Association of triglyceride-driven residual atherosclerotic risk with carotid stiffening assessed using ultrafast ultrasound imaging in individuals with hypertriglyceridemia

Article information

Ultrasonography. 2026;45(3):298-310

Publication date (electronic) : 2026 March 17

doi : https://doi.org/10.14366/usg.26047

Ping Dai^1,*, Zhengqiu Zhu^1,*, Xuezhong Jiang², Hui Gao¹, Xuehui Ma¹, Yinping Wang¹, Bixiao Shen¹, Chong Zou^3,4, Yun Luan¹, Hui Huang^,1, Weiming Ge^,5

¹Department of Ultrasound, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, China

²Department of Ultrasound, Jiangsu Province Geriatric Hospital, Geriatric Hospital of Nanjing Medical University, Nanjing, China

³Department of Cardiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, China

⁴Center of Good Clinical Practice, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, China

⁵Department of Geriatrics, Jiangsu Province Geriatric Hospital, Geriatric Hospital of Nanjing Medical University, Nanjing, China

Correspondence to: Weiming Ge, MD, Department of Geriatrics, Jiangsu Province Geriatric Hospital, Geriatric Hospital of Nanjing Medical University, 65# Jiangsu Road, Nanjing 210009, China Tel, Fax. +86-25-8331-1761 E-mail: 1270332953@qq.com

Hui Huang, MD, Department of Ultrasound, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, 155# Hanzhong Road, Nanjing 210029, China Tel, Fax. +86-25-8661-7141 E-mail: szcrhh007@vip.163.com

*These authors contributed equally to this work.

Received 2026 January 24; Revised 2026 March 13; Accepted 2026 March 16.

Abstract

Graphical abstract

Introduction

Dyslipidemia, particularly elevated low-density lipoprotein cholesterol (LDL-C), is an independent risk factor with a key role in the pathogenesis of atherosclerosis (AS) [1,2]. Mendelian randomization studies have established the critical role of LDL-C in atherosclerotic plaque formation and related cardiovascular events [3]. Extensive evidence from clinical studies [4] and trials [5] has also demonstrated that lowering LDL-C significantly reduces the risk of atherosclerotic cardiovascular disease (ASCVD). However, the Progression of Early Subclinical Atherosclerosis (PESA) study [6] revealed that approximately 50% of participants had atherosclerotic plaques despite having LDL-C levels within the normal range. In addition, multiple large randomized controlled trials have shown that achieving guideline-recommended LDL-C targets reduces only one-third of cardiovascular events, leaving two-thirds of the risk unaddressed—a phenomenon termed cardiovascular residual risk [7–9]. Accordingly, the assessment of residual cardiovascular risk has become a focus of current research.

With increasingly stringent LDL-C control in clinical practice, a substantial proportion of patients with dyslipidemia now present with hypertriglyceridemia. Hypertriglyceridemia, characterized by elevated triglyceride-rich lipoproteins (TGRLs), is considered a potential major contributor to residual atherosclerotic risk. The Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial confirmed that patients with controlled LDL-C but elevated triglyceride (TG) levels retain substantial cardiovascular risk and that targeted TG-lowering therapy is associated with a 25% risk reduction [10]. The PESA study further showed that hypertriglyceridemia is independently associated with subclinical AS even in low-risk individuals with normal LDL-C levels, reinforcing the contribution of TG to residual atherosclerotic burden [11]. However, no established method is currently available for the visual and quantitative assessment of residual atherosclerotic risk in patients with hypertriglyceridemia.

Carotid intima-media thickness (cIMT), obtained by noninvasive ultrasound, is currently recognized as a morphological marker of early AS [12] and is closely associated with ASCVD [13]. However, a large meta-analysis (n=100,667) found that cIMT has limited value for predicting cardiovascular events in the general population [14]. Moreover, the use of cIMT is constrained by limitations such as inter-operator variability, lack of standardization, and insufficient sensitivity for detecting early AS, particularly in low-risk populations [15,16]. Another study [17] indicated that carotid stiffening can occur even in individuals with normal cIMT, suggesting that functional changes in carotid stiffness may precede measurable cIMT thickening. Therefore, new approaches are necessary to assess the early progression of residual atherosclerotic risk in patients with hypertriglyceridemia, including methods that evaluate arterial stiffening.

Ultrafast pulse wave velocity (ufPWV) is a novel, convenient, noninvasive, real-time ultrasound imaging technique for measuring pulse wave velocity (PWV), with good accuracy and reproducibility in the assessment of arterial stiffness [17,18]. Unlike traditional PWV methods, ufPWV uses an ultra-high frame rate (>2,000 frames/s) to track local motion of the common carotid artery (CCA) wall in real time and to accurately measure PWV conduction in the arterial wall, thereby avoiding the large errors introduced by estimated distance and timing in conventional methods [17,19,20]. Previous studies have shown that ufPWV can quantitatively assess the presence and progression of AS in patients with early cardiovascular risk factors such as hypertension [19], chronic kidney disease [20], and diabetes [21]. According to Zhu et al. [17], ufPWV can also be used to assess AS risk in patients without such risk factors, even when LDL-C is controlled at an optimal level. Therefore, it is theoretically feasible that ufPWV could be used to evaluate residual AS risk in individuals with hypertriglyceridemia whose LDL-C levels are normal or even optimal.

This study aimed to assess the association between ufPWV-quantified carotid stiffening and residual atherosclerotic risk driven by elevated TG levels in individuals with hypertriglyceridemia, with the goal of informing timely intervention for AS progression and potentially reducing ASCVD incidence.

Materials and Methods

Study Cohort

This retrospective study initially enrolled 982 participants from the Affiliated Hospital of Nanjing University of Chinese Medicine who underwent ufPWV between January 2019 and December 2024. All participants also underwent carotid ultrasound examinations and laboratory testing, and their clinical data were collected. The following laboratory parameters were obtained after at least 8 hours of fasting: TG, total cholesterol (TC), LDL-C, high-density lipoprotein cholesterol (HDL-C), fasting blood glucose (FBG), and serum creatinine (SCr).

The exclusion criteria were as follows: (1) a history of cardiovascular or cerebrovascular disease (n=12); (2) cancer, kidney dysfunction, liver disease, blood disease, or any other condition that could affect life expectancy (n=36); (3) pregnancy or lactation (n=2); (4) incomplete clinical, laboratory, or imaging data (n=235); and (5) invalid ufPWV measurements (n=179; details are provided in the “Measurements of cIMT and ufPWV” section). After these criteria were applied, 518 participants remained and were divided into three groups according to the Fourth Adult Treatment Panel guidelines for fasting serum TG [22]: TG-high (≥150 mg/dL [1.69 mmol/L], n=150), TG-normal (100–149 mg/dL [1.13–1.68 mmol/L], n=146), and TG-optimal (<100 mg/dL [1.12 mmol/L], n=222) (Fig. 1). To investigate the association between residual atherosclerotic risk and carotid stiffness in individuals with hypertriglyceridemia and explore whether LDL-C influences this association, participants (n=518) were further divided into two subgroups: high LDL-C (≥3.4 mmol/L, n=97) and normal LDL-C (<3.4 mmol/L, n=421). In accordance with previous research [17], cIMT ≥0.050 cm and PWV at the end of systole (PWV-ES) ≥7.0 m/s were used as morphological and biomechanical indicators, respectively, of carotid AS. The prevalence of AS in the study population was then calculated. To evaluate the trend in carotid stiffness across increasing TG levels, participants were additionally categorized into six subgroups at 50 mg/dL intervals: <50 mg/dL (<0.57 mmol/L), 50–99 mg/dL (0.57–1.12 mmol/L), 100–149 mg/dL (1.13–1.68 mmol/L), 150–199 mg/dL (1.69–2.25 mmol/L), 200–249 mg/dL (2.26–2.81 mmol/L), and ≥250 mg/dL (≥2.82 mmol/L). These cutoffs were selected to yield equally spaced intervals while maintaining adequate sample sizes within each subgroup.

Fig. 1.

Flow diagram of study cohort selection.

This retrospective study enrolled 982 participants who underwent clinical and laboratory examinations, as well as concurrent ultrafast pulse wave velocity (ufPWV) and carotid intima-media thickness measurements. After application of the inclusion and exclusion criteria, 518 participants with available data were included in the final analysis. These participants were then divided into three groups according to triglyceride (TG) level: TG-optimal (n=222), TG-normal (n=146), and TG-high (n=150).

Measurements of cIMT and ufPWV

cIMT and ufPWV were measured using an ultrasonic diagnostic system (Supersonic Imagine, Aix-en-Provence, France) equipped with a linear array probe (SL10-2). Participants were examined in the supine resting position with the neck fully exposed. The longitudinal section was adjusted to clearly visualize the intima-media structure of the posterior wall of the distal CCA, 1.0 to 1.5 cm proximal to the bifurcation. cIMT was quantified using automated cIMT measurement software (Aixplorer, Supersonic Imagine), which reduced the substantial bias associated with manual cIMT measurement [17,25]. A white sampling frame (1 cm wide) was placed within the region of interest (ROI), and the cIMT was delineated in real time by two white dotted lines within the frame. The system then automatically measured the mean cIMT of the traced segment. A cIMT value was considered valid when the quality control index, Fit, exceeded 80% (Fig. 2A, C). For each side of the CCA, three repeated measurements were obtained, and the mean value was used as the cIMT for that side. Finally, the average of the left and right cIMT values was used as the participant’s final cIMT.

Fig. 2.

Protocol for measuring carotid intima-media thickness (cIMT) using the Aixplorer automatic cIMT measurement system and carotid stiffness using ultrafast pulse wave velocity (ufPWV).

A. cIMT was measured using the Aixplorer automatic cIMT measurement system. The white region of interest (ROI) box was placed on the posterior wall of the common carotid artery (CCA) near the bulb, while two white dashed lines automatically traced the carotid intima-media structure. The mean cIMT within the ROI was obtained with a Fit value of 98%. B. Pulse wave velocity at the beginning of systole (PWV-BS) and pulse wave velocity at the end of systole (PWV-ES) were measured using ufPWV. The yellow ROI box covered the anterior and posterior walls of the main CCA, and the red line tracked movement of the anterior and posterior walls in real time. PWV-BS and PWV-ES were considered valid when Δ± was ≤1.0 m/s. C, D. Magnified views of the cIMT and ufPWV measurement regions are shown, respectively. LCCA, left common carotid artery; RCCA, right common carotid artery.

The probe was then moved to a straight segment of the CCA in a longitudinal plane that clearly displayed both the anterior and posterior walls. Each participant was asked to hold their breath for 5 seconds while the probe remained motionless and the “PWV” mode was activated. After image acquisition and processing, a yellow sampling frame (3×3 cm) was positioned over the CCA so that the envelopes of the anterior and posterior walls could be automatically traced by two red lines. The system then automatically recorded the PWV parameters, including PWV at the beginning of systole (PWV-BS) and PWV-ES. A quality control index of Δ±≤1.0 m/s was considered indicative of a valid measurement (Fig. 2B, D). Measurements were considered invalid under the following conditions: (1) Δ±>1.0 m/s; (2) failure to acquire PWV-BS and/or PWV-ES; and (3) incorrect ROI placement [17,25]. The CCA on each side was measured three times, and the average value was calculated. The mean of the bilateral CCA values was used as the final PWV-BS and PWV-ES for each participant.

Results

Clinical and Ultrasound Characteristics of Study Participants

A total of 518 participants (47.3% men; mean age, 50.78 years; mean BMI, 23.71 kg/m²) were included and categorized into the TG-optimal, TG-normal, and TG-high groups (Table 1). Clinical and ultrasound characteristics differed significantly among the three groups (all P<0.05), except for PWV-BS (P=0.231). Compared with the TG-optimal group, the TG-normal and TG-high groups had significantly higher age, proportion of men, BMI, SBP, DBP, FRS, TG, TC, LDL-C, FBG, SCr, cIMT, and PWV-ES, as well as lower HDL-C levels (all P<0.05) (Table 1).

Table 1.

Clinical and ultrasound characteristics of study participants grouped by TG level

cIMT and Carotid Stiffening across TG Groups in the Total Population and LDL-C Subgroups

In the total population, both the TG-high and TG-normal groups had significantly higher cIMT values than the TG-optimal group (all P<0.001) (Fig. 3A), as well as higher PWV-ES values (P<0.001 and P<0.01, respectively) (Fig. 3C). A similar pattern was observed in the normal LDL-C subgroup for both cIMT (P<0.01 and P<0.05, respectively) (Fig. 3D) and PWV-ES (P<0.01 and P<0.05, respectively) (Fig. 3F). In contrast, within the high LDL-C subgroup, only PWV-ES was significantly higher in the TG-high group than in the TG-optimal group (P=0.017) (Fig. 3I), whereas cIMT did not differ significantly among the TG groups (all P>0.05) (Fig. 3G). PWV-BS did not differ significantly among the three TG groups in either the total population or the LDL-C subgroups (all P>0.05) (Fig. 3B, E, H). In the finer TG stratification, PWV-ES showed an overall increasing trend with rising TG levels, despite a slight decline at the highest range, in both the total population and the LDL-C subgroups (Fig. 4).

Fig. 3.

Pairwise comparisons of ultrasound parameters among triglyceride (TG) groups in the total population and low-density lipoprotein cholesterol (LDL-C) subgroups.

Boxplots show pairwise comparisons of carotid intima-media thickness (cIMT), pulse wave velocity at the beginning of systole (PWV-BS), and pulse wave velocity at the end of systole (PWV-ES) among TG groups in the total population (A–C), the normal LDL-C subgroup (D–F), and the high LDL-C subgroup (G–I). *P<0.05, **P<0.01, ***P<0.001.

Fig. 4.

Bar and line graphs of pulse wave velocity at the end of systole (PWV-ES) across finer triglyceride (TG) categories in the total population and low-density lipoprotein cholesterol (LDL-C) subgroups.

Bar graphs of PWV-ES by finer TG category are shown for the total population (A), the normal LDL-C subgroup (C), and the high LDL-C subgroup (E); all comparisons were made against TG <0.57 mmol/L. ***P<0.001. Line graphs of PWV-ES by finer TG category are shown for the total population (B), the normal LDL-C subgroup (D), and the high LDL-C subgroup (F).

Carotid Stiffening across cIMT and FRS Subgroups

In the TG-optimal, TG-normal, and TG-high groups, the proportions of participants with cIMT ≥0.050 cm were 59.0%, 82.2%, and 79.3%, respectively (Fig. 5A). The proportions with PWV-ES ≥7.0 m/s increased progressively across these groups, reaching 56.3%, 73.9%, and 77.3%, respectively (Fig. 5C). For both cIMT and PWV-ES, the proportions of intermediate-risk (FRS 10%–20%) and high-risk (FRS >20%) individuals increased with increasing TG levels (Fig. 5B, D). Among participants with cIMT <0.050 cm, PWV-ES differed significantly between the TG-optimal and TG-high groups (P<0.001), whereas no significant differences were observed among the three TG groups when cIMT was ≥0.050 cm (all P>0.05) (Fig. 5E). Similarly, within the low-risk subgroup, PWV-ES differed significantly between the TG-optimal and TG-normal groups (P=0.005) and between the TG-optimal and TG-high groups (P<0.001). No significant differences were observed among the TG groups in the intermediate- or high-risk subgroups (all P>0.05) (Fig. 5F).

Fig. 5.

Carotid stiffening across carotid intima-media thickness (cIMT) and Framingham risk score (FRS) subgroups.

The proportions of participants with cIMT ≥0.050 cm (A) and pulse wave velocity at the end of systole (PWV-ES) ≥7.0 m/s (C) are shown across triglyceride (TG) groups. The proportions of participants with cIMT ≥0.050 cm (B) and PWV-ES ≥7.0 m/s (D) are also shown across TG groups stratified by FRS category. Boxplots show pairwise comparisons of PWV-ES among TG groups within the cIMT (E) and FRS (F) subgroups. **P<0.01, ***P<0.001.

Correlations between cIMT, ufPWV Indices, and Major Cardiovascular Risk Factors in the Total Population

PWV-ES was significantly correlated with age (r=0.545, P<0.001), and this correlation was stronger than that observed for cIMT (r=0.479, P<0.001). PWV-ES was also weakly associated with BMI (r=0.177), SBP (r=0.300), DBP (r=0.175), TG (r=0.158), HDL-C (r=−0.130), FBG (r=0.087), and SCr (r=0.131) (all P<0.05). cIMT showed similarly weak correlations with these variables (r=0.137–0.359, all P<0.05). In contrast, PWV-BS was weakly correlated only with age (r=0.285, P<0.001) and SCr (r=0.156, P<0.001) (Table 2).

Table 2.

Correlations of major cardiovascular risk factors with cIMT, PWV-BS, and PWV-ES in the total population

Association between Carotid Stiffening and TG-Driven Residual Atherosclerotic Risk

Logistic regression analysis showed that increased carotid stiffness was associated with high TG levels in the high LDL-C subgroup (OR, 1.56; P=0.024). This association remained significant after adjustment for LDL-C alone (OR for PWV-ES, 1.57; P=0.023) and after further adjustment for age, sex, BMI, SBP, DBP, FBG, and SCr (OR for PWV-ES, 1.81; P=0.048). In the normal LDL-C subgroup, increased carotid stiffness was also associated with high TG levels (OR, 1.22; P=0.005) and remained significant after adjustment for LDL-C alone (OR for PWV-ES, 1.21; P=0.006), but not after further adjustment for age, sex, BMI, SBP, DBP, FBG, and SCr (OR for PWV-ES, 1.03; P=0.744) (Table 3).

Table 3.

Odds ratios of PWV-ES among TG groups in the total population and LDL-C subgroups

Discussion

Using ufPWV, this study showed that increased carotid stiffness was associated with elevated TG levels even in individuals with normal LDL-C levels, indicating persistent residual atherosclerotic risk in patients with hypertriglyceridemia. In addition, PWV-ES, a technical parameter derived from ufPWV, differentiated atherosclerotic risk across TG strata in both the cIMT <0.050 cm subgroup and the low-risk FRS subgroup, suggesting potential value for early risk detection. These findings further suggest that ufPWV-guided TG-lowering strategies may help reduce residual atherosclerotic risk and enable earlier preventive intervention in patients with hypertriglyceridemia.

The Framingham Heart Study, with 12 years of follow-up, demonstrated a robust positive association between TG levels and atherosclerotic risk after multivariable adjustment [26]. A meta-analysis of 29 Western prospective studies (n=262,525) revealed that each 1 mmol/L increase in TG levels corresponded to an approximately 30% increase in coronary heart disease risk [27]. In the present study, both PWV-ES and cIMT were significantly higher in the TG-high and TG-normal groups than in the TG-optimal group, indicating greater atherosclerotic risk at higher TG levels. This pattern persisted even among participants with normal LDL-C levels, supporting the presence of residual atherosclerotic risk in hypertriglyceridemia. Numerous genetic and epidemiological studies have identified TG and TGRLs as major contributors to residual ASCVD risk [28]. Mechanistically, TGRL metabolism generates atherogenic remnant particles that readily penetrate the arterial intima and accelerate foam cell formation, while elevated TG levels also promote endothelial dysfunction, inflammatory responses, and coagulation activation [29–31]. Together, these TG-mediated processes contribute to increased arterial stiffness and greater residual atherosclerotic risk.

This study is also distinctive in that it identified a significant association between elevated TG levels and increased carotid stiffness, measured using ufPWV rather than the previously used brachial-ankle PWV (baPWV). This association persisted independently of LDL-C concentration. Kawasoe et al. [32] studied a Japanese general population with low LDL-C levels (≤119 mg/dL) and found that high TG levels were independently associated with increased carotid stiffness. Similarly, a Chinese study evaluating the associations of non–HDL-C, TG, and the TC/HDL-C ratio with arterial stiffness showed that TG levels were consistently associated with baPWV, independent of LDL-C levels [33]. Mechanistically, a large UK Biobank cohort study (>502,000 UK residents) [34] estimated that TGRLs and their remnants confer an approximately fourfold higher atherogenic risk than LDL-C particles, which may partly explain the robust association between TG levels and arterial stiffening independent of LDL-C concentrations. However, these atherogenic processes are closely intertwined with traditional cardiovascular risk factors, creating a synergistic environment in which TG-mediated arterial stiffening cannot be mechanistically separated from these factors. Accordingly, the observed association was slightly attenuated after comprehensive adjustment for traditional cardiovascular risk factors, including age, sex, BMI, SBP, DBP, FBG, and SCr. These model-dependent findings underscore the complexity of the relationship between TG and carotid stiffness and its susceptibility to multifactorial influences.

Previous studies have shown a significant positive correlation between TG levels and cIMT, particularly in patients with type 2 diabetes [35] and obesity [36]. The present results also demonstrated that cIMT was correlated with TG (r=0.123). Both cIMT, which reflects arterial wall structure, and PWV-ES, which reflects arterial stiffening, represent key indicators of AS and cardiovascular risk. Zhu et al. [17] reported that carotid stiffening may already be present even when the morphological carotid index remains within the normal range (cIMT <0.050 cm). This finding suggests a pathophysiological sequence in which functional stiffening precedes structural remodeling. Consistent with this interpretation, the present results showed that among participants with normal cIMT, PWV-ES differentiated between the TG-high and TG-optimal groups, with significantly higher values in the former. This discriminatory ability disappeared once structural thickening occurred (cIMT ≥0.050 cm), as no significant differences were observed among the three TG groups. These findings suggest that PWV-ES may enable the accurate quantitative assessment of TG-related atherosclerotic risk at an early stage, before morphological cIMT thickening becomes detectable.

Although both PWV-BS and PWV-ES are derived from the same ufPWV acquisition, only PWV-ES was significantly associated with TG-driven residual risk. This discrepancy may stem from differences in the hemodynamic phases captured by the two parameters: PWV-BS reflects velocity at the onset of systole and thus the artery’s immediate elastic response, whereas PWV-ES reflects end-systolic velocity and therefore represents the cumulative arterial strain during systole [17,25]. In early atherogenesis, functional stiffening typically emerges first during late systole as a result of endothelial dysfunction, altered smooth muscle tone, and extracellular matrix remodeling, often before structural thickening becomes detectable [19,21]. Previous ufPWV studies have similarly shown that PWV-ES is more sensitive than PWV-BS for detecting subclinical arterial stiffening in populations with hypertension [19], diabetes [21], and even no overt risk factors [17]. Accordingly, the subtle biomechanical effects of elevated TG may be better captured by PWV-ES. In contrast, PWV-BS may require more advanced vascular remodeling before it becomes abnormal, which could explain its lack of discriminatory value among TG groups. These findings support PWV-ES as the more informative ufPWV parameter for quantifying early TG-related arterial stiffening and residual atherosclerotic risk.

The FRS remains a cornerstone of cardiovascular risk assessment and is widely used in clinical practice. Although TG is not directly included in the FRS calculation, it may complement FRS-based risk assessment, especially in patients with metabolic syndrome [37]. Previous research has reported a positive correlation between TG concentration and FRS [38]. The present results support a similar relationship, showing progressive increases in the proportions of intermediate-risk and high-risk FRS categories as TG levels increased. A recent study [39] indicated that PWV-ES was significantly associated with FRS-estimated risk, especially in the low-risk FRS group (r=0.517), suggesting that PWV-ES may be useful for cardiovascular risk assessment in low-risk populations. Similarly, in the present study, PWV-ES accurately differentiated carotid stiffness across TG groups within the low-risk FRS subgroup. However, PWV-ES did not clearly distinguish these differences in the intermediate- or high-risk FRS subgroups. These observations support consideration of PWV-ES assessment in low-risk individuals with borderline or elevated TG levels to improve atherosclerotic risk stratification and facilitate timely preventive intervention.

This study has several limitations. First, because this was a retrospective observational study, the association between TG and carotid stiffness should not be interpreted as causal. Second, multiple subgroup comparisons were performed using the least significant difference test without adjustment for multiple testing. Although this approach is sensitive for exploratory analyses, the findings should be regarded as hypothesis-generating and require confirmation in future studies. Third, although some individuals had normal LDL-C levels at the time of assessment, prior long-term exposure to elevated LDL-C may have caused irreversible or only partially reversible vascular structural changes that continued to elevate PWV. Therefore, increased PWV in individuals with normal LDL-C and TG levels may not be attributable solely to TG-driven residual atherosclerotic risk, which could have introduced bias into the results. Fourth, although fasting TG levels were measured after an overnight fast of at least 8 hours according to standard protocols, recent evidence suggests that non-fasting TG measurements may provide superior cardiovascular risk prediction [40]. Finally, this was a single-center study with a limited sample size, which may restrict the generalizability of the findings. Large-scale, multicenter, prospective studies are needed to validate these results.

Elevated carotid stiffness quantified by ufPWV was significantly associated with elevated TG levels in individuals with hypertriglyceridemia, independent of LDL-C, suggesting that PWV-ES, a ufPWV-derived parameter, may be a promising tool for the early quantitative assessment of residual atherosclerotic risk.

Article information Continued

Notes