RESEARCH ARTICLE SA JOURNAL OF DIABETES & VASCULAR DISEASE 18 VOLUME 21 NUMBER 1 • November 2024 group (n = 220). Subjects with MACE showed a higher proportion of smoking, drinking, hypertension and diabetes, and also higher levels of BMI, FBG, TG, Gensini score and TyG index, but lower HDL-C levels (all p < 0.05) (Table 2). Univariable logistic regression analyses showed smoking, drinking, hypertension, diabetes, BMI, FBG, TG, HDL-C and TyG index were associated with MACE. The variables selected by univariable logistic regression (p < 0.05) were analysed in the multivariable logistic regression analysis. FBG, TG and Gensini score were excluded because the TyG index had a strong correlation with FBG, TG and Gensini score (rs = 0.596, 0.881, 0.601; p < 0.001). Multivariable logistic regression analysis showed smoking (OR: 2.387, 95% CI: 1.034–5.510; p = 0.042), hypertension (OR: 2.156, 95% CI: 1.114–4.172; p = 0.023), diabetes (OR: 2.351, 95% CI: 1.151–4.805; p = 0.019) and TyG index (OR: 4.653, 95% CI: 2.541–8.522; p < 0.001) were possible independent risk factors for MACE. HDL-C (OR: 0.130, 95% CI: 0.021–0.808; p = 0.029) was an independent protective factor for MACE (Table 3). The results showed that among the three groups, re-admission, coronary artery revascularisation and in-stent restenosis showed significant differences (all p < 0.05). However, heart failure, arrhythmia and haemorrhagic events showed no significant differences (all p > 0.05) (Table 4). Patients with a high Gensini score (> 24) and patients with MACE were defined as positive, and possessed sensitivity analysis. The area under the ROC curve for predicting severity of PCAD, sensitivity, specificity and Youden index were 0.833 (95% CI: 0.789–0.877), 0.678, 0.801 and 0.479, respectively (Table 5, Fig. 2). The area under the ROC curve for predicting MACE of PCAD, sensitivity, specificity and Youden index were 0.807 (95% CI: 0.752–0.862), 0.500, 0.955 and 0.495, respectively (Table 5, Fig. 2). Discussion PCAD is an aggressive disease with high rates of recurrent events and mortality. The coronary artery lesions of PCAD are unstable plaques, which are prone to develop from single-vessel lesions into new multi-vessel lesions at an early stage. This high rate of MACE has persisted despite the advent of drug-eluting stents, and antiplatelet and lipid-lowering drugs.9 Therefore, compared with treatment of the disease, early prevention of coronary atherosclerosis is very important. Fig. 1. Multivariable regression analysis for association of TyG index with the severity of PCAD. Model 1: adjusted for smoking, drinking, hypertension, diabetes. Model 2: Model 1+ adjusted for BMI, TC, HDL-C. Table 2. Comparison of baseline characteristics of MACE and non-MACE patients MACE non-MACE group group Variables (n = 80) (n = 220) t/χ2/Z p-value Age (year), mean ± SD 49.18 ± 6.75 50.32 ± 7.70 1.174 0.241 Males, n (%) 57 (71.25) 145 (65.91) 0.761 0.383 Smoking, n (%) 44 (55.00) 52 (23.64) 26.521 < 0.001 Drinking, n (%) 32 (40.00) 45 (20.45) 11.747 0.001 Hypertension, n (%) 56 (70.00) 83 (37.73) 24.573 < 0.001 Diabetes, n (%) 35 (43.75) 31 (14.10) 30.074 < 0.001 Family history of CAD, n (%) 26 (32.50) 56 (25.45) 1.466 0.226 BMI (kg/m2), mean ± SD 26.90 ± 3.01 25.61 ± 3.55 –2.898 0.004 FBG (mmol/l), mean (min–max) 7.48 (5.40–10.25) 5.30 (4.71–6.56) –6.047 < 0.001 TC (mmol/l), mean (min–max) 4.11 (3.37–4.91) 3.88 (3.38–4.52) –1.272 0.203 TG (mmol/l), mean (min–max) 2.91 (1.99–4.56) 1.71 (1.22–2.48) –6.810 < 0.001 HDL-C (mmol/l), mean ± SD 0.89 ± 0.19 1.06 ± 0.22 6.034 < 0.001 LDL-C (mmol/l), mean ± SD 2.73 ± 0.91 2.69 ± 0.85 –0.397 0.692 Gensini score, mean (min–max) 46 (32–65) 20 (12–32) –7.993 < 0.001 TyG index, mean ± SD 9.83 ± 0.79 8.96 ± 0.59 –8.920 < 0.001 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.
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