Comparative analysis of right atrial function in arrhythmogenic right ventricular cardiomyopathy and dilated cardiomyopathy using cardiac magnetic resonance-feature tracking

Introduction

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare inherited cardiomyopathy characterized by a progressive fibrofatty replacement that principally involves the right ventricle (RV) (1). Dilated cardiomyopathy (DCM) constitutes a condition characterized by left or biventricular dilation and systolic dysfunction, with the absence of preload conditions or severe coronary artery disease (2). Despite the inclusion of “right ventricular” in the nomenclature, previous studies have demonstrated that ARVC can also manifest left ventricular (LV) involvement (sometimes predominant) or biventricular involvement in an advanced stage, or even before right cardiac dysfunction, leading to LV dilation, dysfunction, and late gadolinium enhancement (LGE) in subepicardial or midmyocardial distribution, which overlap with DCM (3). Meanwhile, right cardiac dysfunction may also be found in severe DCM patients (4). However, these findings have most often been reported in separate studies and have rarely been compared directly.

The right atrium is now recognized as a dynamic structure that assists in RV filling and maintaining hemodynamic stability during the cardiac cycle, serving the following functions: (I) reservoir function, collect and store blood of the systemic venous return during ventricular systole and atrial diastole; (II) conduit function, transfer blood passively and directly from the coronary and systemic veins to the RV during early ventricular diastole; and (III) booster function, pump blood actively into the RV by atrial contraction during late ventricular diastole, thereby completing ventricular filling (5). It has been well established that right atrial (RA) function may provide valuable insights into the diagnosis and prognosis of multiple cardiovascular diseases, such as cardiac amyloidosis, pulmonary artery hypertension, significant tricuspid regurgitation, and myocardial infarction (6-9). Nevertheless, the comparison analysis of RA functional alterations between patient cohorts with ARVC and DCM remains to be thoroughly elucidated.

Recently, cardiac magnetic resonance imaging (MRI) has emerged as the reference standard for cardiac structural and functional assessment due to its unrestricted acquisition window and higher signal-to-noise ratio compared with echocardiography (10). Cardiac magnetic resonance-feature tracking (MR-FT), a novel noninvasive technique for myocardial deformation evaluation based on routinely available steady-state free precession sequences, is becoming extensively utilized among cardiac studies (6,11). There is increasing evidence that MR-FT-derived RA deformation parameters may serve as more sensitive indicators for assessing RA function compared with RA emptying fraction (RAEF) (5,7). However, there is a paucity of comparative research regarding RA dysfunction in ARVC and DCM using this technique. As ARVC and DCM represent distinct pathophysiological entities, the underlying difference in RA dysfunction patterns may provide insights into their tailored management strategies. Therefore, the aim of the present study was to investigate the potential differences in RA functional alterations between ARVC and DCM patients using MR-FT, thereby enhancing the understanding of disease mechanisms. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2133/rc).

Methods

Study population

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This retrospective, observational, and dual-center study was approved by the ethics committee of The First Affiliated Hospital of Zhejiang Chinese Medical University (No. 2022-KLS-207-01) with approval acknowledged by The First Affiliated Hospital of Zhejiang Chinese Medical University and The Second Affiliated Hospital of Zhejiang University School of Medicine, and the requirement for patients’ consent was waived due to its retrospective nature. From June 2018 to December 2022, 46 consecutively diagnosed patients with ARVC and 221 patients with DCM who underwent cardiac MR examination were included from The First Affiliated Hospital of Zhejiang Chinese Medical University and The Second Affiliated Hospital of Zhejiang University School of Medicine. The ARVC diagnosis was defined according to the task force criteria (TFC) revised in 2010: in the presence of 2 major, 1 major and 2 minor, or 4 minor diagnostic criteria from different categories including MRI, echocardiography, and electrocardiogram (1). The DCM diagnostic criteria adhere to the World Health Organization and International Society and Federal of Cardiology definitions (12): (I) a reduced left ventricular ejection fraction (LVEF) <45%; (II) LV end-diastolic volumes >2 standard deviations from normal according to nomograms corrected by body surface area (BSA) and age. The exclusion criteria encompassed the following: (I) ischemic heart diseases (defined as a history of myocardial infarction, or greater than 50% luminal stenosis identified by coronary angiography, or the presence of an infarct pattern of LGE on cardiac MRI; (II) hypertrophic, restrictive, or infiltrative cardiomyopathies; (III) moderate-to-severe valvular heart diseases; (IV) other congenital heart diseases; (V) acute myocarditis or known history of myocarditis; and (VI) other etiologies potentially leading to secondary DCM, including but not limited to alcoholic cardiomyopathy and peripartum cardiomyopathy. Moreover, patients with suboptimal image quality deemed unsuitable for accurate RA MR-FT analysis or combined with atrial fibrillation were initially excluded. Subsequent to age- and sex-matching, the final cohort comprised 38 patients with ARVC and 98 patients with DCM (Figure 1). Meanwhile, we also recruited 72 age- and sex-matched healthy individuals without hypertension, diabetes, or any known cardiovascular diseases to provide a normal standard of cardiac MRI parameters.

Figure 1 Flowchart of ARVC and DCM patient cohorts’ inclusion. ARVC, arrhythmogenic right ventricular cardiomyopathy; DCM, dilated cardiomyopathy.

Additionally, a subgroup analysis was conducted to evaluate the differential diagnostic value of RA strain parameters in distinguishing between patients with ARVC combined with LV dysfunction and those with DCM combined with RV dysfunction. LV dysfunction was defined as an LVEF of less than 50% (13), and RV dysfunction was defined as an RV ejection fraction (RVEF) of less than 40% (14).

Cardiac MRI protocols

All patients underwent cardiac MRI on 3.0T MR scanner (Discovery MR750, GE Healthcare, Chicago, IL, USA) and 1.5T MR scanners (Signa HD Excite, GE, USA and Magnetom Avanto, Siemens, Erlangen, Germany). Breath holds with retrospective electrocardiogram gating were applied for acquiring standard cine images, comprising three long-axis views (2-, 3-, and 4-chamber) and a stack of contiguous parallel short-axis slices covering the whole LV and RV from the base to the apex. The detailed cardiac MRI scan acquisition information is available in Appendix 1.

Cardiac MR analysis for cardiac function

All cardiac MR images were analyzed collaboratively in a random order using dedicated commercial software (CVI42 version 5.14.2; Circle Cardiovascular Imaging, Calgary, Canada) by two researchers (Y.G. and W.L., with 6 and 2 years of cardiac MR-FT analysis experience, respectively), who were blinded to the clinical information. Basic cardiac MR analyses are presented in Appendix 1. RA deformation parameters were assessed using MR-FT in the 4-chamber view. Both RA endocardial and epicardial borders were manually delineated using a point-and-click approach at the phase when RA reaches the minimum volume following atrial contraction, with the superior vena cava and RA appendage excluded from the contours. The software then automatically identified the myocardial tissue in each subsequent frame under visual surveillance, and the initial contours were manually adjusted when considered requisite (15). RA reservoir strain (εs) and peak positive strain rate (SRs), conduit strain (εe) and peak early negative strain rate (SRe), and booster strain (εa) and peak late negative strain rate (SRa) were obtained according to strain-time curves and SR-time curves (Figure 2). Biventricular global radial strain (GRS), global circumferential strain (GCS), and global longitudinal strain (GLS) were measured on short- and long-axis cine images using MR-FT according to previously described methods (15).

Figure 2 Quantification of RA reservoir, conduit, and booster function based on cardiac MR-FT-derived strain and SR parameters. εa, booster strain; εe, conduit strain; εs, reservoir strain; MR-FT, magnetic resonance-feature tracking; RA, right atrial; SR, strain rate; SRa, peak late negative strain rate; SRe, peak early negative strain rate; SRs, peak positive strain rate.

Reproducibility

We randomly selected 30 cases [10 with ARVC, 10 with DCM, and 10 healthy controls (HC)] for assessing reproducibility using intraclass correlation coefficients (ICCs) and Bland-Altman analysis. Inter-observer reproducibility was determined by the same two operators independently to provide a blinded assessment. The intra-observer reproducibility was conducted by one of those operators (Wenqi Liu), 1 month later, blinded to the result from the first measurement to avoid a recall bias.

Statistical analysis

Statistical analyses were performed using the software SPSS 27.0 (IBM Corp., Armonk, NY, USA) and GraphPad Prism (Version 9.5, Graph-Pad software, San Diego, CA, USA). Normally distributed continuous variables were represented as means ± standard deviations (SDs), non-normally distributed variables as medians and interquartile ranges (IQRs), and categorical variables as numbers and percentages. Comparisons of continuous variables among the three groups (ARVC, DCM, and HC) were performed using one-way analysis of variance (ANOVA) with post hoc least significant difference (LSD) tests for normally distributed continuous variables, and Kruskal-Wallis test with post hoc Dunn’s test for non-normally distributed variables. Categorical variables were compared using the chi-square test. Multiple comparisons of continuous variables were tested with Bonferroni correction. The associations of RA strains and RAEFs were investigated using simple linear regression analysis, and the correlation coefficient (r) was calculated using Pearson method and r_s was calculated using Spearman’s method. The association was considered strong, moderate, and weak when |r| ≥0.7, 0.4≤ |r| <0.7, and |r| <0.4, respectively. Receiver operating characteristic (ROC) analysis was applied to evaluate the differential diagnostic value of RA deformation parameters with the calculated area under the curve (AUC). Reproducibility was considered excellent when ICC >0.74, good when ICC =0.60–0.74, fair when ICC =0.40–0.59, and poor when ICC <0.40 (16). Two-tailed P values of <0.05 were considered as statistically significant.

Results

Baseline characteristics

The final study cohort comprised 38 patients with ARVC (mean age 40.1±15.6 years, 68.4% male), 98 patients with DCM (mean age 41.9±9.8 years, 68.4% male), and 72 HC [at a median of 41.0 (IQR, 27.0–52.0) years, 68.1% male] (Table 1). There were no significant differences in age (P=0.466) and male proportion (P=0.999) among the three groups. Compared with ARVC patients and HC, those with DCM showed higher BSA, body mass index (BMI), and heart rate (all P<0.05). Patients with ARVC, in turn, demonstrated higher systolic blood pressure than both HC and patients with DCM (all P<0.05), and lower fasting blood glucose (FBG) compared with the DCM group (P<0.05). Diabetes was more prevalent in DCM compared with ARVC (P=0.020). The frequency of aspirin administration was comparable between patient cohorts with ARVC and DCM (P=0.681), whereas utilizations of β-blockers, angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB), and diuretics were more common in DCM (all P<0.001).

LV and RV volumetric and strain parameters

Compared with HC, both ARVC and DCM patient cohorts exhibited significantly reduced LVEF and RVEF (all P<0.05) (Table 2). No significant difference was observed in LV cardiac index (LVCI) or RV cardiac index (RVCI) between ARVC and HC (P=1.000 and P=0.057, respectively), yet patients with DCM showed the lowest LVCI and RVCI among the three groups (P<0.05). Although DCM exhibited reduced biventricular stroke volume index (SVi) compared with those in the ARVC and HC groups, there was no significant difference found between ARVC and HC in LVSVi (P=0.835). Both patient cohorts with ARVC and DCM exhibited dilated ventricles with higher biventricular end-diastolic volume index (EDVi) and end-systolic volume index (ESVi) compared with HC (all P<0.05). Notably, DCM patients showed greater LV dilation compared with ARVC, with higher left ventricular indexed end-diastolic volume (LVEDVi) and left ventricular indexed end-systolic volume (LVESVi) (both P<0.001), whereas ARVC exhibited greater RV dilatation reflected by a higher right ventricular indexed end-diastolic volume (RVEDVi) (P<0.001). Both patients with ARVC and those with DCM exhibited significantly lower right ventricular global radial strain (RVGRS), right ventricular global circumferential strain (RVGCS), and biventricular GLS, compared with HC, with DCM patients showing more pronounced reductions (all P<0.05). However, no significant differences were observed in LVGRS and LVGCS between the ARVC and HC groups (P=0.113 and P=0.057, respectively), nor in RVGCS between the ARVC and DCM groups (P=0.062).

RA volumetric and deformation parameters

No significant differences were observed in maximum RA volume index (RA Vmaxi) (P=0.691) and pre-atrial contraction RA volume index (RA Vpaci) (P=0.836) among the three groups, yet minimum RA volume index (RA Vmini) in DCM patients was significantly higher compared with HC (P=0.019). Both ARVC and DCM patient cohorts exhibited reduced total RAEF (RAEF total) and active RAEF (RAEF booster) (all P<0.001), with a more pronounced decrease in RAEF total in DCM patients (P<0.05). Although DCM exhibited a significantly reduced passive RAEF (RAEF passive) compared with HC, no significant difference was observed between ARVC and HC (P=0.222) (Table 3).

For RA deformation parameters, patients with DCM had the lowest RA εs, εe, SRs, SRe, and SRa across the three groups (all P<0.05), whereas no significant difference was observed in εa and RA SRa between ARVC and HC (P=0.060 and P=0.257, respectively), nor in εa between ARVC and DCM (P=0.061) (Table 3 and Figure 3). Examples of RA strain and SR curves obtained using MR-FT in patients with ARVC, DCM, and HC are displayed in Figure 4.

Figure 3 Comparisons of RA εs, εe, εa, SRs, SRe, and SRa (A-F) values among ARVC, DCM, and HC Groups. *, P<0.05 when compared with HC. ^†, P<0.05 when compared with DCM patients. εa, booster strain; εe, conduit strain; εs, reservoir strain; ARVC, arrhythmogenic right ventricular cardiomyopathy; DCM, dilated cardiomyopathy; HC, healthy controls; RA, right atrial; SRa, peak late negative strain rate; SRe, peak early negative strain rate; SRs, peak positive strain rate.

Figure 4 Examples of RA strain and SR measurements in HC (A), patient with ARVC (B) and with DCM (C) using cardiac MR-FT in the four-chamber view (left), and the corresponding RA strain (D) and SR (E) curves for each example (right). ARVC, arrhythmogenic right ventricular cardiomyopathy; DCM, dilated cardiomyopathy; HC, healthy controls; MR-FT, magnetic resonance-feature tracking; RA, right atrial; SR, strain rate.

Correlation between RA deformation parameters and RAEF parameters

Simple linear regression analysis demonstrated that RA deformation parameters were moderately to strongly correlated with RAEFs for RA reservoir, conduit, and booster function in all three groups (ARVC, DCM, and HC) (Table S1 and Figure 5). Specifically, RA εs showed a strong correlation with RAEF total across all groups: ARVC (r=0.81), DCM (r=0.74), and HC (r=0.73) (all P<0.001). RA εe moderately correlated with RAEF passive in HC (r=0.66), and strongly correlated in ARVC (r=0.76) and DCM patients (r=0.77, all P<0.001). RA εa exhibited moderate correlations with RAEF booster in DCM (r=0.61) and HC (r=0.55), yet a strong correlation in ARVC (r=0.73, all P<0.001). The results were robust when Spearman correlation was applied, with differences in correlation coefficients between Pearson and Spearman analyses being <0.1 across all groups (Table S1).

Figure 5 Correlation between RA strains (A-C; εs, εe, and εa) and RAEFs for RA Functions across the three Groups (ARVC, DCM, and HC). Specific r values were included. εa, booster strain; εe, conduit strain; εs, reservoir strain; ARVC, arrhythmogenic right ventricular cardiomyopathy; DCM, dilated cardiomyopathy; HC, healthy controls; RA, right atrial; RAEF, right atrial emptying fraction; RAEF booster, right atrial booster emptying fraction; RAEF passive, right atrial passive emptying fraction; RAEF total, right atrial total emptying fraction.

RA deformation parameters in ARVC-LV dysfunction and DCM-RV dysfunction subgroups

A total of 10 of 38 patients with ARVC exhibited LV dysfunction, whereas 77 of 98 patients with DCM presented with RV dysfunction. In the subgroup analysis, ROC analysis demonstrated that RA εs [AUC: 0.71; 95% confidence interval (CI): 0.49–0.92] and εe (AUC: 0.70; 95% CI: 0.47–0.93) showed significant differential diagnostic value in distinguishing ARVC patients with LV dysfunction from DCM patients with RV dysfunction (both P<0.05) (Table S2 and Figure S1).

Reproducibility

Intra- and inter-observer reproducibility for RA strain and SR measurements is presented in Table 4. The inter- and intra-observer reproducibility of RA deformation measurements was excellent, with all ICCs >0.75, along with narrow limits of agreement in Bland-Altman plots, as presented in Figures S2,S3.

Discussion

The importance of evaluating RA function is being increasingly acknowledged, given its role in the diagnosis, prognosis, and risk stratification of a spectrum of cardiovascular diseases (8,17,18). The development of MR-FT has provided a promising approach to assessing RA myocardial mechanics and deformation performance. In the current study, we conducted a comprehensive comparison of RA function alterations among patients with ARVC, DCM, and HC based on MR-FT technique. The primary findings are as follows: (I) patients with both ARVC and DCM exhibited impaired RA reservoir, conduit, and booster function when compared with HC; (II) although RV dilation was observed to be more severe in ARVC, RA dysfunction was more pronounced in patients with DCM; (III) a robust correlation was observed between RA deformation parameters and RAEFs across the cohorts of ARVC patients, DCM patients, and HC.

RA involvement in ARVC

ARVC is histologically characterized by the progressive replacement of the ventricular myocardium by fibrofatty tissue and cardiomyopathic changes that predominantly appear in the RV free wall (1). However, previous animal studies have confirmed atrial involvement in ARVC (in 17% of feline models and in 35% of canine ARVC models) (19,20). Moreover, in autopsy materials of three patients with ARVC, Li et al. (21) found similar pathological changes in RA with fibrofatty tissue replacing cardiomyocytes in addition to RV, which may help to explain the high prevalence of atrial fibrillation in ARVC. Within this context, RA dysfunction in ARVC may be less dependent on global hemodynamic loading conditions and more closely related to intrinsic atrial myocardial substrate abnormalities and impaired electromechanical coupling (21). Zheng et al. (22) reported that ARVC patients exhibited significant RA strain impairment in comparison with HC on cardiac MRI, and that RA εs and RA εa may serve as independent predictors for adverse cardiac events. Using MR-FT, Zghaib et al. (23) characterized RA functions in a large cohort of ARVC patients and found impaired RA deformation parameters, which may predict incident atrial arrhythmia after adjusting for clinical and ventricular characteristics. Consistent with these studies, ARVC patients in our study also exhibited RA involvement with reduced RA εs, εe, and εa in a cross-sectional analysis with HC, suggesting increased RA stiffness and diminished contractility in patients with ARVC.

RA dysfunction in DCM

Analogous to ARVC, DCM is histologically characterized by varying degrees of interstitial fibrosis and fibrofatty infiltration, yet mainly involves LV with substantial hypertrophy and degeneration of myocytes (24). Since the mechanical functional relationship between left atrium (LA) and LV, previous studies on DCM have primarily focused on LA and have confirmed the prognostic value of LA in DCM (25,26). Meanwhile, using two-dimensional speckle tracking, Tigen et al. (27) found a worse RA function in patients with non-ischemic DCM compared with HC; Charisopoulou et al. (28) revealed that low peak RA longitudinal strain was one of the independent predictors of RV assistant device support after LV assistant device implantation in a cohort of 70 patients with advanced chronic heart failure, predominantly consisting of those with DCM. That is to say, RA dysfunction may also be found in DCM. Additionally, a very recent cardiac MR-FT study (11) demonstrated the independent prognostic value of RA εe in patients with DCM, which also provided evidence for RA involvement in these patients. In line with previous studies, we observed that compared with age- and sex-matched HC, DCM patients showed impaired RA deformation ability during the whole cardiac cycle with reduced RA reservoir, conduit, and booster function.

Comparison of RA functional alterations between ARVC and DCM

In the present study, despite more pronounced RV dilation in patients with ARVC, patients with DCM exhibited a more pronounced impairment in RA phasic function than those with ARVC, as reflected by significantly lower RA strain and strain rate parameters. This dissociation in RA functional alteration between the two cardiomyopathies suggests that their RA dysfunction may be driven by distinct pathophysiological substrates rather than by the anatomical origin of disease alone. In DCM, significant impairment in all three functions of RA may be attributed to persistent hemodynamic overload secondary to left heart failure (29). Specifically, significant LV systolic and diastolic dysfunction in DCM leads to chronically elevated pulmonary arterial pressure, resulting in sustained RV overload and increased filling pressure (30). This adverse loading condition gradually promotes RA volume overload, progressive fibrotic remodeling, and functional tricuspid regurgitation, thereby preferentially impairing RA reservoir and conduit function through restriction of passive filling and emptying under a reduced atrioventricular pressure gradient (30,31). By contrast, despite the more marked RV dilation in ARVC, the left heart is less frequently involved and pulmonary hypertension is less prevalent compared with DCM (1); this may allow partial preservation of RA passive mechanics and atrioventricular coupling.

These findings may be further interpreted within a continuous atrioventricular functional framework analogous to a Möbius strip, in which atrial and ventricular mechanics form a bidirectionally coupled system rather than independent compartments (32). The biventricular adverse loading conditions in DCM patients may disrupt this functional continuum and compromise passive phases of RA function. In contrast, the regional RV involvement and in ARVC might allow for partial preservation of atrioventricular coupling. Furthermore, RA dysfunction in DCM may be attributed to the RV dysfunction exacerbated by impaired “ventricular interdependence”—a functional interaction through which LV contraction augments RV contraction due to the shared oblique fibers within the interventricular septum, whereby reduced LV contribution to RV systolic performance in the setting of pulmonary hypertension may further compromise RV function, which in turn impairs RA mechanics (33). By contrast, pathological changes in ARVC involve the interventricular septum in only 20% of patients, and usually start from the epicardium and extend towards the endocardium (3,33), which means RV systolic function in ARVC tends to be less affected, thus has a milder impact on RA compared with DCM.

Association of RA deformation parameters with RAEFs and clinical implications

In the current study, we observed that RA deformation parameters significantly correlated with RAEFs for atrial reservoir, conduit, and booster function, which was consistent with previous studies (34,35). As RAEF reduction has been previously confirmed to predict the risk of adverse events (36), reduced RA deformation parameters may suggest intensified RV support in DCM, including optimizing preload, decreasing afterload, and inotropic interventions (37). In ARVC, the relatively preserved RA booster function may delay overt right heart failure, yet still warrants enhanced arrhythmia monitoring due to the coexisting myocardial fibrosis (3). Notably, subgroup analysis in the current study demonstrated that RA εs and RA εe held certain differential diagnostic value between ARVC and DCM, suggesting the potential incremental utility of RA strain assessment in discriminating these two cardiomyopathies.

In this study, cardiac MR-FT showed excellent intra- and inter-observer reproducibility for RA strain measurements, which was consistent with a previous MR-FT study by Tang et al. involving patients with connective tissue disease (38). Prior speckle-tracking echocardiography studies have reported the clinical and prognostic value of RA strain in pulmonary hypertension and cardiac amyloidosis (7,39). Given its superior reproducibility (40), cardiac MR-FT holds promise for providing more accurate measurements and may further improve the reliability and prognostic stratification and risk assessment.

Limitations

There were several limitations to this study. The retrospective design may have induced potential selection bias, and dedicated RA-specific cine acquisitions were not available. Whereas, RA volumetric and deformation parameters were derived from the standard 4-chamber view using a widely adopted and validated MR feature-tracking approach. Second, the cardiac MRI examinations in this study were performed on 1.5T and 3.0T scanners, which may have introduced variability in strain measurements due to differences in field strength and vendors. Nevertheless, previous investigations have shown that MR-FT myocardial strain assessment is not affected by field strength or vendors (41,42). Third, the sample sizes of patient cohorts with ARVC and DCM were inconsistent due to their variable prevalence rates. However, to enhance the accuracy of comparisons and ensure baseline consistency, we performed age- and sex-matching for these two conditions. Lastly, patients with atrial fibrillation were excluded from this study. Future investigations are warranted to explore the relationship between RA function and atrial fibrillation.

Conclusions

Both patients with ARVC and those with DCM exhibit a decline in RA function compared with HC. Despite the more pronounced RV dilation in ARVC, DCM exhibited a significantly greater impairment in RA reservoir and conduit function. These findings highlight distinct patterns of RA functional alterations between ARVC and DCM, underscoring the utility of MR-FT in quantifying atrial mechanics.

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-aw-2133/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2133/dss

Funding: This study received funding by the National Natural Science Foundation of China (No. 81971600 to M.X.), the “Pioneer” and “Leading Goose” R&D Program of Zhejiang (No. 2022C03046 to M.X.), the Talent Cultivation Program for Outstanding Innovative Individuals at Zhejiang Chinese Medical University (No. 2024YJSBJ002 to Y.G.), and Jinhua public welfare Technology Application Research Project (No. 2025-4-274 to Wanzhen Li).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-aw-2133/coif). Y.G. reports funding support from the Talent Cultivation Program for Outstanding Innovative Individuals at Zhejiang Chinese Medical University (No. 2024YJSBJ002). Wanzhen Li reports funding support from the Jinhua public welfare Technology Application Research Project (No. 2025-4-274). M.X. reports funding support from the National Natural Science Foundation of China (No. 81971600) and the “Pioneer” and “Leading Goose” R&D Program of Zhejiang (No. 2022C03046). The other 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. This study was approved by the ethics committee of The First Affiliated Hospital of Zhejiang Chinese Medical University (No. 2022-KLS-207-01) with approval acknowledged by The First Affiliated Hospital of Zhejiang Chinese Medical University and The Second Affiliated Hospital of Zhejiang University School of Medicine, and the requirement for patients’ consent was waived due to its retrospective nature.

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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