAD showed no significant differences (all p > 0.05) (Table 1). On multivariable logistic regression analysis, with the T1 group as the reference group, the higher tertile of the TyG index was significantly associated with severity of PCAD after unadjusting for any factors (OR: 3.273, 95% CI: 1.745–6.137 for the T2 group, and OR: 5.211, 95% CI: 2.758–9.845 for the T3 group). After further adjustment for other confounding factors, the increased TyG index was associated with an increased risk of suffering from severe PCAD (all p < 0.05) (Fig. 1). According to the presence or absence of MACE, the 300 patients were divided into a MACE group (n = 80) and a non-MACE Table 1. Clinical characteristics and laboratory tests of patients with different TyG levels T1 group T2 group T3 group Variables (n = 100) (n = 100) (n = 100) F/χ2/Z p-value Age (year), mean ± SD 49.83 ± 7.24 50.32 ± 8.06 49.89 ± 7.12 0.128 0.880 Males, n (%) 65 (65.00) 69 (69.00) 68 (68.00) 0.394 0.821 Smoking, n (%) 18 (18.00)ab 32 (32.00)c 46 (46.00) 18.015 < 0.001 Drinking, n (%) 13 (13.00)ab 25 (25.00)c 39 (39.00) 17.751 < 0.001 Hypertension, n (%) 31 (30.00)ab 46 (46.00)c 62 (62.00) 19.331 < 0.001 Diabetes, n (%) 9 (9.00)ab 20 (20.00)c 7 (37.00) 23.193 < 0.001 Family history of CAD, n (%) 24 (24.00) 28 (28.00) 30 (30.00) 0.940 0.625 BMI (kg/m2), mean ± SD 24.44 ± 3.59ab 26.23 ± 3.12c 27.19 ± 3.10 18.129 < 0.001 FBG (mmol/l), mean 4.95ab 5.44c 7.69 94.158 < 0.001 (min–max) (4.39–5.61) (4.95,6.73) (6.19–10.36) TC (mmol/l), mean 3.67ab 3.87c 4.32 23.765 < 0.001 (min–max) (3.15–4.22) (3.38,4.44) (3.64–5.01) TG (mmol/l), mean 1.18ab 1.96c 3.30 201.300 < 0.001 (min–max) (0.94–1.48) (1.66–2.47) (2.61–4.38) HDL-C (mmol/l), mean ± SD 1.12 ± 0.23ab 1.01 ± 0.20c 0.91 ± 0.21 25.068 < 0.001 LDL-C (mmol/l), mean ± SD 2.50 ± 0.74b 2.69 ± 0.88 2.91 ± 0.92 5.601 0.004 Gensini score, mean 17.50ab 24.00c 47.00 90.874 < 0.001 (min–max) (10.00–22.00) (12.50–36.00) (32.00–60.00) CAD: coronary artery disease, BMI: the body mass index, FBG: fasting plasma glucose, TC: total cholesterol, TG: triglycerides, HDL-C: high-density lipoprotein cholesterol, LDL-C: low-density lipoprotein cholesterol. aT2 group vs T1 group, p < 0.05; bT3 group vs T1 group, p < 0.05; cT3 group vs T2 group, p < 0.05.
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