Cardiac involvement in patients with anti-MDA5 Ab+ dermatomyositis: a cross-sectional study with cardiac magnetic resonance

Introduction

Idiopathic inflammatory myopathy (IIM) is a heterogeneous group of autoimmune disorders characterized by systemic inflammation of skeletal muscles, which may also involve other organs, leading to a wide range of clinical manifestations and outcomes (1). Among these, dermatomyositis (DM) is distinguished by its characteristic skin manifestations and muscle involvement. The discovery of myositis-specific autoantibodies has provided a powerful tool for subclassifying IIM, aiding in diagnosis and prognostication. Particular attention has centered on the anti-MDA5 antibody, which was originally identified in 2005 as the anti-CADM-140 antibody (2). Patients with anti-MDA5 antibody-positive dermatomyositis (anti-MDA5 Ab+ DM) exhibit a high mortality rate, largely driven by the strong association with rapidly progressive interstitial lung disease (RP-ILD) (3). Although interstitial lung disease (ILD) is well-documented in anti-MDA5+ DM, cardiac involvement, although less frequently reported, represents an underrecognized and potentially life-threatening manifestation (4,5). Emerging evidence suggests that myocardial involvement (MI) in anti-MDA5+ DM is not uncommon and may contribute to the observed high mortality in these patients (4). Cardiac manifestations in these patients can range from myocarditis and pericarditis to conduction abnormalities (6). However, the prevalence and clinical significance of MI in anti-MDA5 Ab+ DM remain poorly understood due to the lack of systematic studies utilizing advanced imaging modalities.

Cardiac magnetic resonance (CMR) is widely regarded as the reference standard for noninvasive evaluation of myocardial structure and function, with particular strength in detecting inflammation and fibrosis (7). Techniques such as native T1 and T2 mapping provide quantitative metrics for non-invasively evaluating myocardial tissue characteristics and have proven invaluable for diagnosing myocarditis and other myocardial pathologies (8). Moreover, late gadolinium enhancement (LGE) imaging has been widely used to identify focal fibrosis and has shown prognostic value across various cardiovascular conditions (9). Despite the utility of these tools, their application in studying MI in anti-MDA5+ DM has been limited, leaving a critical gap in understanding the burden and impact of cardiac involvement in these patients (10).

Thus, this study aimed to assess MI in anti-MDA5 Ab+ DM patients using CMR techniques, including T1 and T2 mapping and LGE. We hypothesized that myocardial abnormalities would be prevalent even in the absence of overt cardiac symptoms, highlighting the potential of CMR as a sensitive tool for early detection and systematic risk assessment in these patients. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-974/rc).

Methods

This single-center, cross-sectional study was conducted in compliance with the Declaration of Helsinki and its subsequent amendments, and was approved by the Ethics Committee of China-Japan Friendship Hospital (approval No. 2021-KY-060). All participants signed informed consent before the CMR scan. Patients diagnosed with anti-MDA5 Ab+ DM between May 2022 and May 2024 were recruited. The diagnosis of DM was based on the 239th ENMC International Workshop criteria (11). The detection of anti-MDA5 antibodies was performed by the Rheumatology and Immunology Department using the western blot method. The results of this test were used to identify patients with anti-MDA5 antibodies for inclusion in our study. Age- and gender-matched healthy volunteers with normal electrocardiogram and echocardiography findings served as the healthy controls (HCs). All patients underwent non-contrast and contrast-enhanced CMR, whereas HCs underwent noncontrast CMR only. The exclusion criteria were as follows: (I) non-diagnostic CMR image quality; (II) prior coronary stent implantation or coronary artery bypass grafting; (III) confirmed or suspected active infection; (IV) a history of congenital heart disease, coronary heart disease, cardiomyopathy, or malignancy; (V) other connective-tissue diseases or myositis-specific autoantibodies; and (VI) hypothyroidism or renal/hepatic dysfunction. For patients with anti-MDA5 Ab+ DM, laboratory work-up included a cytokine panel [interleukin (IL)-6, IL-8, IL-10, IL-1β, tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ)], inflammatory markers [erythrocyte sedimentation rate (ESR), ferritin (FER), lactate dehydrogenase (LDH)], and N-terminal pro-B-type natriuretic peptide (NT-proBNP). The flowchart of this study is shown in Figure 1.

Figure 1 A flow chart of patient enrollment and study design. Based on the predefined exclusion criteria, 42 patients successfully enrolled in this study. Anti-MDA5 Ab+, anti-MDA5 antibody-positive; CADM, clinically amyopathic dermatomyositis; CMR, cardiac magnetic resonance; DM, dermatomyositis.

High-resolution chest computed tomography imaging analysis

All 42 anti-MDA5 Ab+ DM patients underwent chest high-resolution computed tomography (HRCT) imaging to assess the presence of ILD. The HRCT scans were performed without the use of contrast agents, following standard protocols. The images were reviewed by experienced radiologists, and the presence of interstitial changes was determined based on characteristic features such as ground-glass opacities, reticular patterns, honeycombing, and traction bronchiectasis. Patients were classified as ILD-positive or ILD-negative according to the presence or absence of these findings, consistent with the typical pulmonary manifestations seen in dermatomyositis.

CMR protocol

All examinations were performed on a 1.5-T clinical MR system (MAGNETOM Area, Siemens Healthcare, Erlangen, Germany) using an 18-channel phased-array surface coil. Images were acquired with retrospective electrocardiogram (ECG) gating during end-expiratory breath-holds. The protocol included: (I) conventional sequences: cine imaging in short- and long-axis views and T2-weighted imaging (T2WI); (II) quantitative mapping: native T1 and T2 mapping; (III) LGE. A contiguous short-axis stack covering the left ventricle (LV) from the apex to the level of the mitral annulus was obtained. T2WI and native T1/T2 mapping were prescribed in the same short-axis planes as the cine images.

A contiguous short-axis stack spanning both ventricles from base to apex, together with a 4-chamber long-axis cine was acquired using a balanced steady-state free precession sequence. Typical parameters were as follows: repetition time/echo time (TR/TE) =4.5/1.1 ms, flip angle (FA) =50–60°, slice thickness =6 mm, in-plane spatial resolution =1.8×1.8 mm², temporal resolution =40 ms, and 25 reconstructed cardiac phases. Native T1 mapping employed an ECG-gated, diastole-triggered, single-shot modified Look-Locker inversion recovery (IR) sequence with protocol 3 (3 sec) 3 (3 sec) 5, yielding seven images in 17 heartbeats, with the following acquisition settings: TE =1.2 msec, TR =2.8 ms, field of view (FOV) =360×360 mm, matrix =128×128, FA =35°, bandwidth =100 kHz, slice thickness =8 mm, slice gaP =0 mm. T2 mapping was generated with a double IR fast spine echo sequence with four TE (11, 33, 55.1, and 77.1 msec); total echo train length =16, TR = 1RR, FA =90°, matrix =160×160, bandwidth =83.33 kH, slice thickness =8 mm, slice gaP =3 mm.

LGE imaging used a phase-sensitive IR sequence with TE =1.94 ms, TR =684 ms, FA =20°, and spatial resolution =1.4×1.4×8 mm. The LGE stack was acquired in the same slice position as cine imaging approximately 15 minutes after intravenous gadopentetate dimeglumine (Bayer, Berlin, Germany) at 0.1 mmol/kg, injected at 3 mL/s and followed by a 20-mL saline flush at 2 mL/s.

CMR analysis

CMR images in Digital Imaging and Communications in Medicine (DICOM) format were exported to a syngo.via workstation (Siemens Healthcare). Left ventricular (LV) myocardial native T1 and T2 values were obtained according to the American Heart Association (AHA) 16-segment model (12) (Figure S1). Two cardiac radiologists independently performed manual region of interest (ROI) placement on the T1 and T2 maps, and the mean of the two readings for each segment was recorded as the segmental T1/T2 value.

Endocardial and epicardial contours at end-diastole and end-systole were generated on the serial short-axis stack using syngo.via Cardiac Function, with manual adjustment as needed. Standard LV metrics—including ejection fraction (EF), end-diastolic/systolic volume (EDV/ESV), indexed volumes (EDVI/ESVI), stroke volume (SV), cardiac output (CO), and cardiac index (CI)—were then computed automatically.

LGE was assessed in consensus by two cardiovascular radiologists (each with 10 years of experience) who were blinded to all clinical information. They recorded presence/absence, location, and pattern of enhancement; hyperenhancement seen in two orthogonal planes was regarded as positive LGE.

Moreover, main pulmonary artery diameter (MPA) and ascending aortic diameter (Aao) were respectively measured to the ratio of MPA to Aao (MPA/Aao ratio) (Figure S2).

Statistical analysis

Statistical analyses and graphing were performed using SPSS 29.0 (IBM Corp., Armonk, NY, USA) MedCalc 15.0 (MedCalc Software, Ostend, Belgium), and GraphPad Prism 10.4.1 (GraphPad Software, San Diego, CA, USA). Before inferential testing, data distributions were examined with normality tests and visual inspection of distribution plots. Continuous variables were reported as mean ± standard deviation (SD). Between-group comparisons (anti-MDA5 Ab+ DM vs. HCs) employed the independent-samples t-test when normality was satisfied, and the Mann-Whitney U test otherwise; categorical variables were compared with the Chi-squared test. Interobserver reproducibility was assessed using the intraclass correlation coefficient, interpreted as poor (<0.50), moderate (0.50–0.75), good (0.75–0.90), and excellent (>0.90). A two-sided P<0.05 was considered statistically significant.

Results

Patient characteristics

A total of 42 patients with anti-MDA5 Ab+ DM were finally enrolled in this study, of which 23 (54.76%) were male, and the median age was 45 [23–67] years. The disease duration of the patients ranged from 6 to 13 months. Meanwhile, 29 age-and gender-matched healthy volunteers were grouped into HCs group. The baseline characteristics of all participants are provided in Table 1. Body mass index (BMI), blood pressure, creatine kinase myocardial band (CK-MB), high-sensitivity troponin l (hsTnl) MPA and MPA/Aao ratio, were comparable between the anti-MDA5 Ab+ DM group and HC group. All patients had ILD on HRCT and eight patients had pericardial effusion. Based on predefined biomarker abnormality thresholds, 42 patients with MDA5 Ab+ DM were respectively stratified into three subgroups: (I) cytokine-abnormal group (45.2%, 19/42) versus cytokine-normal group (54.8%, 23/42); (II) inflammatory marker-positive group (45.2%, 19/42) versus inflammatory marker-negative group (54.8%, 23/42); (III) NT-pro-BNP-normal group (21.4%, 9/42) versus NT-pro-BNP-abnormal group (78.6%, 33/43).

LV function

Table 2 shows the LV function metrics between anti-MDA5 Ab+ DM patients and HCs. Compared to HCs, anti-MDA5 Ab+ DM patients had lower LVEF (60.0%±7.0% vs. 66.9%±6.2%, P<0.001), SV (61.3±14.0 vs. 79.8±13.9 mL, P<0.001), CO (4.8±1.1 vs. 5.9±1.3 L/min, P<0.001), and CI (2.8±0.5 vs. 3.0±0.5 L/min/m², P=0.048).

T1, T2 mapping and LGE

A total of 672 LV myocardial segments of 42 patients were available for T1 and T2 measurements. As shown in Table 1 and Figure 2, the mean values of LV global native T1 value (1052.3±43.3 vs. 1019.5±33.1 ms, P<0.001) and T2 (52.5±3.7 vs. 48.7±3.1 ms, P<0.001) value in anti-MDA5 Ab+ DM patients were significantly higher than those in HCs. All parameters demonstrated good inter-observer reproducibility (intraclass correlation coefficients of 0.86 and 0.81 T1 and T2 values, respectively). Cutoff thresholds were set at two SD above the HC mean: T1 =1,085.7 ms and T2 =54.9 ms. Some 200 (29.8%) LV segments from 38 (90.5%) anti-MDA5 Ab+ DM patients manifested elevated native T1 values, and 198 (29.5%) LV segments from 35 (83.3%) patients showed increased T2 values (13).

Figure 2 Scatter plots of native T1 and native T2 of anti-MDA5 Ab+ DM patients and healthy controls. Anti-MDA5 Ab+ DM, anti-MDA5 antibody-positive dermatomyositis.

Figure 3 respectively shows LV myocardial native T1 and T2 value according to the AHA 16-segment model. The native T1 value of segments 1, 3, 4, 7, 8, 9, 10, 11, 12, 14, and 16 were significantly higher in anti-MDA5 Ab+ DM patients than in HCs (P<0.05). The T2 value of segments 1–16 (except segment 14) were significantly elevated in anti-MDA5 Ab+ DM patients compared to HCs (P<0.05).

Figure 3 Native T1 and T2 value in anti-MDA5 Ab+ DM patients and healthy controls. (A) Segmental myocardial native T1 value in anti-MDA5 Ab+ DM patients and healthy controls. (B) Segmental myocardial native T2 value in anti-MDA5 Ab+ DM patients and healthy controls. *, P<0.05 in the comparison between patients and controls. Anti-MDA5 Ab+ DM, anti-MDA5 antibody-positive dermatomyositis; DM, dermatomyositis.

Among the 42 patients with anti-MDA5+ DM, 15 (35.7%) exhibited LGE on CMR imaging. Patients were categorized into two groups based on LGE status: the positive LGE group (35.7%, 15/42) and the negative LGE group (64.3%, 27/42). The LGE predominantly involved the interventricular septum and the left vent inferior wall, as illustrated in Figure 4.

Figure 4 Myocardial T1 (A) and T2 measurement (B) in a 35-year-old female anti-MDA5 Ab+ DM patient, and (C) the patchy LGE in the infer-posterior wall of the left ventricle (arrow). Anti-MDA5 Ab+ DM, anti-MDA5 antibody-positive dermatomyositis; LGE, late gadolinium enhancement.

As detailed in Table 3, patients in the positive LGE group had significantly higher CK-MB levels compared to those in the negative LGE group (18.9±4.0 vs. 13.6±4.1 U/L, P<0.001). Additionally, the positive LGE group exhibited lower CI values (2.5±0.4 vs. 2.9±0.5 L/min/m², P<0.05).

Correlation of LV parameters and clinical biomarkers

In the anti-MDA5 Ab+ DM patients, LVEDVI (r=0.406, P=0.008) and CI (r=0.462, P=0.002) moderately correlated with ESR levels. LVEDVI (r=0.520, P<0.001) and LVESV (r=0.418, P=0.006) demonstrated a moderate correlation with FER, whereas LVEF demonstrated a moderate negative correlation with FER (r=−0.492, P<0.001). No significant associations were observed between the remaining LV functional indices and clinical variables (Figure 5).

Figure 5 Linear correlation analysis among left ventricular function parameters and biochemical examinations. CI, cardiac index; ESR, erythrocyte sedimentation rate; FER, ferritin; LVEDVI/LVESVI, left ventricular end-diastolic/end-systolic volume index; LVEF, left ventricular ejection fraction; LVESV, left ventricular end-systolic volume.

Within biomarker-based groups, LV indices were compared. Patients positive for inflammatory markers had significantly elevated LVEDVI and decreased CI compared with marker-negative patients. (LVEDVI: 64.0±17.1 vs. 54.8±10.1 mL/m², P=0.047; CI: 2.6±0.5 vs. 3.0±0.6 L/min/m², P=0.006), as shown in Figure 6.

Figure 6 Mean estimation plot and heatmap. The mean estimation plot compares the LVEDVI and CI between the inflammatory marker-positive and negative groups. The heatmap displays the absolute values of LVEDVI and CI for each patient, with blue indicating higher values and green indicating lower values. +, positive; −, negative. CI, cardiac index; LVEDVI, left ventricular end-diastolic volume index.

No significant differences in LV function indices were detected across the remaining cytokine- or NT-proBNP-defined subgroups.

Discussion

In this cross-sectional study, we compared LV function, myocardial T1 and T2 value, as well as LGE on CMR between anti-MDA5 Ab+ DM patients and HCs. Furthermore, we analyzed the correlation of those CMR metrics and biomarkers. There were several findings, as follows: I. Compared to HCs, LV functional metrics were significantly impaired in anti-MDA5 Ab+ DM patients; II. Myocardial native T1 and T2 values were elevated in anti-MDA5 Ab+ DM patients compared to the HCs. III. LGE was a common finding in anti-MDA5 Ab+ DM patients, with a prevalence of 35.7%. IV. Compared with the inflammatory marker-negative group, the inflammatory marker-positive group exhibited a significant increase in LVEDVI and a reduction in CI. To our best knowledge, this study represents the largest cohort to date that evaluates MI in patients with anti-MDA5 Ab+ DM using CMR.

Cardiac involvement in anti-MDA5 Ab+ DM has historically been considered infrequent, with most evidence derived from case reports and small cohort studies. Zhou et al. (4) reported a 15.8% prevalence of cardiac involvement using transthoracic echocardiography in a Chinese cohort, suggesting that MI may be more common than previously assumed. Our study, utilizing more sensitive CMR techniques, demonstrated an even higher prevalence of myocardial abnormalities, supporting the hypothesis that subclinical cardiac involvement is underdiagnosed in anti-MDA5 Ab+ DM patients. Importantly, our findings align with recent studies emphasizing the role of myocardial T1 and T2 mapping as sensitive biomarkers for detecting diffuse myocardial abnormalities in rheumatological diseases (8,14).

Quantitative T1/T2 mapping has been extensively applied to aid the detection of diffuse MI. Native T1 values increase in areas affected by oedema, scarring, or fibrosis (15-18). Recently, T1 mapping has been increasingly used to detect MI in rheumatological diseases, with increasing attention from rheumatologists on managing cardiac complications in their patients. Early clinical intervention in cases of myocardial inflammation or diffuse interstitial fibrosis has the potential to reduce the risk of irreversible myocardial damage (19). CMR T1 mapping, which demonstrates high intra- and inter-observer agreement, may play a valuable role in the noninvasive monitoring of histological changes following specific clinical interventions. This technique holds particular promise for patients with IIM who present with cardiac inflammation and reversible diffuse interstitial fibrosis (20). In our cohort of anti-MDA5 Ab+ DM patients, both the global mean T1 value and segmental T1 values were elevated compared to HCs, indicating that native T1 mapping is a sensitive imaging marker for assessing MI in these patients.

T2 mapping is more specific for detecting acute oedema and has been widely used in the study of conditions such as acute myocardial infarction, myocarditis, and sarcoidosis (21,22). Additionally, T2 mapping has been employed in rheumatological diseases, such as systemic sclerosis, significantly enhancing the sensitivity for detecting MI (22,23). Verhaert et al. (24) reported that a T2 value of 62 ms may serve as an appropriate cutoff for identifying edema on T2 mapping. In our study, both the global mean T2 value and segmental T2 values in anti-MDA5 Ab+ DM patients were significantly higher than those in HCs, suggesting that myocardial oedema is a common feature in anti-MDA5 Ab+ DM patients.

Positive LGE on CMR has been shown to be a surrogate marker for myocardial fibrosis and is widely recognized as a valuable diagnostic tool as well as a reliable risk marker of adverse outcomes in cardiovascular disease of various origins. However, in the early stages of the disease, diffuse fibrosis may occur without detectable positive LGE signals (20). In our study, 35.7% of anti-MDA5 Ab+ DM patients exhibited positive myocardial LGE on CMR. In contrast, increased native T1 and T2 values were observed in 90.5% and 83.3% of patients, respectively, highlighting the utility of T1 and T2 mapping in detecting early myocardial changes, even in the absence of LGE.

It is noteworthy that patients with elevated inflammatory markers exhibited significantly poorer LV function, as evidenced by raised LVEDVI and reduced CI. FER levels demonstrated a moderate correlation with impaired of LV function. These results align with the well-recognized paradigm that inflammation aggravates myocardial damage, as indicated by elevated biomarkers post-intervention. Mechanistically, inflammatory cytokines aggravate ischemia–reperfusion injury by enhancing oxidative stress and promotion of fibrotic remodeling (25). In DM patients, hyperferritinemia (>1,500 ng/mL) independently predicts mortality (26), potentially through fibrosis driven by the iron-mediated Fenton reaction (27). The combined impact of cytokine-driven oxidative stress and iron toxicity may hasten myocardial stiffening, emphasizing the necessity for early detection using sensitive tools such as CMR. However, establishing cytokine thresholds is challenging, and different cytokines may reflect distinct patient phenotypes. For example, patients with elevated interleukin-10 (IL-10) might represent a relatively more benign subset, whereas those with elevated TNF-α or interleukin-1β (IL-1β) might experience more inflammation and muscle weakness (28).

The other interesting finding was that both LGE+ and LGE− DM patients had similar T1 and T2 values, LVEF, and LVEDV, but a significant reduction in LV CI. Positive LGE indicated myocardial fibrosis. The extent and distribution of myocardial fibrosis can vary significantly between patients, which could explain the lack of marked differences in functional parameters (such as LVEDV and T1 mapping) between LGE+ and LGE− groups. Moreover, fibrosis is not the only factor affecting the diastolic function in these patients. Other underlying pathological processes, such as inflammation and immune response, may also contribute to myocardial alterations. Inflammatory processes, which are a hallmark of DM, could potentially affect the diastolic function of the LV, regardless of the presence of myocardial fibrosis. The complex interplay between these factors might lead to similar functional parameters between LGE+ and LGE− patients, despite the difference in myocardial fibrosis presence.

Dysfunction of the systemic microvasculature is widely documented across a range of rheumatic and autoimmune diseases (29). This dysfunction is particularly prominent in anti-MDA5 Ab+ DM patients (30), often in association with RP-ILD that may lead to respiratory failure. In anti-MDA5+ DM, ILD-related pulmonary hypertension can produce cardiac pressure overload, whereas direct autoimmune injury to the myocardium may coexist as an additional pathogenic pathway. In our study, comparable MPA values and MPA/AAo ratios in anti-MDA5+ patients and HCs imply that the subclinical dysfunction mainly arises from direct autoimmune injury to the myocardium. The marked decline in LV function highlights the potential prognostic value of these markers in predicting adverse outcomes. Future research should investigate the incorporation of ventricular function parameters and T1/T2 mapping into routine clinical practice to enhance risk stratification and prognosis in this patient population. Although CMR can identify myocardial changes before clinical symptoms appear, the relationship between subclinical cardiac involvement and long-term outcomes, such as the risk of heart failure or cardiovascular events, has not been fully established. Therefore, further research is needed to determine whether subclinical cardiac abnormalities detected by CMR are predictive of adverse outcomes and how they should influence clinical management.

Several limitations should be acknowledged. First, the study cohort comprised only mild cases without respiratory failure, and the relatively small sample size may limit the generalizability of the findings; large, multicenter studies are warranted to confirm these results. Second, the absence of longitudinal follow-up precludes evaluation of temporal changes in LV dysfunction and their relationship to long-term clinical outcomes. Finally, integrating CMR with additional imaging modalities, alongside comprehensive clinical and laboratory assessments, could enhance diagnostic accuracy and provide a more complete appraisal of biventricular function.

Conclusions

This study indicates that patients with anti-MDA5 Ab+ DM exhibit subclinical LV dysfunction, predominantly reflecting impaired systolic performance. Elevated native myocardial T1 and T2 values serve as sensitive indicators of cardiac involvement. In light of these findings, CMR should be considered for the early detection of subclinical cardiac involvement in anti-MDA5+ DM.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-974/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-974/dss

Funding: This work was supported by General Program of the National Natural Science Foundation of China (grant Nos. 82272398 and 82472349); National High Level Hospital Clinical Research Funding (grant No. 2022-NHLHCRF-YS-02); the Elite Medical Professionals project of China-Japan Friendship Hospital (grant No. ZRJY2021-GG14).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-974/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. This single-center, cross-sectional study was conducted in compliance with the Declaration of Helsinki and its subsequent amendments, and was approved by the Ethics Committee of China-Japan Friendship Hospital (approval No. 2021-KY-060). All participants signed informed consent before the CMR scan.

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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