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. 2026 May 22;105(21):e48949. doi: 10.1097/MD.0000000000048949

Epidemiological characteristics of serum small dense low-density lipoprotein cholesterol: From 2017 to 2019 in Chengdu adults, China

Jing Li a, Zhaoji Lv a, Enping He a, Huanhuan Wang b,c, Liping Wu a, Yi Wei a, Hui Quan a, Shaocheng Zhang a,d,*
PMCID: PMC13201054  PMID: 42175474

Abstract

Small dense low-density lipoprotein cholesterol is a better indicator in monitoring atherosclerotic cardiovascular disease. This study was designed to explore the distribution patterns of small dense low-density lipoprotein cholesterol (SdLDL-C), SdLDL-C/(low-density lipoprotein cholesterol [LDL-C]; SLR), SdLDL-C/(high-density lipoprotein cholesterol [HDL-C]; SHR), and SdLDL-C/(apolipoprotein B; SBR) in adults in Chengdu, China. The retrospective study enrolled 1549 adults (aged 20–69 years) in Chengdu, China from 2017 to 2019. The subjects were first divided into 5 age groups to evaluated the distribution patterns of SdLDL-C, SLR, SHR, and SBR in adults in Chengdu, China, then divided into normal and dyslipidemia groups to compare the differences, and multiple lipid parameters were quantitatively analyzed the differences further. Finally, we had evaluated the correlations among SdLDL-C, SLR, SHR, and SBR and other lipids. The median concentrations of serum SdLDL-C, SLR, SHR, and SBR were 0.71 mmol/L, 0.29, 0.54, and 0.83, respectively, in adults in Chengdu, China. The levels of serum SdLDL-C, SLR, SHR, and SBR increased with age. Men had higher levels of SdLDL-C, SLR, SHR, and SBR than women. The dyslipidemia group had higher levels of SdLDL-C, SLR, SHR, and SBR than the normal group. And in the subgroups of dyslipidemia, the differences in SdLDL-C, SLR, SHR, and SBR among subgroups were statistically meaningful. SdLDL-C, SLR, SHR, and SBR were positively correlated with total cholesterol, triglycerides, LDL-C, apolipoprotein B, and non-high-density lipoprotein cholesterol, whereas inverse correlations were observed with HDL-C and apolipoprotein A1. Our study showed the distribution characteristics of serum SdLDL-C, SLR, SHR, and SBR in adults in Chengdu, China, which contributed to the growing body of evidence supporting the incorporation of advanced lipid markers into cardiovascular risk assessment frameworks, particularly for Chinese populations with unique metabolic characteristics.

Keywords: atherosclerotic cardiovascular disease, cardiovascular disease, dyslipidemia, small dense low-density lipoprotein cholesterol

1. Introduction

Cardiovascular disease (CVD) rank as the primary contributor to mortality and health complications globally. During the 3-decade period, the global prevalence of CVD exhibited a substantial increase, representing an ~2-fold growth. and cardiovascular deaths demonstrated a 1.54-fold increase.[1,2] In 2019, CVD accounted for 44.26% and 46.76% of total mortality in urban and rural regions of China, respectively,[3] and there were ~100 million Chinese adults who required cholesterol-lowering treatment to reduce their risk of CVD.[4]

Higher low-density lipoprotein cholesterol (LDL-C) or total cholesterol (TC) features of dyslipidemia are important determinants of risk for atherosclerosis and atherosclerotic cardiovascular disease (ASCVD),[5,6] which can increase the risk of death and morbidity due to CVD.[7-13] In accordance with professional consensus statements,[14,15] the reduction of LDL-C levels represents a clinically validated intervention strategy for managing lipid metabolism disorders.[16,17] LDL-C comprises 3 distinct subfractions characterized by varying particle density and size: large buoyant LDL, intermediate-density LDL and small dense low-density lipoprotein cholesterol (SdLDL-C).[18] SdLDL-C is smaller than other LDL-C subtypes and is the main component of LDL-C, which exhibits a higher invasion of blood vessel walls, lower affinity to LDL-C receptors, longer plasma half-life, and lower tolerance for oxidative stress than large buoyant LDL-C.[19] SdLDL-C particles demonstrate enhanced atherogenic potential due to their increased capacity for vascular endothelial infiltration and subsequent plaque formation.[20] SdLDL-C – level exceeding 50 mg/dL represents a meaningful and independent risk enhancer for ASCVD,[21] which suggests that SdLDL-C is a better indicator in monitoring ASCVD.[22-24] The routine evaluation of SdLDL-C levels represents an essential component of comprehensive cardiovascular risk assessment.[25]

Earlier studies in the Chinese population revealed that among patients with type 2 diabetes mellitus (T2DM) aged ≥65 years, higher levels of SdLDL-C were significantly and independently associated with the risk of cardiovascular or cerebrovascular death, acute coronary syndrome, coronary stent implantation, and stroke. Additionally, both lbLDL-C and SdLDL-C were identified as independent risk factors for the development of T2DM.[26,27] Several biological properties of Small dense low-density lipoprotein (SdLDL) could confer heightened coronary heart disease (CHD) risk. SdLDL appears to enter the arterial intima faster than large buoyant LDL (lbLDL), concentrations of SdLDL but not lbLDL predicted incident CHD independent of LDL-C, SdLDL is preferentially enriched in ApoC-III and glycated apolipoprotein B (ApoB) relative to lbLDL.[19] So, our study aimed to investigate the dispersion characteristics of SdLDL-C, along with 3 clinically significant ratios SdLDL-C/LDL-C(SLR), SdLDL-C/high-density lipoprotein cholesterol (HDL-C; SHR), and SdLDL-C/ApoB (SBR) in adults in Chengdu, China, which could provide some valuable information for CVD prevention and control in China.

2. Materials and methods

2.1. Subjects

The retrospective study enrolled adults (aged 20–69 years) from the Second Affiliated Hospital of Chengdu Medical College (Nuclear Industry 416 Hospital) for medical checkups from September 1, 2017 to August 31, 2019 (Fig. 1). The health data (physical examination, laboratory examination, and auxiliary examination) were extracted through the hospital information system. The authors did not have access to any information that could identify individual participants during or after data collection.

Figure 1.

Figure 1.

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Sampling and data obtained flowchart.

Inclusion and exclusion criteria were based on China guidelines for clinical lipid profile testing.[28,29] Briefly, the inclusion criteria were as follows: adults were permanent residents and household registrants in Chengdu, China, and the participants took part in physical examination, laboratory examination, and auxiliary examination. The exclusion criteria encompassed the following conditions: unavailability of complete clinical records or missing essential data elements. Had a fever, severe infection, or recent major surgery; pregnant or within 6 weeks after delivery; recent excessive drinking or overeating; and used hypolipidemic agents in the last 4 months. This study was approved by the Ethics Committees at the Second Affiliated Hospital of Chengdu Medical College (Nuclear Industry 416 Hospital; 201722).

2.2. Sampling and testing

The fasting blood (5 mL, heparin lithium–anticoagulated) samples were obtained by trained nurses. Centrifugation was conducted to separate serum (3000 rpm, 10 minutes). Then, serum lipids were measured within 2 hours. The concentrations of serum lipids (TC, triglycerides [TG], HDL-C, LDL-C, apolipoprotein A1 [ApoA1], ApoB, and SdLDL-C) were detected using Mindray BS2000M analyzer (Mindray Bio-Medical Electronics Co., Ltd., Shenzhen, China) to calculate non–high-density lipoprotein cholesterol, SLR, SHR, and SBR. Reagents and calibrators were purchased from Beijing Strong Biotechnologies Co., Ltd. (Beijing, China). The instructions for detection range, accuracy r, precision variation coefficient (CV) %, and R are presented in Table S1.

2.3. Statistical analysis

The normal and dyslipidemia groups were divided based on TC, TG, LDL-C, and HDL-C concentrations; then, the dyslipidemia group was divided into 6 subgroups. The lipid grouping was according to the criteria of the Joint Committee on the Chinese Guidelines for Lipid Management (2023).[5] Normal group was defined as TC < 5.2mmol/L, TG < 1.7 mmol/L, LDL-C < 3.4 mmol/L, and HDL-C > 1.0 mmol/L, and dyslipidemia group was defined as TC ≥ 5.2mmol/L, or TG ≥ 1.7 mmol/L, or LDL-C ≥ 3.4 mmol/L, and or HDL-C ≤ 1.0 mmol/L. The dyslipidemia group was divided into 6 subgroups: high TC(≥ 5.2mmol/L), high TG(≥ 1.7 mmol/L), high TC and TG(≥ 5.2mmol/L, ≥ 1.7 mmol/L), high TC and LDL-C(≥ 5.2mmol/L, ≥ 3.4 mmol/L), high TC, TG and LDL-C(≥ 5.2mmol/L, ≥ 1.7 mmol/L, ≥ 3.4 mmol/L), decreased HDL-C(≤ 1.0 mmol/L).

All statistical analyses were performed using the SPSS 26.0 statistical software (IBM, New York). Continuous variables demonstrating normal distribution were presented as mean ± standard deviation, in which intergroup comparisons were performed using independent samples t-tests, whereas the comparison involving multiple groups used 2-way analysis of variance. Median with interquartile range was used to exhibit the skewed distribution variables, in which the Mann–Whitney U test was served as analysis between 2 groups, and the Kruskal–Wallis rank sum test was used for comparison among multiple groups. Spearman’s rank correlation analysis was used to evaluate the correlation among SdLDL-C, SLR, SHR, and SBR and other lipids. The threshold for statistical significance was set at P < .05 (2-tailed) for all analyses.

3. Results

3.1. General characteristics of the study population

The study cohort comprised 1549 participants, including 1016 men and 533 women at 20 to 69 years, included 290 participants aged 20 to 29 years old, 347 participants aged 30 to 39 years old, 444 participants aged 40 to 49 years old, 277 participants aged 50 to 59 years old, and 191 participants aged 60 to 69 years old (Table S2). The median levels of TC, TG, LDL-C, HDL-C, ApoA1, ApoB, and non-HDL-C in adults were 4.65, 1.22, 2.44, 1.32, 1.39, 0.85, and 3.32 mmol/L, respectively. Men had higher TC (4.69 vs 4.57 mmol/L), TG (1.35 vs 0.94 mmol/L), LDLC (2.54 vs 2.25 mmol/L), ApoB (0.88 vs 0.78 mmol/L), and non-HDL-C (3.44 vs 3.09 mmol/L) but lower ApoA1 (1.34 vs 1.50 mmol/L; all P < .05) than women. Moreover, TC, TG, LDL-C, HDL-C, ApoA1, ApoB, and non-HDL-C increased stably with age (all P < .05, except for HDL-C) and peaked at 50 to 59 years of age (TC, 4.86; TG, 1.34; LDL-C, 2.63; HDL-C, 1.33; ApoA1, 1.42; ApoB, 0.92; and non-HDL-C, 3.53 mmol/L) and then decreased at 60 to 69 years of age.

3.2. The distribution of SdLDL-C, SLR, SHR, and SBR in adults in Chengdu, China

The median levels of SdLDL-C, SLR, SHR, and SBR in adults were 0.71 mmol/L, 0.29, 0.54, and 0.83, respectively. Men had higher median levels of SdLDL-C (0.79 vs 0.55 mmol/L), SLR (0.31 vs 0.26), SHR (0.65 vs 0.38), and SBR (0.88 vs 0.73) than women (all P < .05; Table S3).

SdLDL-C, SLR, SHR, and SBR increased stably with age (all P < .05; Fig. 2). On the one hand, among men, the concentration of SdLDL-C elevated from 0.65 mmol/L at 20 to 29 years of age to a maximum of 0.86 mmol/L at 50 to 59 years of age, the level of SLR increased from 0.28 at 20 to 29 years of age to a maximum of 0.32 at 40 to 49 years of age, the level of SHR increased from 0.54 at 20 to 29 years of age to a maximum of 0.70 at 40 to 49 years of age, and the level of SBR increased from 0.82 at 20 to 29 years of age to a maximum of 0.93 at 40 to 49 years of age. On the other hand, women followed the same pattern. The level of SdLDL-C increased from 0.45 mmol/L at 20 to 29 years of age to a maximum of 0.74 mmol/L at 50 to 59 years of age, the level of SLR increased from 0.25 at 20 to 29 years of age to a maximum of 0.30 at 60 to 69 years of age, the level of SHR increased from 0.30 at 20 to 29 years of age to a maximum of 0.53 at 60 to 69 years of age, and the level of SBR increased from 0.70 at 20 to 29 years of age to a maximum of 0.84 at 50 to 59 years of age.

Figure 2.

Figure 2.

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The comparison of SdLDL-C, SLR, SHR, and SBR in men and women in different age groups. The effect of gender was evaluated at significance levels of P < .001 (***), P < .01 (**), and P < .05 (*). SdLDL-C (A), SLR (B), SHR (C), and SBR (D) for distribution patterns. ApoB = apolipoprotein B, HDL-C = high-density lipoprotein cholesterol, LDL-C = low-density lipoprotein cholesterol, SBR = SdLDL-C/ApoB, SHR = SdLDL-C/HDL-C, SdLDL-C = small and dense low-density lipoprotein cholesterol, SLR = SdLDL-C/LDL-C.

3.3. The distribution of SdLDL-C, SLR, SHR, and SBR levels in the normal and dyslipidemia groups

First, the dyslipidemia group had significantly elevated median concentrations of of SdLDL-C, SLR, SHR, and SBR than the normal group in total (Table S4 and Fig. 3; SdLDL-C, 0.96 vs 0.53 mmol/L; SLR, 0.34 vs 0.26; SHR, 0.80 vs 0.39; and SBR, 0.99 vs 0.72), man (SdLDL-C, 0.98 vs 0.59 mmol/L; SLR, 0.35 vs 0.27; SHR, 0.85 vs 0.46; and SBR, 1.02 vs 0.76), and women (SdLDL-C, 0.86 vs 0.48 mmol/L; SLR, 0.30 vs 0.24; SHR, 0.62 vs 0.32; and SBR, 0.93 vs 0.69; all P < .001). Second, the distribution of SdLDL-C, SLR, SHR, and SBR levels in the normal and dyslipidemia groups followed the same pattern: the level of SdLDL-C increased from 0.45 mmol/L to a maximum of 0.62 mmol/L, SLR increased from 0.25 to a maximum of 0.27, SHR increased from 0.32 to a maximum of 0.48, and SHR increased from 0.70 to a maximum of 0.77 at 20–29 to 50 to 59 years of age in the normal group. The concentration of SdLDL-C increased from 0.83 mmol/L to a maximum of 1.02 mmol/L, SLR increased from 0.32 to a maximum of 0.36, SHR increased from 0.74 to a maximum of 0.86, and SHR increased from 0.95 to a maximum of 1.02 at 20–29 to 50–59 years of age in the dyslipidemia group (Table S4). Furthermore, the dyslipidemia group demonstrated significantly elevated concentrations of SdLDL-C, SLR, SHR, and SBR compared to normal group in all age groups. (all P < .001; Fig. 4).

Figure 3.

Figure 3.

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The comparison of SdLDL-C, SLR, SHR, and SBR levels in total between the normal and dyslipidemia groups. The effects of the groups were evaluated at the significance level of P < .001 (***). SdLDL-C (A), SLR (B), SHR (C), and SBR (D) for distribution patterns. ApoB = apolipoprotein B, HDL-C = high-density lipoprotein cholesterol, LDL-C = low-density lipoprotein cholesterol, SBR = SdLDL-C/ApoB, SHR = SdLDL-C/HDL-C, SdLDL-C = small and dense low-density lipoprotein cholesterol, SLR = SdLDL-C/LDL-C.

Figure 4.

Figure 4.

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The comparison of SdLDL-C, SLR, SHR, and SBR at different age groups between the normal and dyslipidemia groups. The effects of the groups were evaluated at the significance level of P < .001 (***). SdLDL-C (A), SLR (B), SHR (C), and SBR (D) for distribution patterns. ApoB = apolipoprotein B, HDL-C = high-density lipoprotein cholesterol, LDL-C = low-density lipoprotein cholesterol, SBR = SdLDL-C/ApoB, SHR = SdLDL-C/HDL-C, SdLDL-C = small and dense low-density lipoprotein cholesterol, SLR = SdLDL-C/LDL-C.

3.4. The distribution of SdLDL-C, SLR, SHR, and SBR in the subgroups of dyslipidemia

Then, we analyzed SdLDL-C, SLR, SHR, and SBR in the subgroups of dyslipidemia, statistically significant differences were observed among the subgroups (all P < .001). The highest level of SdLDL-C (1.40 mmol/L) was in Subgroup 5, and the lowest level of SdLDL-C (0.69 mmol/L) was in Subgroup 6. The highest level of SLR (0.39) was in subgroup 3, and the lowest level of SLR (0.28) was in subgroup 1. The highest level of SHR (1.15) was in subgroup 5, and the lowest level of SHR (0.57) was in subgroup 1. The highest level of SBR (1.14) was in subgroup 3, and the lowest level of SBR (0.85) was in subgroup 1 (Table S5, Fig. 5).

Figure 5.

Figure 5.

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The comparison of SdLDL-C, SLR, SHR, and SBR in the subgroups of dyslipidemia. SdLDL-C (A), SLR (B), SHR (C), and SBR (D) for distribution patterns. ApoB = apolipoprotein B, HDL-C = high-density lipoprotein cholesterol, LDL-C = low-density lipoprotein cholesterol, SBR = SdLDL-C/ApoB, SHR = SdLDL-C/HDL-C, SdLDL-C = small and dense low-density lipoprotein cholesterol, SLR = SdLDL-C/LDL-C.

3.5. The correlation of SdLDL-C, SLR, SHR, and SBR with lipids in Chinese population

The levels of SdLDL-C, SLR, SHR, and SBR were positive associations with TC, TG, LDL-C, ApoB, and non-HDL-C while showing inverse relationships with HDL-C and ApoA1 (all P < .001; Table S6, Fig. 6).

Figure 6.

Figure 6.

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The correlation between SdLDL-C, SLR, SHR, and SBR and lipids in the Chinese population. The effects of the groups were evaluated at the significance level of P < .001 (***). ApoA1 = apolipoprotein A1, ApoB = apolipoprotein B, HDL-C = high-density lipoprotein cholesterol; LDL-C = low-density lipoprotein cholesterol, non-HDL-C = non-high-density lipoprotein cholesterol, SBR = SdLDL-C/ApoB, SHR = SdLDL-C/HDL-C, SdLDL-C = small and dense low-density lipoprotein cholesterol, SLR = SdLDL-C/LDL-C, TC = total cholesterol, TG = triglycerides.

4. Discussion

Our study investigated the distributions of SdLDL-C, SLR, SHR, and SBR in adults in Chengdu, China. The results indicated a steady increase in SdLDL-C, SLR, SHR, and SBR levels with age. Men exhibited higher median serum lipid levels than women. Furthermore, individuals with dyslipidemia demonstrated significantly elevated concentrations of SdLDL-C, SLR, SHR, and SBR than normal lipid profiles. At the same time, the levels of SdLDL-C, SLR, SHR, and SBR had obvious differences in the dyslipidemia subgroups. Furthermore, SdLDL-C, SLR, SHR, and SBR were positive associations with TC, TG, and LDL-C while showing inverse relationships with HDL-C and ApoA1.

Our study identified that age and gender were crucial and influential elements for variations of SdLDL-C, SLR, SHR, and SBR in the Chinese population. On the one hand, age-related trends of SdLDL-C and SLR were similar to the findings of Toshihide Izumida’s research[30]; we found that SdLDL-C, SLR, SHR, and SBR exhibited an age-dependent rise, SdLDL-C reached its maximum at 50 to 59 years of age, SLR attained peak levels at 60 to 69 years of age. Toshihide Izumida’s research showed that in men, SdLDL-C and SLR increased with aging, culminated at 50 to 54 years of age, subsequently declined; SdLDL-C and SLR increased until 65 years of age and then decreased among women. On the other hand, men had elevated concentrations of SdLDL-C, SLR, SHR, and SBR compared to women, which may be the reason that estrogens enhance vascular endothelial function through upregulation of nitric oxide synthesis, thereby promoting maintenance of favorable lipoprotein homeostasis.[31] However, these protective physiological mechanisms undergo significant attenuation following menopause, consequently leading to an elevated susceptibility to cardiovascular disorders in postmenopausal women.[32]

These trends highlight age- and sex-specific variations in cardiovascular risk factors. The study reveals significant sex-based disparities in atherogenic lipid markers, with men maintaining consistently higher levels. Both sexes demonstrate age-dependent increases, but women show delayed peak levels compared to men (typically 10–20 years later).

The present sduty explored the levels of SdLDL-C, SLR, SHR, and SBR between the dyslipidemia and normal groups. The findings of the present investigation demonstrated that the dyslipidemia group significantly elevated concentrations of SdLDL-C, SLR, SHR, and SBR compared to the normal group, and elevated concentrations of SdLDL-C, SLR, SHR, and SBR that may be related to smoking, increased energy intake, and reduced physical activity levels were more prevalent among men.[33,34] In contrast, women had a lower prevalence of dyslipidemia, which may be linked to the protective effect of estrogens.[35,36] Furthermore, we found that age and gender play roles in variations of SdLDL-C, SLR, SHR, and SBR with dyslipidemia, and these findings are consistent with Munire Mutalifu’s findings.[37] Previous studies have confirmed metabolic disorders with high SdLDL-C concentrations, for example, obesity,[20,38] metabolic syndrome,[39,40] systemic hypertension,[41] hepatic diseases,[42,43] and CHD.[44] SLR has been extensively utilized as a reliable surrogate biomarker in multiple investigations, demonstrating significant associations with various cardiovascular-related comorbidities.[38,41-46] Moreover, SBR is considered an atherogenic marker of dyslipidemia in participants with underlying chronic conditions.[47]

These findings confirm that dyslipidemia is linked to significantly elevated levels of atherogenic lipids (SdLDL-C, SLR, SHR, SBR) in both sexes, with men generally showing higher values than women. These findings highlighted the importance of considering both age and sex when assessing cardiovascular risk profiles. The dyslipidemia group exhibited consistently higher atherogenic lipid markers than the normal group, regardless of sex, reinforcing its association with increased cardiovascular risk. The persistent elevation of these atherogenic markers in dyslipidemia patients across all age groups underscores their potential utility in Clinical Relevance. Such as risk stratification, therapeutic monitoring, and cardiovascular prognosis.

The distributions of SdLDL-C, SLR, SHR, and SBR in the subgroups of dyslipidemia were also analyzed, which showed the significant differences in SdLDL-C, SLR, SHR, and SBR. Recent epidemiological data indicate persistently elevated prevalence rates of dyslipidemia among the adult population in China, maintaining a consistently high level.[48,49] The results of a national survey in 2018 suggested that the total prevalence of dyslipidemia in adults ≥18 years old was 35.6%.[49] The management of lipids should primarily focus on the measurement of SdLDL-C to enhance the controlling and managing of CVD risk factors.[21,23,24,50,51]

The substantial variations (SdLDL-C 2.03-fold difference between extremes, SLR 39% relative difference, SHR: 2.02-fold difference, SBR: 34% relative difference) highlight the importance of subgroup stratification in dyslipidemia management. The significant inter-subgroup variations suggest distinct metabolic patterns within dyslipidemia populations. We hoped to provide SdLDL-C, SLR, SHR, SBR relative differences for references of clinical significance.

Finally, the relationships between SdLDL-C and lipids were estimated. SdLDL-C, SLR, SHR, and SBR were positive associated with TC, TG, and LDL-C, whereas were negative linked to HDL-C and ApoA1. Existing research has consistently demonstrated significant associations between elevated SdLDL-C concentrations and multiple lipid biomarkers, including TG,[20,39] TC,[39,42] LDL-C,[20,39,42] and ApoB.[40,47]

The measured markers (SdLDL-C, SLR, SHR, SBR) share common metabolic pathways with conventional lipid parameters. Their inverse relationship with protective lipids (HDL-C, ApoA1) reinforces their atherogenic potential. And the parallel positive/negative associations with conventional lipid parameters support the validity of these markers in cardiovascular risk assessment.

This study had some limitations. As a retrospective study, there is a limitation regarding causality and the ability to have detailed control over variables during data collection. Moreover, there is a limitation regarding the lack of data on atherosclerotic cardiovascular diseases associated with SdLDL-C, which would undoubtedly enrich the results. Despite these shortcomings, we showed the distribution of SdLDL-C, SLR, SHR, and SBR concentrations in adults in Chengdu, China at present. We provide some clinical implications and the potential impact on cardiovascular risk assessment and management in Chinese population.

5. Conclusions

We investigated the distribution characteristics of serum SdLDL-C, SLR, SHR, and SBR in adults in Chengdu, China. The established associations between these atherogenic markers and conventional lipid parameters suggest their potential utility in: early cardiovascular risk detection, precision medicine approaches for dyslipidemia management, and monitoring therapeutic interventions. These results contribute to the growing body of evidence supporting the incorporation of advanced lipid markers into cardiovascular risk assessment frameworks, particularly for Chinese populations with unique metabolic characteristics.

Acknowledgments

We acknowledge all the recruited adults for participating in this project, and we also thank LetPub (www.letpub.com.cn) for its linguistic assistance during the preparation of this manuscript.

Author contributions

Conceptualization: Jing Li, Hui Quan, Shaocheng Zhang.

Data curation: Enping He, Liping Wu, Yi Wei.

Formal analysis: Zhaoji Lv.

Funding acquisition: Jing Li, Huanhuan Wang, Shaocheng Zhang.

Methodology: Huanhuan Wang.

Supervision: Hui Quan, Shaocheng Zhang.

Writing – original draft: Jing Li, Zhaoji Lv.

Writing – review & editing: Huanhuan Wang, Hui Quan, Shaocheng Zhang.

medi-105-e48949-s001.docx (19.5KB, docx)
medi-105-e48949-s002.docx (18.5KB, docx)
medi-105-e48949-s003.docx (18.5KB, docx)
medi-105-e48949-s004.docx (19KB, docx)
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medi-105-e48949-s006.docx (17.3KB, docx)

Abbreviations:

ApoA1
apolipoprotein A1
ApoB
apolipoprotein B
ASCVD
atherosclerotic cardiovascular disease
CVD
cardiovascular disease
HDL-C
high-density lipoprotein cholesterol
LDL-C
low-density lipoprotein cholesterol
SdLDL-C
small and dense low-density lipoprotein cholesterol
TC
total cholesterol
TG
triglycerides
SBR
SdLDL-C/ApoB
SHR
SdLDL-C/HDL-C
SLR
SdLDL-C/LDL-C

This work was supported by the Special Scientific Research Foundation of Chengdu Medical College, China (FYZX17016), the Clinical Science Research Project of Chengdu Medical College, China (24LHBBYY1-03), the Special Scientific Research Project of Sichuan Medical Association, China (2024HR21), and the Chengdu Medical Research Project of Chengdu Health Commission, China (2025588).

This study was approved by the Ethics Committees at the Second Affiliated Hospital of Chengdu Medical College (Nuclear Industry 416 Hospital; 201722). The study involves the retrospective study analysis of archived medical records and samples, the data were fully anonymized before access and analysis. And this research complies with the ethical exemption requirements outlined in the “Ethical Review Measures for Life Sciences and Medical Research Involving Humans” issued in China, the requirement for informed consent has been waived by the ethics committee.

The authors have no conflicts of interest to disclose.

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

Supplemental Digital Content is available in the online version of this article (http://dx.doi.org/10.1097/MD.0000000000048949).

How to cite this article: Li J, Lv Z, He E, Wang H, Wu L, Wei Y, Quan H, Zhang S. Epidemiological characteristics of serum small dense low-density lipoprotein cholesterol: From 2017 to 2019 in Chengdu adults, China. Medicine 2026;105:21(e48949).

JL, ZL, EH, and HW contributed to this article equally.

Contributor Information

Jing Li, Email: lijing0081@126.com.

Zhaoji Lv, Email: lvzhaoji416@163.com.

Enping He, Email: 912213736@qq.com.

Huanhuan Wang, Email: 102022065@cmc.edu.cn.

Liping Wu, Email: wing.g7@163.com.

Yi Wei, Email: 318661071@qq.com.

Hui Quan, Email: 734363678@qq.com.

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