Reversible left ventricular trabecular remodeling after bariatric surgery in obesity: a prospective cohort study using quantitative cardiac MRI
Introduction
Obesity is a chronic metabolic disorder characterized by excessive adipose tissue accumulation and has become a major global public health concern (1). By increasing cardiac output and hemodynamic load, obesity contributes to structural and functional cardiac abnormalities, including left ventricular hypertrophy, diastolic dysfunction, and heart failure (2,3). However, the structural basis of these changes and their quantitative imaging correlation remain incompletely understood.
Myocardial trabeculae are an integral structural component of the left ventricle, yet their physiological and clinical significance has not been fully clarified. Left ventricular non-compaction (LVNC) is traditionally regarded as a congenital cardiomyopathy resulting from arrested myocardial compaction during embryonic development (4). However, recent imaging studies have demonstrated substantial inter-individual variation in trabeculation within the general population, with notably higher degrees observed in athletes, pregnant women, and obese individuals (5-7). These observations suggest that myocardial trabeculation, beyond classical congenital LVNC, may exhibit structural variability under different physiological or pathological conditions. In this context, obesity-related hemodynamic load and metabolic stress have been proposed to be associated with increased trabeculation. Such changes may differ from classical congenital LVNC; however, their clinical significance and potential reversibility remain to be clarified.
Cardiac magnetic resonance imaging (CMR) is regarded as the reference standard for evaluating cardiac morphology and function, allowing accurate and reproducible quantification of left ventricular structure and trabeculation (8). Although previous studies have indicated a close association between obesity and left ventricular dysfunction, whether obesity-related cardiac dysfunction is associated with structural alterations such as increased trabeculation remains uncertain. Quantitative imaging evidence regarding the relationship between trabeculation and obesity-related cardiac dysfunction is currently limited.
This study used quantitative CMR to assess left ventricular trabeculation and cardiac function in individuals with obesity and to evaluate changes following bariatric surgery. We aimed to examine whether trabeculation was associated with cardiac functional parameters and whether it was related to the observed association between obesity and cardiac dysfunction. Mediation analysis was performed as an exploratory statistical approach to assess whether trabeculation statistically explained part of this association. A conceptual diagram illustrating the variables examined in this study is provided in Figure S1. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2534/rc).
Methods
Study participants
This prospective single-center study with matched healthy controls consecutively enrolled 59 patients with obesity who were scheduled for bariatric surgery at Hebei Medical University Second Hospital between November 2022 and January 2025. All participants underwent baseline CMR within 1 week before surgery and follow-up examinations 11–13 months postoperatively. According to predefined criteria, 29 patients were excluded: 8 did not complete preoperative CMR, 17 were lost to follow-up or declined follow-up, and 4 had poor image quality. Finally, 30 patients were included in the analysis.
Concurrently, 30 healthy volunteers with a body mass index (BMI) <30 kg/m2 and no chronic diseases were recruited as controls. Basic clinical data, including age, sex, height, weight, and blood pressure, were collected for all participants. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The Second Hospital of Hebei Medical University (No. 2022-R100), and all participants provided written informed consent.
The inclusion criteria for the obesity group were as follows: (I) meeting the indications for laparoscopic sleeve gastrectomy (LSG) according to the Clinical Multidisciplinary Diagnosis and Treatment Consensus for Obesity (2021 Edition); (II) age 16–65 years, regardless of sex; and (III) no history of cardiovascular disease, chronic respiratory disease, type 2 diabetes, hypertension, or other chronic conditions.
The inclusion criteria for the control group were as follows: (I) BMI <30 kg/m2 and no chronic diseases; and (II) age and sex distribution broadly matched to those of the severe obesity group.
The exclusion criteria were as follows: (I) contraindications to CMR, including claustrophobia or implanted metallic devices incompatible with CMR, such as cardiac pacemakers or aneurysm clips; (II) inability to complete CMR for any reason, such as poor breath-holding capacity; and (III) poor image quality, severe artifacts, or missing data that could substantially affect data extraction and analysis. The participant inclusion flowchart is shown in Figure 1.
Imaging equipment and acquisition protocol
All examinations were performed using a 3.0-T magnetic resonance imaging (MRI) scanner (Signa™ Architect, GE Healthcare, USA) equipped with an AIR coil. Participants were positioned supine, instructed to remove all metallic objects, and trained to perform breath-holding before scanning. Imaging was performed during end-expiratory breath-hold with respiratory and electrocardiographic gating.
Black blood sequence
A single-shot fast spin-echo (SSFSE) sequence was used. The main acquisition parameters were as follows: repetition time, approximately 1,400 ms; echo time, 68 ms; flip angle, 90°; slice thickness, 5 mm; and 26 slices covering the region from the aortic arch to the diaphragmatic dome.
Bright blood sequence
Bright-blood images were acquired using a fast imaging employing steady-state acquisition (FIESTA) cine sequence. The main acquisition parameters were as follows: repetition time, approximately 3.1 ms; echo time, 1.2 ms; flip angle, 45°; slice thickness, 10 mm; and field of view, 300 × 300 mm2. Short-axis images continuously covered 8–10 levels from the cardiac base to the apex, with 25 frames acquired per cardiac cycle. Long-axis images included two-chamber, three-chamber, and four-chamber views, with one slice acquired for each view.
Image analysis
Images were independently analyzed by two radiologists with more than 5 years of experience in cardiac CMR diagnosis using Medis Suite (version 4.0, Leiden, the Netherlands). In the QMass module, endocardial and epicardial contours were manually delineated on each short-axis slice, and time-volume curves were automatically generated.
The following parameters were derived: left ventricular ejection fraction (LVEF); end-diastolic volume and end-systolic volume (LVEDV and LVESV) and their indexed values (LVEDVi and LVESVi); stroke volume (SV) and stroke volume index (LVSVi); early and late diastolic peak filling rates (PFR1 and PFR2, respectively), with corresponding filling volumes (FV1 and FV2, respectively); and total filling volume (FV). Left atrial diameter (LAD) was measured on axial black-blood images at the largest cross-sectional plane of the left atrial body, representing the anteroposterior diameter.
The left ventricular global function index (LVGFI) was calculated according to the following equation (9):
The body surface area (BSA) was calculated using the Du Bois formula:
In patients with severe obesity, increased circulating blood volume and preload may influence LVEF through physiological changes related to volume status (10). To obtain a body-size-normalized index for exploratory comparison, we calculated BSA-indexed LVEF (LVEF/BSA) to account for differences in body habitus (11,12). LVEF/BSA was analyzed as an exploratory functional parameter and should not be interpreted as a guideline-recommended clinical metric.
After manual contour adjustment, trabeculated myocardial mass and left ventricular mass (LVM) were calculated. The trabeculated-to-total myocardial mass ratio (TM/M) was calculated by dividing trabeculated myocardial mass by total myocardial mass. Using aligned four-chamber and two-chamber views, the non-compacted to compacted layer ratio (NC/C) was measured at the thickest segment of trabeculated myocardium in the distal left ventricle for subsequent analysis (13) (Figure 2A,2B).
Myocardial feature tracking was performed using the QStrain module to obtain global longitudinal strain (GLS), global circumferential strain (GCS), and global radial strain (GRS) (Figure 2C).
Bariatric surgery
All participants in the obesity group underwent LSG performed by the same surgical team. CMR was repeated approximately 12 months after surgery to assess changes in cardiac structure and function.
Reproducibility
All CMR images were analyzed and post-processed using third-party cardiac magnetic resonance post-processing software (Medis Suite, version 4.0) by two experienced radiologists. A random subset of 25 participants was selected to assess inter-observer and intra-observer reproducibility.
Statistical analysis
All data were imported into R software (version 4.4.3) for statistical analysis. Continuous variables are presented as mean ± standard deviation or median with interquartile range, and categorical variables are presented as frequency and percentage. Between-group comparisons were performed using independent-samples t-tests or Mann-Whitney U tests, as appropriate. Within-group pre-post comparisons were assessed using paired t-tests or Wilcoxon signed-rank tests. Categorical variables were compared using the chi-square test or Fisher’s exact test, as appropriate.
Baseline characteristics were also compared between participants included in the final analysis and those excluded to assess potential selection bias.
To evaluate whether the extent of trabecular regression was associated with functional improvement, patients were stratified according to the median change in the NC/C. Differences between groups were assessed using the Mann-Whitney U test, and correlations between changes in the NC/C and changes in GLS or the PFR1/PFR2 ratio were examined using Spearman’s rank correlation.
Pearson or Spearman correlation analyses were used to assess associations between left ventricular trabeculation and cardiac functional parameters. Bootstrap 95% confidence intervals (CIs) were estimated using 5,000 resamples.
Mediation analyses were performed using standardized z-score variables, with BMI as the independent variable, NC/C as the primary mediator, and LVEF as the dependent variable. Covariates included age, sex, diastolic blood pressure, and systolic blood pressure. Nonparametric bootstrap resampling with 5,000 iterations was used to estimate indirect effects and their 95% CIs.
Additional exploratory mediation analyses were conducted using LVEF/BSA, LVGFI, GLS, and the PFR1/PFR2 ratio as alternative outcomes, and LVM and TM/M as alternative mediators. A reverse model specification was also explored as a supplementary analysis. These mediation analyses reflect statistical decomposition of associations and do not establish temporal, biological, or causal relationships.
To avoid potential mathematical coupling or multicollinearity among body-size variables that could affect the mediation analysis, variance inflation factor (VIF) tests were conducted for BMI, BSA, and NC/C before model construction. All variables had VIF values below 5, indicating no substantial multicollinearity and supporting the stability of the model estimates.
Results
Baseline characteristics
A total of 60 participants underwent CMR examinations, including 30 individuals in the obesity group and 30 healthy controls. There were no statistically significant differences between the two groups in sex, age, height, or systolic blood pressure (P>0.05). Body weight, BMI, and diastolic blood pressure were significantly higher in the obesity group than in the control group (P<0.05). The general clinical characteristics of the participants are presented in Table 1.
Table 1
| Parameter | Obese group (n=30) | Control group (n=30) | t/χ2 | P |
|---|---|---|---|---|
| Male sex | 17 (57) | 17 (57) | 0.00 | >0.999 |
| Age (years) | 27.30±6.81 | 28.37±7.97 | −0.55 | 0.580 |
| Height (cm) | 170.26±7.39 | 167.60±10.53 | 1.13 | 0.262 |
| Weight (kg) | 128.50±23.25 | 69.90±12.27 | 12.20 | <0.001*** |
| BMI (kg/m2) | 44.22±6.71 | 24.78±3.16 | 14.33 | <0.001*** |
| SBP (mmHg) | 128.23±13.46 | 121.93±10.80 | 1.99 | 0.050 |
| DBP (mmHg) | 81.83±8.00 | 75.56±8.66 | 2.90 | 0.005** |
Data are presented as number (percentage) or mean ± standard deviation. **, P<0.01; ***, P<0.001. BMI, body mass index; DBP, diastolic blood pressure; SBP, systolic blood pressure.
Baseline characteristics were also compared between participants included in the final analysis and those excluded to assess potential selection bias. Differences were observed in sex, height, and weight, whereas key variables, including BMI and blood pressure, were comparable between groups (Table S1).
Comparison of left ventricular structural and functional parameters
In quantitative structural analysis, the NC/C and LVM were significantly higher in the obesity group than in the control group (P<0.05) (Figure 3A), indicating more pronounced myocardial trabeculation and hypertrophy in individuals with obesity. Although the TM/M did not differ significantly between groups (P=0.08), a similar trend was observed.
Regarding systolic function, LVGFI and LVEF were significantly lower in the obesity group than in the control group (P<0.05) (Figure 3B), with a more pronounced difference after correction for body surface area (LVEF/BSA, P<0.05). LVSVi was also reduced in the obesity group (P<0.05).
Regarding diastolic function, PFR1 and the PFR1/PFR2 ratio were significantly lower in the obesity group (P<0.05) (Figure 3C), accompanied by a significant increase in LAD (P<0.05).
Strain analysis demonstrated lower absolute values of GLS and GCS in the obesity group (P<0.05) (Figure 3D), while GRS was also significantly lower in the obesity group (P<0.05). Detailed quantitative results are provided in Table S2.
Correlations among body mass index, trabeculation, and CMR-derived parameters
Pearson correlation analysis revealed significant linear associations between BMI and multiple cardiac functional parameters. BMI was negatively correlated with LVEF, LVEF/BSA, LVGFI, and the PFR1/PFR2 ratio (P<0.05). In contrast, BMI was positively correlated with GLS and PFR2 (P<0.05), reflecting impaired myocardial strain and increased late diastolic filling in individuals with obesity.
Similarly, the NC/C showed significant correlations with several CMR-derived functional indices. It was negatively correlated with LVEF, LVEF/BSA, LVGFI, LVSVi, and the PFR1/PFR2 ratio (P<0.05), and positively correlated with GLS, GCS, PFR2, and FV2 (P<0.05). Detailed results are shown in Figure 4 and Table S3, and the 95% bootstrap CIs for all correlation coefficients are provided in Table S4.
Mediation analysis of trabeculation between body mass index and cardiac function
Pearson correlation analysis showed significant associations among BMI, the NC/C, and cardiac functional parameters, supporting subsequent mediation analysis. BMI was positively correlated with the NC/C (r=0.81, P<0.05) and negatively correlated with LVEF (r=−0.29, P<0.05). The NC/C was also negatively correlated with LVEF (r=−0.44, P<0.05) (Figure 5A-5C).
After adjustment for age, sex, and blood pressure, a mediation model was constructed with BMI as the independent variable, NC/C as the primary mediator, and LVEF as the dependent variable. The total effect of BMI on LVEF was −0.29 (P<0.05). The indirect effect via NC/C was statistically significant (β=−0.46, 95% CI: −0.81 to −0.09), whereas the direct effect was not statistically significant (β=0.17, 95% CI: −0.25 to 0.59). Detailed regression coefficients and bootstrap results are presented in Tables 2,3, and the mediation path is illustrated in Figure 5D.
Table 2
| Model | BMI | NC/C | R2 | F | |||||
|---|---|---|---|---|---|---|---|---|---|
| β | t | P | β | t | P | ||||
| Model 1: LVEF (total effect) | −0.29 | −2.16 | 0.03 | − | − | − | 0.15 | 3.08 | |
| Model 2: NC/C (mediator) | 0.83 | 9.74 | <0.001 | − | − | − | 0.65 | 23.33 | |
| Model 3: LVEF (direct effect) | 0.17 | 0.81 | 0.42 | −0.55 | −2.74 | 0.008 | 0.24 | 4.13 | |
All variables were standardized before entry into the mediation model. Models were adjusted for age, sex, systolic and diastolic blood pressure. BMI, body mass index; LVEF, left ventricular ejection fraction; NC/C, non-compacted-to-compacted layer ratio.
Table 3
| Path | Effect estimate | SE | Bootstrap 95% CI | |
|---|---|---|---|---|
| Lower | Upper | |||
| Total effect | −0.29 | 0.13 | −0.56 | −0.02 |
| BMI→NC/C | 0.83 | 0.08 | 0.66 | 1.00 |
| NC/C→LVEF | −0.55 | 0.20 | −0.95 | −0.14 |
| Indirect effect | −0.46 | 0.18 | −0.81 | −0.09 |
| Direct effect | 0.17 | 0.13 | −0.25 | 0.59 |
All variables were standardized before entry into the mediation model. Models were adjusted for age, sex, systolic and diastolic blood pressure. Post-hoc power for the indirect effect was 0.79. Mediation effects were tested using the bootstrap method with 5,000 resamples. Post-hoc power for the indirect effect was calculated based on the standardized indirect effect (β/SE) at a two-sided significance level of 0.05. BMI, body mass index; CI, confidence interval; LVEF, left ventricular ejection fraction; NC/C, non-compacted-to-compacted layer ratio; SE, standard error.
When LVEF/BSA was used as the dependent variable, both the direct and indirect effects of BMI were statistically significant. The indirect effect via NC/C remained significant, and the direct association between BMI and LVEF/BSA persisted after accounting for NC/C.
Sensitivity analyses showed no significant indirect effects when LVEF was used as the outcome. In the reverse model specification, with LVEF modeled as the predictor and NC/C as the outcome, only a modest pattern consistent with statistical mediation was observed. Additional analyses using LVEF/BSA as the outcome showed a similar pattern, with both direct and indirect effects remaining statistically significant (Tables S5,S6).
Mediation analyses for other cardiac functional parameters, including LVGFI, GLS, and the PFR1/PFR2 ratio, showed similar trends but did not reach statistical significance (P>0.05) (Table S7).
Changes in cardiac CMR parameters before and after bariatric surgery
At approximately 12 months after surgery, patients with obesity showed significant improvements in left ventricular structure and function compared with preoperative values. LVM, NC/C, and TM/M all decreased significantly (P<0.05), with a large effect size observed for the reduction in NC/C (Cohen’s d=0.82) (Table S8). LVGFI and LVEF increased significantly (P<0.05), with a more pronounced improvement in LVEF/BSA (P<0.05; Cohen’s d=1.73). LVSVi also increased significantly (P<0.05), reflecting improved systolic performance.
GLS improved significantly (P<0.001), GCS showed an upward trend (P=0.06), and GRS remained unchanged. PFR1 and the PFR1/PFR2 ratio increased significantly (P<0.05), accompanied by a reduction in LAD (P<0.05). Detailed results are presented in Figure 6 and Table S9.
Trabecular regression and functional improvement
To further evaluate the relationship between structural changes and functional recovery, patients were stratified according to the median change in NC/C. The magnitude of functional improvement did not differ significantly between the high- and low-change groups. Median change in GLS was 2.49 (1.39, 2.65) in the high-change group and 2.90 (1.86, 3.56) in the low-change group (P=0.32). Median change in the PFR1/PFR2 ratio was −0.64 (−0.75, −0.39) vs. −0.33 (−0.51, −0.11), respectively (P=0.13) (Figure S2A,S2B).
Spearman correlation analysis further showed no statistically significant association between changes in NC/C and changes in the PFR1/PFR2 ratio (r=−0.25, 95% CI: −0.58 to 0.09, P=0.17) or GLS (r=−0.21, 95% CI: −0.57 to 0.06, P=0.28) (Figure S2C,S2D).
Reproducibility analysis
Intra-observer and inter-observer reproducibility of NC/C measurements was evaluated using the intraclass correlation coefficient (ICC) and Bland-Altman analysis. Intra-observer reliability was excellent (ICC =0.99, 95% CI: 0.98 to 0.99), and inter-observer reliability was also excellent (ICC =0.97, 95% CI: 0.95 to 0.99). Bland-Altman analysis demonstrated excellent reproducibility for NC/C measurements. Inter-observer agreement showed a mean bias of −0.021 (P=0.17), with 95% limits of agreement ranging from −0.17 to 0.13. Intra-observer agreement showed a mean bias of 0.004 (P=0.62), with 95% limits of agreement ranging from −0.07 to 0.08, indicating minimal systematic bias and high measurement consistency (Figure S3).
Discussion
This study evaluated longitudinal changes in left ventricular structure and function before and after bariatric metabolic surgery in patients with severe obesity using multiparametric quantitative CMR. Compared with healthy controls, individuals with obesity showed increased left ventricular trabeculation and impaired cardiac function, including reduced systolic performance, impaired myocardial strain, and abnormal diastolic filling. Approximately 12 months after surgery, both structural and functional parameters improved, with reductions in trabeculation and LVM, together with improvements in systolic function, myocardial strain, and diastolic filling. These findings suggest that severe obesity is associated with measurable alterations in cardiac structure and function, some of which may improve after weight loss.
Large-scale population-based CMR studies have shown that trabeculated myocardial mass varies with BMI, cardiovascular risk factors, and age (5). Our findings are broadly consistent with these observations; however, differences in population characteristics should be considered when interpreting and generalizing these results.
Participants with obesity exhibited reduced LVEF together with impaired strain and diastolic filling parameters, supporting the presence of subclinical functional impairment. Notably, global longitudinal strain and diastolic indices appeared more sensitive than conventional systolic measures, consistent with prior reports describing early myocardial dysfunction in obesity (14,15). These findings suggest that obesity-related cardiac remodeling involves both structural alteration and early impairment of myocardial mechanics.
Following bariatric surgery, both structural and functional parameters improved. Trabeculation and LVM decreased, while systolic function, myocardial strain, and diastolic filling indices improved (16). However, the reduction in trabeculation was modest, and no significant association was observed between changes in trabeculation and improvements in functional parameters. These results suggest that structural and functional recovery may occur in parallel but are not necessarily directly coupled at the individual level.
Mediation analyses were performed to explore whether trabeculation statistically explained part of the association between obesity and cardiac function. When LVEF was used as the outcome, the results were not consistent across models, and sensitivity analyses did not support stable indirect effects. Reverse modeling showed only modest signals, which may reflect underlying correlations rather than directional relationships. When BSA-indexed LVEF was used as an alternative outcome, both direct and indirect effects were observed. Overall, these findings suggest that trabeculation may be related to part of the association between obesity and cardiac function; however, the evidence was inconsistent and should be interpreted as exploratory rather than as indicative of a causal pathway. This interpretation is important because LVEF is a more established functional parameter than BSA-indexed LVEF. In this study, LVEF was treated as the primary outcome, whereas BSA-indexed LVEF was considered a complementary measure accounting for body-size-related variability and should not be interpreted as a substitute for conventional functional indices.
The mechanisms underlying increased trabeculation and functional impairment in obesity are likely multifactorial and remain incompletely understood. Chronic hemodynamic loading, including increased preload and ventricular wall stress, may contribute to adaptive structural changes. In addition, lipotoxicity, chronic low-grade inflammation, and metabolic dysregulation may influence myocardial remodeling and contractile performance (17). Experimental evidence has implicated inflammatory mediators and signaling pathways, such as Notch and Wnt, in myocardial compaction, suggesting that metabolic stress may affect trabecular morphology through interacting biological pathways (18-21). Beyond intrinsic myocardial factors, increased thoracoabdominal adiposity may impose external mechanical constraints on the heart, further contributing to impaired myocardial strain and diastolic function (22). Reductions in these hemodynamic, metabolic, and mechanical influences after bariatric surgery may contribute to the observed improvements in cardiac function. However, these mechanisms were not directly assessed in the present study and should therefore be regarded as hypothesis-generating.
The increased trabeculation observed in obesity may differ from that seen in classical congenital LVNC. While LVNC has traditionally been considered a congenital abnormality (23,24), recent data suggest that trabeculation exists on a continuum and may also be influenced by acquired factors. In this context, obesity-related trabeculation may represent a dynamic remodeling phenotype rather than a fixed structural abnormality. However, whether this reflects an acquired remodeling process remains uncertain and requires further investigation. This observation may have implications for imaging interpretation. Current LVNC diagnostic criteria are based on static morphological thresholds (13,25). Although these criteria remain widely used, additional factors such as clinical context, metabolic status, functional parameters, and longitudinal imaging changes may help inform the interpretation of prominent trabeculation. From a clinical perspective, quantitative CMR assessment of trabeculation may provide additional information on obesity-related cardiac remodeling and its evolution after weight loss. However, its incremental value beyond established parameters remains uncertain and requires further investigation.
Limitation
This study has several limitations. It was a single-centre, prospective, exploratory investigation with a relatively small sample size, which may limit the generalisability of the findings. The study population consisted predominantly of relatively young individuals with severe obesity and without major cardiometabolic comorbidities, which may restrict extrapolation to older populations or to patients with conditions such as diabetes, hypertension, or heart failure with preserved ejection fraction (HFpEF), where additional factors may influence myocardial remodeling.
Although standardised CMR post-processing protocols were used to assess left ventricular trabeculation, the measurements remain operator-dependent, and repeatability was evaluated only for NC/C. In addition, the absence of histological or molecular data precludes direct assessment of the biological mechanisms underlying trabecular changes. Future studies integrating multiparametric imaging with molecular approaches are warranted to further elucidate the relationship between obesity, trabeculation, and cardiac function.
Conclusions
Severe obesity was associated with increased left ventricular trabeculation and impaired cardiac function, including reduced LVEF and abnormalities in myocardial strain and diastolic indices. Following weight loss, a modest reduction in trabeculation and improvements in cardiac function were observed, suggesting that aspects of obesity-related cardiac remodeling may be modifiable. Exploratory analyses indicate that trabeculation may be related to cardiac functional changes and may account for part of the association between obesity and cardiac function; however, these findings were not consistent and should be interpreted with caution. These findings support the characterization of obesity-related trabecular remodeling as a dynamic imaging phenotype, although further studies are required to clarify its clinical significance and underlying mechanisms.
Acknowledgments
None.
Footnote
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2534/rc
Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2534/dss
Funding: This work was supported by
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2534/coif). The authors have no conflicts of interest to declare.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The Second Hospital of Hebei Medical University (No. 2022-R100), and written informed consent was obtained from all participants.
Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
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