Impaired diastolic filling and adverse event risks in patients with ST-segment-elevation myocardial infarction: insights from four-dimensional flow magnetic resonance imaging

Introduction

Acute myocardial infarction (AMI) is the primary cause of mortality and morbidity (1). The immediate implementation of reperfusion therapy for ST-segment elevation myocardial infarction (STEMI) holds the potential to save lives; however, the incidence of long-term heart failure remains elevated, thus significantly increasing the risk of poor prognosis (2). This underscores the crucial need to develop an accurate and early risk stratification method. Enhanced risk stratification of STEMI patients following hospital discharge could significantly advance clinical research aimed at informing long-term treatment decision on indications for novel therapies for mitigating residual cardiovascular risk beyond conventional treatment modalities.

Previous studies have demonstrated that alterations in intra-cavity blood flow in patients with AMI are significantly associated with adverse left ventricular (LV) remodeling (3). The sudden loss of LV contractility following AMI increases preload and triggers a cascade of adaptive neurohormonal responses. Failure to regulate elevated blood pressure can result in progressive LV dilation, which interacts with intracavity blood flow disturbances, further exacerbating ventricular dilation. Adverse events, including death, occur when the heart becomes structurally and functionally decompensated, impairing its ability to adequately supply blood. While the exact mechanisms driving these maladaptive changes remain unclear, sudden alterations in intracavity blood flow are believed to play a critical role in the pathophysiology.

Four-dimensional flow (4D-Flow) cardiac magnetic resonance (CMR) imaging facilitates three-dimensional (3D) quantification of LV intracavity flow kinetic energy (KE) across various phases of the cardiac cycle (4). The 4D-Flow KE parameter enables early detection of heart flow disorder, highlighting flow abnormalities before significant ventricular mechanical changes such as stiffness and dilatation become evident (5-7). By measuring systolic and diastolic blood flow components beyond LV ejection fraction (EF), this method is well-suited to explore mechanisms driving poor remodeling. Previous studies have demonstrated that patients with myocardial infarction (MI) exhibit increased in-plane KE compared to controls, likely due to asymmetric contraction of the LV post-MI (8). Additionally, an increase in residual blood volume has been associated with LV thrombus formation (9), and the proportion of in-plane KE is independently associated with extracellular volume (ECV) in hypertensive patients (5). The impact of LV flow disorders on adverse event risks has not yet been investigated and remains unknown.

The Global Registry of Acute Coronary Events (GRACE) risk score is the most established and widely validated tool, strongly recommended by international guidelines for risk stratification in acute coronary syndrome (ACS) patients (10,11). The higher the GRACE risk score, the greater the adverse event risks, including death and MI, during medium- to long-term follow-up (12,13). It remains essential for accurate risk assessment and management in patients with STEMI. Our aims were: (I) to investigate changes in LV flow KE in patients with STEMI at different adverse event risks, aiming to identify imaging markers for risk stratification in patients with STEMI; and (II) to elucidate the relationship between LV flow KE parameters and the adverse event risks. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2695/rc).

Methods

Patient population

This study was approved by the ethics committee of Beijing Chaoyang Hospital, Capital Medical University (Beijing, China) (No. 2021-164). Informed consent was obtained from all patients or their guardians. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. From January 2022 to January 2023, patients presenting with ST-segment elevation were included for CMR imaging within 5–7 days following percutaneous coronary intervention (PCI). The inclusion criteria were as follows: (I) first episode of STEMI symptoms; (II) symptom onset within <12 hours; (III) proximal occlusion lesion in the culprit vessel; and (IV) thrombolysis in myocardial infarction (TIMI) grades 0 or 1 flow in the culprit vessel. The exclusion criteria were as follows: (I) previous MI; (II) evidence of systemic disease (malignancy, syphilis, etc.); (III) other evidence of heart disease (hypertrophic cardiomyopathy, dilated cardiomyopathy, valvular heart disease, etc.); and (IV) severe renal failure, claustrophobia, and so forth not suitable for enhanced CMR. Further, 20 age/gender matched healthy participants who underwent an identical CMR protocol were recruited as healthy controls (Figure 1).

Figure 1 Flow chart of patient selection. CMR, cardiac magnetic resonance; STEMI, ST-segment elevation myocardial infarction.

GRACE risk score analysis

The GRACE risk score was analyzed by a cardiologist (J.H.) blinded to CMR results. We employed the GRACE risk score (available at https://www.mdcalc.com/grace-acs-risk-mortality-calculator), including factors such as age, heart rate, systolic blood pressure upon admission, creatinine levels, cardiac arrest at admission, ST-segment deviation on electrocardiogram, abnormal cardiac enzyme levels, and Killip classification, as the baseline risk assessment tool due to its superior performance in predicting long-term mortality among patients with ACS (14). Adverse event risks were calculated in accordance with the criteria (GRACE risk model version 2.0) and endorsed by the Coordinating Center of the Global Registry of Acute Coronary Events (15). Based on the GRACE risk score, 40 patients with STEMI were eventually enrolled and categorized into two subgroups (16): (I) STEMI-low risk group (GRACE risk score <128, n=27); and (II) STEMI-high risk group (GRACE risk score ≥128, n=13) (Figure 1). Comprehensive medical records and laboratory data were collected for all study participants.

CMR imaging protocols

CMR scans were conducted 5–7 days post-PCI using a 3.0 T scanner (MAGNETOM Prisma, Siemens Healthcare, Erlangen, Germany) equipped with an 18-channel body coil. The CMR scanning sequences included 4D-Flow, cine, and late gadolinium enhancement (LGE). Further, 4D-Flow imaging was executed using a free-breathing, retrospective electrocardiogram-triggered and respiratory-gated sequence. Cine imaging used a balanced steady-state free precession (SSFP) sequence, encompassing standard long-axis 4-chamber, 3-chamber, and 2-chamber views, alongside contiguous cine short-axis (SA) sequences. LGE imaging covered SA slices across both ventricles, extending from the base to the apex. The main parameters of the CMR are showed in Appendix 1.

CMR image analysis

All CMR images were analyzed by two experienced radiologists (X.L. and B.Z.), both blinded to clinical results. The 4D-Flow data analysis was performed using the MASS post-processing software (Version 2022-EXP, Medis Medical Imaging, The Netherlands). The region of interest (ROI) was manually segmented to include the entire LV cavity from the mitral valve annulus to the apex, excluding the LV outflow tract. Cine SA segmentation defined the boundaries for estimating LV flow parameters. Before conducting these calculations, any spatial misalignment between the cine SA stack and 4D-Flow CMR data was corrected through rigid registration (17).

The KE was computed using the following formula: KE =1/2 ρ_blood × V_voxel × v², where ρ_blood represents the blood density (1.06 g/cm³), V_voxel signifies the voxel volume, and v indicates the velocity magnitude. The cumulative KE within the LV was calculated in each stage by summing the KE of individual voxels. Subsequently, KE values from all voxels throughout the cardiac cycle were totaled, generating time-resolved KE curves that allowed for extracting physiologically vital data.

In-plane LV KE was obtained by summing the KE across all SA planes from the basal to the apical LV, expressed as a proportion of the total LV KE. Additionally, the LV cavity was segmented into three equal sections: base, middle, and apex, where KE values were computed separately. Furthermore, the time difference (TD) between the basal ventricular and peak midventricular peak E-wave KE was calculated. To standardize, all KE parameters were indexed by LV end-diastolic volume (LV EDV) in µJ/mL (KE_EDV). The E/A ratio was defined as the peak of E-wave divided by the peak of A-wave. The details of the 4D-Flow measurements are provided in Figure 2 and Table S1.

Figure 2 Left ventricular flow KE parameters used in this study. EDV, end-diastolic volume; KE, kinetic energy; KE_EDV, kinetic energy at end-diastole volume; LV, left ventricular; TD, time difference.

The cine, global strain and LGE data were analyzed using the post-processing software Cvi42 (Circle Cardiovascular Imaging Inc., Calgary, Canada). The cine data were used to analyze LV function and mass parameters. LV function and structural parameters were analyzed by semi-automated contouring of the endocardial and epicardial borders from SA stacks obtained at both end-systole and end-diastole. The LV cavity included both large trabeculae and papillary muscles. The parameters analyzed in the study were as follows: LV EF, LV EDV, LV end-systolic volume (LV ESV), LV stroke volume (LV SV), LV cardiac index (LV CI), and LV mass. LV volume measurements were standardized to body surface area (BSA). Global longitudinal strain (GLS), global circumferential strain (GCS), and global radial strain (GRS) were based on standard cine SSFP images acquired in long-axis and SA views. GLS was assessed from the apical 2-, 3-, and 4-chamber views, while GCS and GRS were derived from SA slices. Global strain values were calculated by averaging peak strain values across segments for each direction. LGE data were used to analyze myocardial MI size percentage and microvascular obstruction (MVO). MI size and MVO were determined based on the criteria involving 5 standard deviations (SDs) above the signal intensity of remote myocardial tissue and the identification of low-signal areas within the MI size (18). The MI size percentage was calculated by dividing the MI size by the total LV mass, aiming to eliminate individualized differences.

Statistical analyses

The statistical analyses were performed using SPSS 26.0 (SPSS Inc., IL, USA), GraphPad Prism 8.0 for Windows (CA, USA), and Origin 2022 (Origin Lab, MA, USA).

The continuous variables were presented as mean ± SD for normally distributed variables, whereas non-normally distributed variables were presented as median with interquartile range (IQR). The categorical variables were presented as total numbers (percentages). The continuous variables between groups were compared using either the independent-samples t-test or the Wilcoxon signed-rank test. The categorical variables between groups were compared using the Chi-squared test. The correlation of CMR parameters with GRACE risk score was analyzed using Pearson or Spearman’s correlation test. Significant variables (P<0.05) derived from the univariate forward regression method were integrated into the multivariable analysis. Multicollinearity among independent variables was assessed using the variance inflation factor (VIF). A VIF value greater than 5 was considered indicative of potential collinearity. Statistical significance was defined as P<0.05 (2-tailed tests). The consistency of quantitative CMR parameters was assessed using the intraclass correlation coefficient (ICC).

Results

Clinical characteristics

A total of 60 participants were evaluated in this study, including 20 healthy controls, 27 patients in the STEMI-low risk group, and 13 patients in the STEMI-high risk group (Figure 1). Healthy controls and patients with STEMI were matched for age (50.40±7.66 vs. 54.35±11.68 years, P=0.176) and sex [18 (90.0%) male vs. 38 (95.0%) male, P=0.464). Patients in the STEMI-high risk group exhibited significantly higher Killip classification at admission (P=0.008) compared with patients in the STEMI-low risk group. Further, patients in the STEMI-high risk group exhibited significantly lower diastolic blood pressure (69.92±6.68 vs. 81.07±11.53 mmHg, P=0.003) compared with patients in the STEMI-low risk group (Table 1).

Global LV functional and structural parameters in STEMI

As illustrated in Table 2, LVEF was reduced in patients with STEMI compared with healthy controls (47.41%±7.63% vs. 66.38%±2.46%, P<0.001). Additionally, certain functional parameters, such as left ventricular end-diastolic volume index (LV EDVi), left ventricular end-systolic volume index (LV ESVi), and left ventricular stroke volume index (LV SVi), significantly increased in the STEMI group (all P<0.05). However, there were no significant differences in the conventional parameters expressing diastolic and systolic function, such as LV EDVi, LV ESVi, EF and LV mass between the two subgroups of STEMI patients (all P>0.05). GLS, GCS, and GRS values were significantly impaired in STEMI patients compared to healthy controls (all P<0.001); however, no significant differences were observed among patient subgroups stratified by GRACE risk levels. The tissue Doppler-derived E/A ratio showed only borderline significance between GRACE-defined risk groups (P=0.050). A significant correlation was observed between E/A and KE-derived E/A (r=0.54, P<0.001) (Figure S1). No significant differences were observed in MI size percentage and MVO between the two subgroups [25.78%±12.71% vs. 17.38%±16.81%, P=0.087; 2.06 (0–7.03) vs. 3.32 (0–8.09) g, P=0.396].

Global LV flow KE parameters in STEMI

Global LV flow KE parameters associated with diastolic function suggested remarkable impaired diastolic filling. The E-wave KE_EDV and E/A ratio significantly decreased in patients with STEMI compared with healthy controls [7.48 (6.08–9.42) vs. 11.33 (10.10–13.61) µJ/mL, P<0.001; 0.81±0.42 vs. 1.85±0.32, P<0.001]. A-wave KE_EDV and TD were significantly greater in patients with STEMI than in healthy controls [9.89 (7.82–14.48) vs. 6.15 (4.99–8.27) µJ/mL, P=0.001; 34.20 (0–49.50) vs. 0 (0–0) milliseconds, P<0.001]. Furthermore, TD was significantly greater in the STEMI-high risk group than in the STEMI-low risk group [58.60 (36.20–68.50) vs. 32.50 (0–35.70) milliseconds, P=0.003]. E/A was significantly decreased in the STEMI-high risk group than in the STEMI-low risk group (0.64±0.34 vs. 0.89±0.44, P=0.036). E-wave KE_EDV was significantly lower in the STEMI-high risk group than in the STEMI-low risk group [6.71 (5.30–8.10) vs. 7.74 (6.50–10.28) µJ/mL, P=0.038]. The global LV flow KE parameters related to systolic function indicated the presence of LV systolic dysfunction. Systolic KE_EDV was significantly lower in patients with STEMI compared with healthy controls [10.20 (8.86–13.03) vs. 15.49 (13.19–16.72) µJ/mL, P<0.001]. In-plane LV KE, a parameter indicating LV flow disturbance, was significantly higher in patients with STEMI than in healthy controls (34.83%±11.35% vs. 26.48%±2.22%, P<0.001) (Table 3 and Figures 3-5).

Figure 3 Bar charts of LV flow KE_EDV parameters between healthy controls and patients with STEMI. **, P<0.001; *, P<0.05. EDV, end-diastolic volume; KE, kinetic energy; LV, left ventricular; STEMI, ST-segment elevation myocardial infarction; TD, time difference.

Figure 4 LV KE component curves in healthy controls and patients in the STEMI subgroup. Total LV flow KE (blue polyline) and in-plane KE (red polyline) curves. EDV, end-diastolic volume; EF, ejection fraction; GRACE, Global Registry of Acute Coronary Events; KE, kinetic energy; LV, left ventricular; STEMI, ST-segment elevation myocardial infarction.

Figure 5 Three levels of the LV KE curve in healthy controls and patients in the STEMI subgroup. Base (blue polyline), mid (red polyline), and apical level (orange polyline) curves. The vertical dashed lines indicate mid-level cardiac phase LV KE, and the horizontal red line represents the TD. EDV, end-diastolic volume; EF, ejection fraction; GRACE, Global Registry of Acute Coronary Events; KE, kinetic energy; LV, left ventricular; STEMI, ST-segment elevation myocardial infarction; TD, time difference.

Correlation between LV flow KE parameters and the GRACE risk score

The univariate analysis revealed a positive correlation of TD with the GRACE risk score (r=0.625, P<0.001). Conversely, the E-wave KE_EDV and E/A ratio demonstrated negative correlations with the GRACE risk score (r=–0.325, P=0.040; r=–0.398, P=0.011). The multivariate regression analysis demonstrated independent correlations of both E/A ratio and TD with the GRACE risk score (β*=–0.38, P=0.003; β*=0.57, P<0.001) (Tables 4,5 and Figure 6).

Figure 6 Scatter plots revealing correlations of structural and flow KE parameters with GRACE risk score. EDV, end-diastolic volume; GRACE, Global Registry of Acute Coronary Events; KEi_EDV, kinetic energy indexed to end-diastolic volume; MI, myocardial infarction; TD, time difference.

Inter‑observer reliability in LV KE parameters

All LV KE parameters exhibited robust intraclass and interclass correlations (ICC >0.800, P<0.001). The ICCs of all LV KE parameters are displayed in Table S2.

Discussion

The complex mechanisms underlying adverse events following STEMI, particularly the role of LV flow disorders in increasing adverse event risks, remain unclear. Afte MI, local myocardial contraction is often compromised, accompanied by histological changes such as fibrosis and scarring. These alterations may contribute to the progression towards heart failure. Additionally, disorders in LV flow patterns, resulting from various pathological mechanisms including myocardial fibrosis, impaired contractility, and ventricular remodeling post-MI, may serve as surrogate indicators for predicting heart failure in these patients. This prospective study is the first to systematically investigate the correlation between LV flow KE parameters and adverse event risks post-STEMI, using the GRACE risk score for risk assessment. The primary findings of the study are as follows:

• The LV flow KE parameters representing both diastolic and systolic functions were impaired in the STEMI group compared healthy controls.
• In the two subgroups exposed to different adverse events risks, no significant differences were observed in conventional LV functional and structural parameters. However, LV flow KE parameters, such as E/A and TD, which demonstrate diastolic function, exhibited significant differences.
• The LV flow KE parameters, particularly the E/A ratio and TD, which served as indicators of diastolic function, exhibited a remarkable correlation with the GRACE score in patients with STEMI.

Impaired diastolic filling and risk of adverse events

In patients with STEMI, despite reperfusion therapy, which alleviates severe coronary artery stenosis, the active diastolic function of the myocardium remains diminished and is challenging to restore within a short timeframe. Under normal physiological conditions, LV filling depends on active ventricular dilation. LV filling flow (from the left atrium into the LV) consists of two components: (I) early diastole due to ventricular relaxation, which forms peak E; and (II) late diastole due to atrial contraction, which forms peak A. TD is the time of peak E-wave propagation from the base to the midventricular region. Several abnormal 4D-Flow KE parameters, such as diastolic, E-wave, A-wave KE, E/A ratio, and TD, may indicate LV impaired diastolic filling. In this study, the LV flow KE parameters, indicative of both LV diastolic and systolic functions, exhibited functional impairment in patients with STEMI. Further, impaired diastolic filling was more obvious in patients with STEMI.

Our findings revealed that STEMI patients exhibited significantly longer TD and significantly lower E-wave KE, and E/A ratio compared with healthy controls. In addition, subgroup analysis showed that the high-risk STEMI group had significantly longer TD and significantly lower E-wave KE and E/A ratio compared with the low-risk STEMI group. Early diastolic flow rapidly entered the LV cavity in healthy controls due to a substantial intraventricular pressure gradient. However, in patients with STEMI, reduced LV active diastolic capacity resulted in a decline in mitral valve propagation velocity and elongation of propagation time. This observation was consistent with the study of Garg et al. (9), demonstrating that an increase in TD indicated delayed LV filling. Additionally, the present study included an analysis of the association between TD and the risk of adverse events. Nguyen identified LV impaired diastolic filling, detected by diastolic structural abnormalities in CMR, as a prognostic predictor of major adverse cardiovascular events (MACE) (19). The present study reported no substantial differences in EDV among subgroups of patients with STEMI categorized according to their risk of adverse events. However, remarkable differences were observed in flow KE indicators, suggesting changes in flow patterns before structural alterations.

We further investigated the correlation between LV diastolic function KE parameters and GRACE score to gain deeper insight into the correlation between LV KE parameters and the risk of adverse events. We revealed an independent correlation of the E/A ratio and TD with the GRACE risk score, implying a potentially stronger correlation of impaired diastolic filling with the risk of adverse events compared with systolic dysfunction. The use of a collaborative approach integrating 4D-Flow diastolic function parameters with conventional EF, infarct area, and MVO in future studies may enhance risk stratification among patients with STEMI.

Mechanisms associated with impaired diastolic filling and risk of adverse events

MI exacerbates impaired diastolic filling through various mechanisms (20). It disrupts the active diastolic process in the LV. Impaired diastolic filling often increases ventricular filling pressure, contributing to LV remodeling. Elevated ventricular filling pressure due to impaired diastolic filling may signify a cycle that exacerbates LV remodeling and impacts systolic function. Furthermore, systolic function may partially be recovered due to myocardial healing; however, persistent impaired diastolic filling is likely due to fibrotic changes in the healing phase, resulting in increased LV compliance (21). Beitnes et al. revealed a noticeable improvement in overall LV systolic strain 3 months post-infarction, whereas overall LV diastolic function was not remarkably recovered even after 1 year (22).

Systolic dysfunction and risk of adverse events

LV systolic KE, indicative of systolic function, obviously decreased in patients with STEMI compared with healthy controls. This was comprehensible because MI led to reduced myocardium contractility, resulting in a decline in LV systolic KE. However, despite subgroup analyses, patients with STEMI from varying risk strata had no obvious alterations in LV systolic KE.

Our findings revealed a positive correlation between larger infarct size and increased in-plane LV KE subsequent to MI. This observation aligned with the findings of Garg (9) among patients experiencing acute infarction. In-plane LV KE serves as an indicator of intraventricular hemodynamic inhomogeneity, encompassing various in-plane blood movements within the LV flow cycle. The LV contractility becomes asymmetric with reduced myocardial contractility among patients with STEMI, causing an uneven distribution of stresses on the myocardial wall within the chambers. This asymmetric contraction can induce heterogenous hemodynamics in the proximity of LV wall. A previous study established a correlation between in-plane LV KE and poor ventricular remodeling during a 12-month period (3). A progressive decline in LV myocardial function and subsequent enlargement of the LV cavity occur in cases of prolonged myocardial remodeling among patients with STEMI. Consequently, blood flow turbulence increases, resulting in more heterogeneous intraventricular hemodynamics and further increase in in-plane LV KE. However, the subgroup analysis in this study revealed no substantial differences in in-plane LV KE among patients with STEMI with differing risk levels. This finding suggested a potential correlation with the multifaceted causes contributing to adverse cardiovascular events, implying that adverse ventricular remodeling might not be the sole cause of such events. This highlighted the need for combining structural and functional parameters, as well as systolic and diastolic KE parameters, in our stratified analysis of patients with STEMI.

MVO and abnormal LV flow KE

This study reported a substantial correlation between MVO and in-plane LV flow KE; however, no considerable correlation was observed with the GRACE risk score. The observed strong correlation between MVO and in-plane LV flow KE might be attributed to the MI size percentage. The potential contribution of MVO to additional disturbances in LV flow, beyond the MI size percentage, remains uncertain and requires further investigation.

Limitations

Despite providing various valuable insights, there are several limitations in this study. First, this was a small-sample cross-sectional analysis investigating the correlation between LV KE parameters and GRACE risk score. It partially elucidated the correlation between diastolic KE parameters and the risk of adverse events. Future research should focus on expanding the sample size and conducting longitudinal follow-ups for a more accurate evaluation of the predictive value of diastolic KE parameters in determining MACE. Second, despite meeting the requirements, the 40-millisecond temporal resolution of the 4D-Flow data presented challenges in precisely measuring KE parameters and TD. As a result, small intergroup differences in TD should be interpreted with caution, and future studies with higher temporal resolution are needed to validate these findings. Additionally, this study addressed spatial alignment errors; however, discrepancies between LV geometry defined by LV stacks using the breath-hold cine technique and 4D flow acquired through free respiration may persist due to variations in heart rate and physiological conditions. These unresolved disparities can influence uncorrected time-varying flow characteristics, potentially impacting the accuracy of the obtained data.

Conclusions

Anomalies in early LV diastolic function KE parameters were significantly correlated with the GRACE risk score among patients with STEMI in this study. Therefore, 4D-Flow KE parameters may serve as novel and complementary indicators for predicting adverse events in patients with STEMI, enabling individualized stratification based on CMR multiparameter and providing valuable clinical guidance.

Acknowledgments

The authors thank all the participants in the study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2695/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2695/dss

Funding: This study was supported by grants from the National Natural Science Foundation of China (grant Nos. 82025018 and 82427804) and the National Key Research and Development Program of China (Nos. 2021YFF0501400 and 2021YFF0501404).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2695/coif). C.Z. is an employee of Siemens Healthineers, a for-profit company. 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. This study was approved by the ethics committee of Beijing Chaoyang Hospital, Capital Medical University (Beijing, China) (No. 2021-164). Informed consent was obtained from all patients or their guardians. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

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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