Macrovascular complications are the main cause of death and disability in patients with T2DM, with their pathological basis being AS. Carotid AS is known to be the hallmark of systemic AS and is a strong predictor of cardiovascular events. It has been reported that the incidence of carotid plaque correlates significantly with the existence of AS, which closely reflects the overall severity of AS in the vascular system [
4‐
7]. Endothelial injury and dysfunction caused by metabolic disorders associated with diabetes are important causes for initiating and promoting AS [
8]. In this study, age, sex, WHR, hypertension, diabetic nephropathy, Lip (a), LDL-C, HDL-C, HDL-C/LDL-C, residual cholesterol, HbA1c, and the HOMA index were evaluated in hospitalized T2DM patients The relationship between IR, CEA, CA199, and carotid AS and the predictive power of each risk factor was evaluated. The results showed that inpatients with T2DM had poor blood glucose control with the mean HbA1c of the two groups being greater than 9%. T-test analysis showed that the blood glucose levels 2 h after a meal in patients with carotid artery plaque were significantly higher than that measured in patients without carotid artery plaque. The proportions of either male patients with carotid plaque or patients with hypertension were significantly higher in the group without carotid plaque. Previous studies have reported that low eGFR or high albuminuria are high-risk factors for cardiovascular events in patients with diabetes [
9,
10]. Another observational study showed no significant association between eGFR level and atherosclerotic lesions in T2DM, although albuminuria was associated closely with AS in these patients [
11].
The current study showed that eGFR in patients with carotid plaque was significantly lower than that in the group without carotid plaque, with the proportion of urinary microalbumin/creatinine ≥ 30 mg/g in the group with carotid plaque being significantly higher than that in the group without carotid plaque. However, eGFR and high albuminuria were not risk factors for carotid plaque after adjustment for confounding factors. Follow-up studies are therefore needed for further analysis of these relationships. We also found that the CEA level in the carotid plaque group was higher than that in the control group, although to date no correlation between these two variables has been reported. The specific mechanism, therefore, needs to be studied in greater detail. Multivariate analysis showed that age, duration of diabetes, blood pressure, WHR, and Lip (a) level were independent risk factors for T2DM patients with carotid artery plaque (
P < 0.05). HDL is an anti-AS plasma lipoprotein and a protective factor of coronary heart disease, and is commonly known as a “vascular scavenger”. In this study, there was no significant difference in HDL-C levels in hospitalized T2DM patients. We observed that advanced age was a risk factor for carotid arteriosclerosis, again emphasizing age as a clinical risk factor for ASCVD events [
12]. LDL-C level has always been the main lipid target for preventing CVD in patients with T2DM [
13]. However, in the current study, there was no statistically significant difference between the two groups, although the mean value of LDL-C in patients without carotid plaque was close to 2.6 mmol/L while the value in patients with carotid plaque was greater than 1.8 mmol/L. From the perspective of the latest CDS guidelines, LDL-C combined with carotid plaque does not achieve the goal of control. The HDL-C/LDL-C ratio, a CVD predictor, reflects the protective and atherogenic lipoprotein balance [
14] and is also considered a predictor of plaque vulnerability and coronary fatty plaque [
15]. However, we observed no significant difference in the HDL-C/LDL-C ratio between the two groups. There is increasing evidence that Lip(a) may be a determinant of the risk of residual CVD when LDL-C is controlled at standard targets [
16]. We, therefore, investigated the relationship between plasma Lip(a) levels and carotid AS in patients with T2DM. However, there have been conflicting results regarding the relationship between Lip(a) levels and CVD risk in patients with diabetes, with some studies reporting a positive correlation between carotid AS and Lip(a) levels in both the general population and patients with diabetes [
17], whereas some studies have reported no significant correlation between the two variables [
18]. For example, a large prospective study over 10 years showed only a moderately positive or no correlation [
19] between Lip(a) levels and future CVD in patients with T2DM [
20,
21]. The current study further confirmed the positive effect of Lip (a) in promoting carotid plaque formation, although the mechanism of this effect requires further investigation. Studies have suggested that oxidized Lip(a) is related to the promotion of an anti-fibrinolytic environment, foam cell formation, generation of fatty streaks, and an increase in smooth muscle cells, that together promote the formation of AS [
22]. However, the specific mechanism of this effect needs to be further investigated in our follow-up studies. IR has been proved to be common before the onset of T2DM and plays an important role in the occurrence and development of AS [
23,
24]. In the current study, no significant difference was observed in the HOMA index between the two groups, a result inconsistent with the conclusions of previous studies. This difference may be related to the non-onset patients and the influence of insulin and other drugs used by patients in our study. We also found that the WHR correlated strongly with carotid plaque load. There is evidence that an increased WHR is a key determinant of atherosclerotic burden in overweight subjects [
25,
26] with studies also showing that the ratio is more strongly associated with all-cause mortality and incidence of myocardial infarction in obese subjects [
27] than that of BMI. The pathophysiological association between abdominal obesity and CVD remains challenging. Adipocyte hypertrophy may be the first marker of mitochondrial dysfunction, which may lead to adipose tissue dysfunction and inflammatory response [
28]. Previous studies have shown that WHR has good diagnostic consistency with abdominal fat measured by CT [
29], although we did not use CT scans or whole-body dual energy X-ray absorptiometry to assess abdominal fat in our study. However, taken together, the above results show that patients with abdominal obesity and T2DM are at greater risk of developing AS. At the same time, our analysis found that the prediction of T2DM with carotid plaque after four risk factors of age, WHR, disease duration and Lip (a) was high (AUC: 0.816; P < 0.001).