Perivascular versus nonperivascular hepatocellular carcinoma treated with liver resection: a retrospective propensity score matching comparison of long-term outcomes
Introduction
Primary liver cancer ranks the sixth most prevalent cancer globally and is the third leading cause of cancer-related mortality, and hepatocellular carcinoma (HCC) accounts for 75–85% of these cases (1). Despite the vital role of radical treatments such as surgery in managing HCC, the 5-year survival rate remains disappointingly low (2). The high mortality rate, largely attributed to the propensity for recurrence, continues to pose a significant challenge (3,4). Identifying risk factors associated with HCC recurrence is crucial for devising effective treatment strategies, facilitating timely interventions, and enhancing patient outcomes (5,6).
The crosstalk between vasculature and tumors plays a pivotal role in modulating the biological behavior of cancers (7). HCC can induce angiogenesis, thereby providing conditions conducive to their growth and metastasis (8,9). Moreover, the vasculature serves as a reservoir for immune cells within the body, and the infiltration of immune cells in the perivascular region can significantly impact the prognosis of patients with HCC (10). Both macrovascular and microvascular invasion (MVI) exert a substantial influence on the prognosis of HCC patients (11,12), suggesting that the relationship between blood vessels and tumor has a vital impact on the survival of HCC patients. Perivascular HCC could be regarded as a special pathological state (13). Previous studies on perivascular HCC have primarily focused on evaluating the efficacy of various treatment modalities, including surgical resection, radiofrequency ablation (RFA), and microwave ablation, with the prevailing opinion suggesting that surgical resection offers superior outcomes compared to other methods (14-17). However, after surgical procedures, few studies have addressed whether perivascular HCC represents a risk factor for poor prognosis when compared to nonperivascular HCC.
The objective of our study was to bridge this gap by further categorizing HCC cases and assessing tumor proximity to intrahepatic blood vessels using preoperative imaging, after excluding cases with pathological evidence of vascular invasion. This assessment could provide preoperative critical insights into the imaging-based evaluation of HCC risk factors, ultimately informing more precise clinical decisions and improving patient outcomes. Although advanced functional imaging techniques such as 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography-computed tomography (PET-CT) have shown value primarily in radiotherapy planning and metastasis detection (18), our focus remains on the prognostic implications of anatomical tumor-vessel relationships on standard cross-sectional imaging. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-2085/rc).
Methods
Patients and design
The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee at West China Hospital (No. 2022-264). The requirement for informed consent was waived in this retrospective study. This cohort study was registered at Chinese Clinical Trial Registry (ChiCTR2400092010), and retrospectively collected the information of 1,056 HCC patients who received hepatectomies in division of liver surgery of West China Hospital from January 2008 to November 2020. All enrolled patients were confirmed as having HCC by an experienced pathologist. In order to assess the tumor condition, each patient underwent abdominal contrast-enhanced CT or magnetic resonance imaging (MRI) examination. Two seasoned doctors analyzed the venous phase of the CT or MRI images to ascertain the relationship between the tumor and blood vessels. The tumor adjacent to the vascular branch was defined as a tumor with any contact with first- or second-degree branches of a portal or hepatic vein that were 3 mm or greater in axial diameter (19,20) (Figure 1). The relationship of the tumor with the portal and hepatic veins was compared. According to the location of the tumor relative to the hepatic and portal veins, patients were divided into a radiologically nonadjacent hepatic vein (nHV) group and a radiologically adjacent hepatic vein (aHV) group regardless the portal vein condition, or a radiologically nonadjacent portal vein (nPV) group and a radiologically adjacent portal vein (aPV) group regardless of the hepatic vein condition.
A proportion of tumors, due to their size or central location, could be adjacent to both major vessel types. To assess the specific prognostic influence of each vessel, two independent propensity score matching (PSM) analyses were conducted. In the portal vein analysis, patients were stratified by portal vein (PV) adjacency regardless of hepatic vein (HV) status, and vice versa for the hepatic vein analysis. The adjacency status of the counterpart vessel was included as a covariate (subvascular) in each respective PSM model to control for its potential effect.
Inclusion and exclusion criteria
The inclusion criteria were as follows: (I) patients without other treatment before hepatectomy; (II) patients with Child-Pugh stage A or B; (III) patients with pathologically confirmed HCC; and (IV) patients with normal cardiopulmonary function and could withstand surgery.
The exclusion criteria were as follows: (I) patients with a pathologically positive resection margin; (II) patients with recurrence within one month after the operation; (III) patients with postoperative deaths from non-tumor-related causes, including perioperative and distant postoperative deaths; and (IV) patients with other malignancies.
Surgical procedure and endpoints
The surgical procedure was conducted as reported previously (21). The surgical approaches encompass anatomical hepatectomy and non-anatomical hepatectomy, with the specific selection determined by tumor location, hepatic functional reserve, and intraoperative evaluation. The adjacent Glisson pedicle and hepatic vein were preserved. All resection margins were negative (R0 resection), which was confirmed by the pathology. The primary endpoints of this study were defined as disease-free survival (DFS) and overall survival (OS). DFS was defined as the period from the completion of surgery until the time of HCC recurrence or death due to any cause, and OS was defined as the time from completion of surgery to death or last follow-up. Patients were followed up in the first month after surgery, and those who experienced recurrence or death were excluded from the study. Routine abdominal ultrasound, alpha-fetoprotein (AFP), and abnormal prothrombin time tests are conducted on patients, and follow-up visits are scheduled every 3 months.
Statistical analysis
Categorical variables were compared using the χ2 test or Fisher exact test, and continuous variables were compared using the Mann-Whitney U test. Kaplan-Meier method was used to compare the DFS and OS, and log-rank analysis was applied to identify significant differences. Univariate and multivariate Cox proportional hazards regression analyses were performed to investigate the significant and independent risk factors of prognosis, and the significant (P<0.1) variables were subjected to stepwise multivariate analysis. A PSM was applied using the nearest-neighbor matching method with a caliper of 0.02 (22), and the confounder variables including MVI, cirrhosis, satellite nodules, tumor number, AFP, tumor diameter, albumin (ALB), gender, lymphocyte (LYM) count, total bilirubin (TBIL) level, subvascular (in portal vein PSM, it was defined as whether the tumor was adjacent to the hepatic vein or not, in hepatic vein PSM, it was defined as whether the tumor was adjacent to the portal vein or not). Analyses were performed using R (v4.4.0; R Foundation for Statistical Computing, Vienna, Austria) and RStudio (v2024.04.1+748).
Results
Characteristics of patients
A total of 1,056 HCC patients who underwent hepatectomy from January 2008 to April 2020 at West China Hospital were retrospectively enrolled. After screening these patients, 714 cases were finally selected for analysis. As shown in Figure 2, the reasons for exclusion including incomplete data (n=208), portal vein tumor thrombus (n=73), death within 3 months (n=15), pathological confirmation of mixed-type liver cancer (n=14), recurrence within one month (n=7), and combination with other malignancies (n=5). In portal vein comparison, there were 257 patients in the nPV group and 457 patients in aPV group, as shown in Table S1. The baseline characteristic data before PSM analysis showed significant differences, including differences in gender (P=0.005), MVI level (P=0.005), satellite nodules (P=0.001), and tumor diameter (P<0.001). In hepatic vein comparison, there were 307 patients in the nHV group group and 407 patients in the aHV group, as shown in Table S2, the baseline characteristic data before PSM analysis showed significant differences, including differences in cirrhosis (P<0.001), MVI level (P=0.035), satellite nodules (P=0.014), AFP (P=0.031), tumor diameter (P<0.001), platelet (PLA; P<0.001), and TBIL (P<0.001). After PSM, as shown in Tables 1,2, both comparisons had comparable baseline characteristics. The detailed scores of matched and unmatched units in each group are shown in Figure S1. Given the tumor size or location, lesions can be simultaneously adjacent to both the portal and hepatic veins; when analyzing the portal vein, these patients were enrolled into the aPV group and when analyzing the hepatic vein, these patients were enrolled into the aHV group; as shown in Tables 1,2, there were no significant differences in each analysis.
Table 1
| Variable | nPV (n=249) | aPV (n=249) | P value |
|---|---|---|---|
| Gender (male) | 203 (81.5) | 205 (82.3) | 0.907 |
| High differentiation | 143 (57.4) | 137 (55.0) | 0.652 |
| Lymphatic metastasis | 2 (0.8) | 1 (0.4) | 1.000 |
| Cirrhosis | 163 (65.5) | 163 (65.5) | 1.000 |
| MVI | 56 (22.5) | 60 (24.1) | 0.750 |
| Satellite nodules | 18 (7.2) | 14 (5.6) | 0.584 |
| Tumor number (single) | 216 (86.7) | 216 (86.7) | 1.000 |
| Invading adjacent organs | 5 (2.0) | 2 (0.8) | 0.446 |
| Positive HBsAg | 205 (82.3) | 212 (85.1) | 0.466 |
| Positive HBeAg | 40 (16.1) | 39 (15.7) | 1.000 |
| AFP (>400 ng/mL) | 81 (32.5) | 83 (33.3) | 0.924 |
| Hepatic vein (adjacent) | 102 (41.0) | 115(46.2) | 0.398 |
| Age (years) | 51.0 (43.0–60.0) | 50.0 (42.0–60.0) | 0.982 |
| Tumor diameter (cm) | 4.1 (2.8–5.5) | 4.0 (2.5–6.0) | 0.997 |
| NEU count (109/L) | 3.19 (2.47–4.15) | 3.08 (2.41–3.91) | 0.259 |
| LYM count (109/L) | 1.46 (1.16–1.92) | 1.45 (1.16–1.84) | 0.439 |
| PLA count (109/L) | 129.0 (84.0–170.0) | 122.0 (89.0–171.0) | 0.735 |
| TBIL level (mmol/L) | 14.2 (11.0–18.8) | 14.1 (10.5–17.9) | 0.332 |
| ALB (g/dL) | 42.2 (39.4–45.4) | 41.8 (39.5–44.4) | 0.735 |
Data are presented as median (IQR) or n (%). AFP, alpha fetoprotein; ALB, albumin; aPV, adjacent portal vein; HBeAg, hepatitis B virus e antigen; HBsAg, hepatitis B virus surface antigen; IQR, interquartile range; LYM, lymphocyte; MVI, microvascular invasion; NEU, neutrophil granulocyte; nPV, nonadjacent portal vein; PLA, platelet; TBIL, total bilirubin.
Table 2
| Variable | nHV (n=268) | aHV (n=268) | P value |
|---|---|---|---|
| Gender (male) | 229 (85.4) | 230 (85.8) | 1.000 |
| High differentiation | 147 (54.9) | 143 (53.4) | 0.795 |
| Lymphatic metastasis | 1 (0.4) | 1 (0.4) | 1.000 |
| Cirrhosis | 190 (70.9) | 184 (68.7) | 0.638 |
| MVI | 69 (25.7) | 63 (23.5) | 0.616 |
| Satellite nodules | 25 (9.3) | 22 (8.2) | 0.760 |
| Tumor number (single) | 228 (85.1) | 229 (85.4) | 1.000 |
| Invading adjacent organs | 2 (0.7) | 4 (1.5) | 0.681 |
| Positive HBsAg | 229 (85.4) | 233 (86.9) | 0.707 |
| Positive HBeAg | 44 (16.4) | 40 (14.9) | 0.722 |
| AFP (>400 ng/mL) | 96 (35.8) | 104 (38.8) | 0.532 |
| Portal vein (adjacent) | 148 (58.7) | 155 (61.5) | 0.585 |
| Age (years) | 51.0 (43.0–60.0) | 51.0 (42.8–60.0) | 0.995 |
| Tumor diameter (cm) | 4.10 (2.77–5.82) | 4.50 (2.88–6.00) | 0.388 |
| NEU count (109/L) | 3.07 (2.45–3.89) | 3.11 (2.39–4.13) | 0.706 |
| LYM count (109/L) | 1.42 (1.13–1.90) | 1.46 (1.18–1.84) | 0.517 |
| PLA count (109/L) | 123.0 (79.0–169.0) | 124.0 (87.0–166.0) | 0.447 |
| TBIL level (mmol/L) | 14.7 (11.5–19.4) | 13.5 (10.4–17.9) | 0.092 |
| ALB (g/dL) | 42.2 (39.4–44.9) | 41.8 (39.1–44.2) | 0.283 |
Data are presented as median (IQR) or n (%). AFP, alpha fetoprotein; aHV, adjacent hepatic vein; ALB, albumin; HBeAg, hepatitis B virus e antigen; HBsAg, hepatitis B virus surface antigen; IQR, interquartile range; LYM, lymphocyte; MVI, microvascular invasion; NEU, neutrophil granulocyte; nHV, nonadjacent hepatic vein; PLA, platelet; TBIL, total bilirubin.
Portal vein and prognosis
According to the tumor location relative to the portal vein, the patients were divided into the nPV group and the aPV group. After the PSM analysis, there were 249 pairs of patients in each group. The median follow-up time was 44 months [interquartile range (IQR), 32–67 months] in the nPV group and 42 months (IQR, 33–65 months) in the aPV group. For nPV group patients, 1-, 3-, and 5-year recurrence rates after surgery were 25.3%, 46.4%, and 58.5%, respectively, whereas those for the aPV group, the recurrence rates were 27.3%, 56.3%, and 69.3%, respectively (P=0.0084) (Figure 3A). This trend was also found in OS; there was a significant difference between the two group patients. For nPV group patients, the 1-, 3-, and 5-year mortality rates after surgery were 6.8%, 27.7%, and 39.0%, respectively, whereas those in the aPV group were 13.7%, 32.2%, and 48.6%, respectively (P=0.023) (Figure 3B). Multivariate analysis demonstrated that adjacency to the portal vein, tumor number, lymphatic metastasis, MVI, satellite nodule, hepatitis B virus e antigen (HbeAg), TBIL, and tumor diameter were the independent risk factors of DFS, adjacency to the portal vein, tumor number, MVI, satellite nodule, adjacent organ invasion, HbeAg, tumor diameter, and TBIL were the independent risk factors of OS (Table 3). In addition, we further analyzed the prognosis of patients with portal vein invasion and found that the closer the relationship between the tumor and the portal vein, the worse the prognosis of patients (Figure S2).
Table 3
| Variable | Univariate | Multivariate | |||
|---|---|---|---|---|---|
| HR (95% CI) | P value | HR (95% CI) | P value | ||
| DFS | |||||
| Subportal, adjacent vs. nonadjacent | 1.371 (1.100–1.709) | 0.005 | 1.374 (1.091–1.730) | 0.007 | |
| Subvein, adjacent vs. nonadjacent | 1.194 (0.911–1.565) | 0.198† | |||
| Gender, male vs. female | 1.298 (0.951–1.771) | 0.100 | |||
| Tumor number, single vs. multiple | 0.526 (0.390–0.708) | <0.001 | 0.575 (0.423–0.783) | <0.001 | |
| Lymphatic metastasis, yes vs. no | 5.409 (1.724–16.970) | 0.004 | 4.249 (1.324–13.641) | 0.015 | |
| MVI, yes vs. no | 1.921 (1.502–2.457) | <0.001 | 1.652 (1.268–2.152) | <0.001 | |
| Satellite nodule, yes vs. no | 2.934 (1.983–4.342) | <0.001 | 2.621 (1.751–3.921) | <0.001 | |
| HBeAg, positive vs. negative | 1.558 (1.174–2.068) | 0.002 | 1.772 (1.329–2.364) | <0.001 | |
| Organ invasion, yes vs. no | 2.301 (1.024–5.169) | 0.044 | |||
| Tumor diameter, cm (continuous) | 1.102 (1.056–1.149) | <0.001 | 1.081 (1.034–1.131) | <0.001 | |
| NEU, 109/L (continuous) | 1.093 (1.011–1.181) | 0.026 | |||
| TBIL, U/L (continuous) | 1.006 (1.002–1.010) | 0.002 | 1.005 (1.001–1.009) | 0.017 | |
| OS | |||||
| Subportal, adjacent vs. nonadjacent | 1.367 (1.043–1.791) | 0.024 | 1.434 (1.086–1.893) | 0.011 | |
| Subvein, adjacent vs. nonadjacent | 1.122 (0.896–1.405) | 0.317† | |||
| Gender, male vs. female | 1.542 (1.030–2.309) | 0.036 | |||
| Tumor number, single vs. multiple | 0.535 (0.377–0.758) | <0.001 | 0.604 (0.423–0.863) | 0.006 | |
| MVI, yes vs. no | 2.046 (1.541–2.716) | <0.001 | 1.589 (1.166–2.166) | 0.003 | |
| Satellite nodule, yes vs. no | 2.734 (1.718–4.350) | <0.001 | 2.440 (1.516–3.927) | <0.001 | |
| HBeAg, positive vs. negative | 1.433 (1.018–2.015) | 0.039 | 1.679 (1.187–2.376) | 0.003 | |
| Organ invasion, yes vs. no | 3.843 (1.701–8.681) | 0.001 | 2.858 (1.206–6.775) | 0.017 | |
| Tumor diameter, cm (continuous) | 1.152 (1.098–1.209) | <0.001 | 1.130 (1.071–1.192) | <0.001 | |
| PLA, 109/L (continuous) | 1.002 (1.000–1.004) | 0.034 | |||
| NEU, 109/L (continuous) | 1.084 (0.989–1.188) | 0.083 | |||
| TBIL, U/L (continuous) | 1.007 (1.003–1.011) | <0.001 | 1.005 (1.001–1.009) | 0.014 | |
†, multivariate Cox analysis was not included. CI, confidence interval; DFS, disease-free survival; HBeAg, hepatitis B virus e antigen; HR, hazard ratio; MVI, microvascular invasion; NEU, neutrophil granulocyte; OS, overall survival; PLA, platelet; TBIL, total bilirubin.
Hepatic vein and prognosis
In comparison with the portal vein, according to the tumor location relative to the hepatic vein, the patients were divided into an nHV group and an aHV group. After the PSM analysis, there were 268 pairs of patients in each group. The median follow-up time was 42 months (IQR, 38–63 months) in the nHV group and 42 months (IQR, 35–65 months) in the aHV group. We did not find a significant difference in DFS; for nHV group patients, 1-, 3-, and 5-year recurrence rates after surgery were 30.2%, 53.3%, and 63.0%, whereas for those in the aHV group, the recurrence rates were 25.7%, 51.6%, and 64.7%, respectively (P=0.980) (Figure 3C). This trend was also found in OS, for which there was no significant difference between the two groups of patients. For nHV group patients, the 1-, 3-, and 5-year mortality rates after surgery were 9.3%, 30.7%, and 46.0%, and those for the aHV group were 9.0%, 30.7%, and 46.5% (P=0.810) (Figure 3D).
Discussion
Vascular invasion is a recognized prognostic risk factor for HCC according to major medical guidelines (23-26), and numerous clinical studies have consistently demonstrated that patients exhibiting vascular invasion had a significantly poorer prognosis (27,28), indicating the significant role that the tumor and hepatic blood vessel relationship plays in patient prognosis. However, when the tumor is adjacent to the vessel yet without vascular invasion, it could be regarded as a perivascular pathological change (10,29). As for perivascular HCC, Kang et al. compared the prognosis of perivascular and nonperivascular HCC treated with percutaneous RFA, reporting that there was no significant between the two group of patients (20); however, the survival rate of periportal HCC was reported as poor compared with that of nonperiportal HCC treated with percutaneous RFA (30). It has also been reported that after microwave ablation treatment, peribiliary HCC had worse long-term tumor control compared with non-peribiliary HCC (31). Several studies have reported that hepatectomy has better prognostic results compared with RFA in perivascular HCC (19,32). After hepatectomy, there is a lack of research demonstrating the prognosis differences between perivascular HCC and nonperivascular HCC. The ongoing digital transformation in surgery, including concepts such as the Internet of Things (IoT), aims to enhance procedural precision and data integration, which may further refine treatment selection for complex cases such as perivascular HCC (33). In our study, a retrospective analysis of preoperative imaging data from a substantial cohort of HCC patients revealed that tumors in proximity to the portal vein were indeed associated with patient prognosis. However, no significant correlation was observed between tumors adjacent to the hepatic vein and patient outcomes.
We hypothesized that the difference in prognosis between portal and hepatic veins may be related to the anatomical structure of the Glisson’s capsule (34). It is possible that when HCC is adjacent to the portal vein, the tumor could potentially infiltrate the surrounding perivascular fibrous tissue or spread along the Glisson’s capsule, leading to intrahepatic metastases and consequently poorer surgical outcomes, including decreased DFS and OS. This speculative mechanism suggests that patients with tumors adjacent to the portal vein might undergo meticulous preoperative evaluation using imaging techniques to assess the feasibility of completely resecting the invaded vessel and the extent of hepatic tissue involved (35). Such an approach could potentially enhance the surgical prognosis. Understanding the biological mechanisms that drive liver regeneration, such as the role of Toll-like receptors, may be key to improving functional recovery after such extensive resections (36). In contrast, when the tumor is adjacent to the hepatic vein, surgical dissection can often be performed without involving the Glisson’s capsule, which might explain why no significant prognostic difference was observed in this group. However, this hypothesis remains speculative and requires further mechanistic studies for validation.
Currently, there is still no clear and uniform definition of periovascular invasion in various current HCC staging systems. According to our findings, we found that tumors adjacent to the portal vein displayed more invasion and migration characteristics. As detailed in Table 3, beyond the tumor’s relationship with the portal vein, multivariate analysis has identified additional independent prognostic risk factors including the number of tumors, lymphatic metastasis, MVI, adjacent organ invasion, and the presence of satellite nodules. Collectively, these factors are recognized as indicators of the tumor’s invasive and metastatic potential (37-40), further emphasizing the multifaceted nature of cancer progression and its impact on patient outcomes. In addition, clinical observations have revealed a higher prevalence of tumor thrombus within the portal vein compared to the hepatic vein (11,41), suggesting a propensity for HCC to infiltrate the portal venous system. Therefore, the potential expansion of definition of vascular invasion should be considered. We hope that high-quality prospective studies will be available to compare and clarify the definition of vascular invasion.
Beyond conventional imaging evaluation, artificial intelligence is revolutionizing liver cancer diagnosis by enhancing the analysis of CT and MRI data for more accurate lesion detection and characterization (42). In this study, preoperative imaging assessments were conducted using enhanced CT and MRI scans, with the majority of patients undergoing these examinations within one week prior to surgery. Two seasoned doctors meticulously analyzed the venous phase of the CT or MRI images to ascertain the relationship between the tumor and blood vessels. Both CT and MRI were reported to have shown moderate sensitivity and high specificity in the detection of macroscopic tumors in veins (43). A clear demarcation between the tumor and the secondary branches of the intrahepatic vasculature was established. In instances where no discernible boundary was observed between the tumor and the intrahepatic blood vessels, the cases were classified as either aPV or aHV groups. For those cases that presented ambiguity, a consensus was reached through a collaborative review process. These cases were further confirmed by correlating with intraoperative surgical notes and postoperative pathological findings. Ultimately, this meticulous approach ensured that all cases were accurately classified and well characterized.
This study also had several limitations: firstly, its retrospective nature hindered the comprehensive collection of clinical data, which carries the potential for informative censoring despite balanced follow-up times between groups. Unmeasured factors or differential follow-up patterns related to patient or disease characteristics could affect survival estimates. These limitations should be considered when interpreting the reported DFS and OS outcomes, necessitating validation through prospective studies. Additionally, both CT and MRI were utilized for imaging assessments, providing valuable insights into tumor and liver vessel conditions; the inherent differences between these modalities could introduce some variability in the results, although the postoperative pathology ruled out cases of vascular invasion. Finally, and importantly, approximately 80% of the patients in our cohort had underlying chronic hepatitis B virus infection. Therefore, the generalizability of our results may be limited when applied to HCC populations with different etiologies, such as hepatitis C virus infection, non-alcoholic fatty liver disease, or alcohol-related liver disease. Future prospective multicenter studies including patients with diverse etiologies are warranted to confirm and extend our findings.
Conclusions
The preoperative radiological evaluation revealed that in HCC patients, tumor adjacency to the portal vein had a detrimental effect on the patient’s prognosis, whereas the hepatic vein did not seem to exert a similar impact.
Acknowledgments
None.
Footnote
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-2085/rc
Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-2085/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-2025-2085/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 at West China Hospital (No. 2022-264). Informed consent was waived in this retrospective study.
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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