Isolated tricuspid regurgitation in structurally normal fetal hearts: a systematic review

Introduction

The widespread availability of high-resolution fetal echocardiography has made valvular regurgitation an increasingly common finding in prenatal assessment, particularly involving the tricuspid valve. Because the right ventricle (RV) plays a dominant role in fetal circulation, small and transient degrees of tricuspid regurgitation (TR) may appear even in structurally normal hearts and often resolve without clinical significance (1,2). At the same time, TR can also serve as an early clue to congenital heart disease (CHD), myocardial dysfunction, or evolving fetal compromise (3,4). This dual nature, physiological in some cases, pathological in others, creates an important diagnostic challenge for fetal cardiologists and obstetricians.

Although several studies describe TR in association with structural heart defects, chromosomal abnormalities, or hemodynamic disorders, much less attention has been given to TR occurring in fetuses whose cardiac anatomy is otherwise normal. The available evidence suggests that isolated TR may behave differently depending on gestational age, hemodynamic context, and Doppler characteristics, but the true clinical relevance of this finding remains uncertain (5,6). For clinicians, distinguishing between a benign variant and an early marker of dysfunction has practical implications for counseling, follow-up, and delivery planning.

Despite its frequency in routine practice, the literature on isolated fetal TR is sparse and heterogeneous, with most publications focusing on specific conditions rather than on structurally normal hearts. This lack of consolidated evidence creates a gap in understanding the diagnostic value, natural history, and prognostic meaning of TR in fetuses without CHD. To address this gap, we conducted a structured review of the literature to examine the diagnostic and prognostic significance of TR in structurally normal fetal hearts. The review was guided by a Population Evaluation/Exposure Comparison Outcome (PECO) question focused on whether isolated TR in structurally normal fetuses clinically meaningful or a physiological finding. We present this article in accordance with the PRISMA reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0202/rc).

Methods

Electronic searches

A literature search was carried out in PubMed/MEDLINE and Embase.

These databases were selected because, within fetal cardiology and obstetric imaging, they consistently index the journals where most relevant studies are published, including Prenatal Diagnosis, Ultrasound in Obstetrics and Gynecology, and Fetal Diagnosis and Therapy. In practice, almost all investigations addressing fetal TR in structurally normal hearts are found in these two sources, making them sufficient for a comprehensive retrieval of the available evidence.

Other platforms, such as Scopus and Web of Science, were considered during the planning phase. Test searches performed in both demonstrated substantial overlap with PubMed/MEDLINE and Embase, without adding unique records. Additionally, institutional access constraints created differences in retrieval that could compromise consistency. For these reasons, the search was intentionally limited to PubMed/MEDLINE and Embase, prioritizing methodological coherence while still following recommendations.

Search strategy

A search strategy was constructed to identify the studies focusing on Doppler characteristics of tricuspid insufficiency in fetuses structural normal heart published. The complete search strategies for both databases are provided in Table 1. They were conducted for studies published in English, between January 1, 2016, and January 31, 2026, and studies unrelated to the prenatal period were excluded. The search was limited to studies published from 2016 onward to ensure inclusion of data reflecting contemporary ultrasound technology and current fetal echocardiographic practice. Earlier studies were reviewed for background context but excluded from the systematic analysis to maintain methodological consistency.

Study selection

The titles and abstracts of all the publications obtained from the electronic search and the list of references of these studies were screened extensively by the authors. To assist with the screening process and ensure a consistent and blinded evaluation of titles and abstracts, all records retrieved from the electronic search were imported into the Rayyan platform (Rayyan Systems Inc.), which facilitated duplicate detection and independent reviewer classification. The tool was used exclusively to organize the screening workflow; all inclusion and exclusion decisions were made by the reviewers according to the predefined eligibility criteria. The pre-established inclusion and exclusion criteria were applied, and articles with complete available texts were selected to be examined and included in this review. Initially, the selected manuscripts were reviewed and verified by two authors. Indeed, the studies selected were assigned to the quality of the research design. Any discrepancies were resolved by consensus among the authors. Risk of bias was evaluated using appropriate methodological tools depending on study design. In addition to database searching, we performed manual screening of reference lists from relevant studies and reviews.

Eligibility criteria

We included original studies that evaluated TR in fetuses with structurally normal hearts, using echocardiography or Doppler ultrasound as the diagnostic method. Studies were excluded if they involved structural CHD, such as Ebstein anomaly (EA) or tricuspid valve dysplasia, or if they included fetuses with chromosomal abnormalities or were primarily focused on aneuploidy screening. Articles reporting exclusively neonatal or pediatric findings, as well as studies that mixed fetal and postnatal data without allowing fetal results to be analyzed separately, were also excluded. Nonoriginal publications (including reviews, editorials, commentaries, and conference abstracts) were not considered eligible.

Data extraction and synthesis

The results of the review were presented descriptively. For each included study, we summarized the design, sample characteristics, gestational age at diagnosis, echocardiographic criteria used to define TR, associated findings, and reported perinatal outcomes. We initially considered the possibility of performing a pooled quantitative synthesis. However, the studies differed substantially in design, gestational age, Doppler criteria used to define TR, and clinical context. Because of this heterogeneity and the limited number of eligible studies, formal meta-analysis was deemed inappropriate. Therefore, a summary table (Table 2) was prepared to provide an organized overview of the main characteristics and key results of the included articles.

Results

A total of 42 records were identified through the electronic searches (PubMed/MEDLINE =32; Embase =10). After removing four duplicates, 38 studies remained for title and abstract screening. Most were excluded at this stage because they either focused on neonatal or pediatric populations, or evaluated TR in the context of structural CHD, chromosomal abnormalities, or aneuploidy screening rather than in structurally normal fetal hearts.

After screening titles and abstracts, eight studies were selected for full-text review. Four of these full texts did not meet eligibility criteria, either because TR was not assessed in structurally normal fetuses or because the regurgitation was not analyzed as an isolated finding. We performed manual screening of reference lists from relevant studies and reviews. Through this process, one additional eligible study aligned with all predefined inclusion criteria was identified and incorporated into the final dataset. Ultimately, five studies fulfilled all inclusion criteria and were retained for qualitative synthesis (Figure 1).

Figure 1 PRISMA flowchart.

The final set comprises observational cohorts evaluating isolated TR in fetuses with structurally normal cardiac anatomy, using Doppler echocardiography across different gestational ages.

Study selection and overall characteristics

The search strategy identified observational studies reporting Doppler-defined TR in fetuses with structurally normal hearts, spanning all trimesters of pregnancy. Most cohorts were single-center, retrospective or prospective observational series, including low-risk or unselected pregnancies, with sample sizes that together encompassed more than one thousand fetuses (Table 2).

Across the included studies, TR was defined by color Doppler and confirmed with pulsed or continuous-wave Doppler, usually requiring a systolic jet directed from the RV to the right atrium. Mild or “physiologic” regurgitation was generally characterized by a short jet, confined near the valve, with peak velocity <2.0–2.5 m/s and non-holosystolic duration, in the setting of normal valve morphology and normal right-sided chamber size. Moderate or severe TR was defined by a longer, turbulent jet with higher velocities and, in some series, by an estimated regurgitant gradient >20 mmHg, often accompanied by right-sided dilation or altered venous Doppler. Echocardiographic criteria for physiological versus pathological TR are described in Table 3.

Clinical outcomes included perinatal survival, need for neonatal cardiac intervention, neonatal echocardiographic findings, and, in some studies, broader obstetric and neonatal endpoints such as birthweight, amniotic fluid abnormalities, and early neonatal adaptation.

First-trimester isolated TR

In the first trimester, Park et al. (7) evaluated 435 singleton pregnancies between 11+0 and 13+6 weeks, excluding fetuses with aneuploidy, structural anomalies or major maternal disease. Mild TR was present in a minority of cases and was specifically analyzed in the subgroup with structurally and chromosomally normal fetuses. Compared with fetuses without TR, those with mild first-trimester TR showed slightly lower gestational age- and sex-adjusted birthweight and a higher frequency of borderline or reduced amniotic fluid index, but there were no significant differences in major perinatal outcomes, including preeclampsia, gestational hypertension, small for gestational age, or preterm birth. The authors interpreted mild isolated TR in this context as a possible marker of subtle placental hemodynamic differences, rather than a predictor of major fetal compromise.

No study in our set demonstrated an increased rate of structural CHD when TR was isolated and first-trimester screening for aneuploidy and CHD had been otherwise reassuring.

Second-trimester isolated TR

Clerici et al. (2) reported a prospective series of 675 fetuses examined in mid-gestation. Isolated TR was found in approximately 5% of structurally normal hearts, usually with non-holosystolic jets, velocity <200 cm/s and mild to moderate intensity. On serial follow-up, regurgitation disappeared before 34 weeks in all cases, neonatal echocardiograms were normal, and there were no excess adverse perinatal outcomes compared with fetuses without TR. Taken together, the second-trimester data support the concept that short-lived, low-velocity TR in an otherwise normal heart behaves as a transient physiological finding, with spontaneous resolution and excellent postnatal cardiac outcome (Figure 2).

Figure 2 Color and spectral Doppler showing the tricuspid regurgitation in a normal fetus at 27 weeks of gestation.

Mid- to late-gestation TR and hemodynamic burden

Cui et al. (8) focused on fetuses in mid and late pregnancy with TR used as a surrogate to estimate pulmonary artery systolic pressure (PASP). Fifty-two fetuses with moderate or greater, high-velocity TR (group A) were compared with 88 fetuses with mild or trivial TR and symmetric ventricular size (group B). In group A, TR velocity, regurgitant pressure gradient and calculated PASP were significantly higher, whereas acceleration time (AT) and AT/ejection time (ET) ratio were lower, indicating increased right ventricular afterload. Gestational age, TR velocity and regurgitant gradient correlated positively with PASP, while AT and AT/ET showed negative correlations. The authors proposed that fetuses with moderate or greater TR and a regurgitant gradient >20 mmHg, particularly when PASP ≥70 mmHg, should be followed closely and considered for delivery if signs of right heart failure appear. These findings underscore that the prognostic meaning of TR in later gestation depends strongly on jet intensity and associated right-sided remodeling: mild or small-volume TR with low velocities is compatible with normal hemodynamics, whereas high-velocity regurgitation identifies fetuses with significant pulmonary hypertension and potential decompensation.

Third-trimester isolated TR

Tague et al. (9) longitudinally evaluated 40 fetuses with structurally normal hearts between 24 and 38 weeks. Each fetus had an echocardiogram before and after 34 weeks. After 34 weeks, trivial or mild TR became very common, increasing from 35% to 80% of fetuses, in parallel with progressive right-to-left atrial and atrioventricular valve disproportion and subtle ductal and isthmic flow changes.

de Melo Lopes et al. (10) conducted a cross-sectional study including 330 singleton low-risk pregnancies and found a 10% prevalence of mild TR in the third trimester. Postnatal transthoracic echocardiography was performed in 66.7% of neonates, and 92.9% of these examinations were normal; only one neonate (7.1%) had persistent TR without additional findings. The authors concluded that third-trimester TR in fetuses with normal cardiac anatomy is not associated with structural cardiac abnormalities or need for neonatal intervention. Crucially, these findings occurred in hearts known to be structurally normal and were not associated with adverse perinatal outcomes. The authors concluded that isolated trivial or mild TR in late gestation is most likely a normal manifestation of third-trimester cardiovascular remodeling and should be interpreted with caution when found in isolation.

Discussion

The widespread use of high-resolution fetal echocardiography has increased the recognition of TR during routine examinations. Because the RV is the dominant chamber in fetal life, small degrees of regurgitation may appear even in structurally normal hearts. The challenge lies in separating transient physiological findings from early markers of pathological conditions. This review focused strictly on fetuses with normal cardiac anatomy, which allows a more precise understanding of TR in the absence of structural disease.

Findings from the studies included in this review

Across the five included studies, the pattern is remarkably consistent: when TR occurs in fetuses with structurally normal hearts, it tends to be mild, transient, and clinically benign. Clerici et al. (2) documented spontaneous resolution in the majority of cases, with no associated perinatal complications. Park et al. (7), who evaluated first-trimester TR, also found no meaningful impact on neonatal outcomes when the heart was otherwise normal. In late gestation, Tague et al. (9) and de Melo Lopes et al. (10) described mild TR as a common finding, likely reflecting the physiological hemodynamic shifts of the third trimester. Cui et al. (8), although evaluating PASP elevation, reinforced the importance of monitoring hemodynamic changes without linking isolated TR itself to adverse outcomes.

Taken together, these studies show that isolated TR in fetuses with normal cardiac anatomy does not behave as a pathological marker, regardless of the gestational period in which it is detected. The regurgitation tends to be soft, of low velocity, and not accompanied by chamber enlargement or downstream Doppler abnormalities, features that align with physiological adaptation rather than disease.

Characteristics of the broader literature and screening studies

Beyond the narrow set of structurally normal fetuses included in this review, a larger body of literature has explored TR in different gestational windows and clinical contexts, particularly in first-trimester screening and third-trimester functional assessment.

In the first trimester, TR has been repeatedly described as a potential marker of aneuploidy and major CHD. Minnella et al. (4) showed that TR, when combined with increased nuchal translucency (NT) and abnormal ductus venosus (DV) flow, is strongly associated with severe CHD in large screening cohorts. In a systematic review and meta-analysis including 101 studies, Scala et al. (3) concluded that first-trimester TR, when combined with other markers used in routine screening, has a high positive predictive value for chromosomal abnormalities and major CHD, but exhibits suboptimal sensitivity when used alone, limiting its role as an isolated screening tool. Evaluating chromosomally normal fetuses, Karadzov Orlic et al. (11) reported a sensitivity of 55% for CHD when TR was added to a simple cardiac scan alongside NT and DV Doppler, reinforcing the importance of incorporating tricuspid valve Doppler into comprehensive first-trimester cardiac screening. Teixeira and Guedes-Martins (12) emphasized that standardized Doppler criteria (regurgitation lasting >50% of systole and jet velocity >60 cm/s) are fundamental to minimize false positives and to interpret first-trimester TR consistently across centers.

In mid- and late gestation, TR has also been investigated as a surrogate for right-sided loading conditions. Cui et al. (8) concluded that abnormal increases in PASP in middle and late pregnancy can be assessed by color Doppler echocardiography of fetal TR, and that fetuses with PASP ≥70 mmHg plus clinical signs of right heart failure require close monitoring up to 35–36 weeks and possible consideration of early delivery. Tague et al. (9) described mild TR as a common echocardiographic finding after 34 weeks of gestation and interpreted isolated mild TR as a consequence of physiological hemodynamic alterations that occur late in the third trimester, advocating cautious interpretation in otherwise low-risk pregnancies. Wang et al. (13) further demonstrated that right atrial enlargement in late gestation may be physiological, and that these fetuses show TR with lower velocities than those with true volume overload, identifying a significant difference in TR velocity between groups (1.85±0.45 m/s in the volume-overload group vs. 0.88±0.45 m/s in the physiological group).

Functional correlates have also been explored. Respondek-Liberska et al. (14) evaluated 100 newborns who had undergone third-trimester fetal echocardiography and had structurally normal hearts. Fetuses were divided into groups with and without functional abnormalities, including TR. The authors observed that tricuspid valve regurgitation behaves as a functional prenatal finding that warrants attention, and they reported elevated neonatal bilirubin levels in the group with functional abnormalities, suggesting that fetal cardiovascular adaptation may have subtle perinatal repercussions even when structural anatomy is normal.

Clinical context from the broader literature

Although the included studies provide reassurance about isolated TR in structurally normal fetal hearts, clinical practice demands a careful distinction between physiological and pathological forms. The broader literature, outside the scope of the four studies included in this review, describes TR as pathological when Doppler demonstrates a holosystolic, turbulent jet extending several millimeters into the right atrium, with peak velocity ≥2.5–3.0 m/s, and when it is associated with right-sided chamber enlargement, abnormal DV flow, or obvious valvar malformation. In conditions such as EA, tricuspid valve dysplasia, and ductal constriction, TR represents hemodynamic stress or structural dysfunction rather than a benign variation (15-17).

From a morphological perspective, the main tricuspid valve anomalies identified in fetal life are non-Ebstein tricuspid dysplasia and EA. Differentiation between tricuspid valve dysplasia and EA is based on the implantation of the tricuspid valve, best assessed in the four-chamber view. In EA, the septal and posterior leaflets are displaced inferiorly relative to the normal tricuspid annulus (Figure 3). Vettraino et al. (18) described a normal offset range of 1.2–5.0 mm in the second trimester and 2.2–6.9 mm in the third trimester in normal fetuses. Displacement of the valve orifice into the RV divides the chamber into a proximal “atrialized” portion and a distal functional ventricle, whose size depends on the degree of displacement (19). In tricuspid valve dysplasia, the atrioventricular ring remains in its usual position, but the ventricular myocardium appears more echogenic due to dysplasia. In borderline cases, distinction between these entities can be challenging, especially in early gestation. Three-dimensional ultrasound techniques such as Spatio-Temporal Image Correlation (STIC), high definition (HD) live, HD flow and Fetal Intelligent Navigation Echocardiography (FINE) facilitate detailed visualization of valve leaflets and the atrialized portion of the ventricle in EA, and STIC color Doppler with vitreous body rendering mode is useful for grading TR severity and identifying associated defects such as ventricular septal defects (20,21).

Figure 3 Color and spectral Doppler showing the tricuspid regurgitation in a fetus with Ebstein’s anomaly at 35 weeks of gestation.

Premature constriction or closure of the ductus arteriosus (DA) is another important hemodynamic condition in which TR may signal significant right-sided overload. DA constriction is not a structural defect but a functional anomaly that must be considered in fetuses with right chamber enlargement, TR, signs of heart failure and edema. The severity depends on the degree and duration of ductal narrowing and may culminate in fetal heart failure, hydrops or even fetal/neonatal death. Maternal exposure to anti-inflammatory drugs during pregnancy—indomethacin, nimesulide, diclofenac, ibuprofen, aspirin and even paracetamol—can constrict the DA by interfering with prostaglandin pathways (22-25).

In addition to drugs, maternal diets rich in polyphenols in late pregnancy have been linked to ductal constriction. Flavonoid polyphenols, abundant in herbal teas, mate tea and dark chocolate, have anti-inflammatory and antioxidant properties but may inhibit cyclo-oxygenase and prostaglandin synthesis [particularly prostaglandin E2 (PGE2)], promoting ductal constriction (26-28). Several authors, therefore, recommend limiting excessive intake of polyphenol-rich foods in the third trimester to prevent ductal constriction (27). Ventricular asymmetry due to right ventricular enlargement in the four-chamber view should raise suspicion of early ductal constriction. Assessment of the ductal arch in the sagittal plane is crucial; increased systolic and diastolic Doppler peaks with reduced ductal pulsatility index confirm the diagnosis. Severe hemodynamic compromise is characterized by RV dilatation and hypertrophy with significant TR and/or pulmonary regurgitation.

From a functional standpoint, fetal assessment of TR relies on color Doppler for detection, pulsed- and continuous-wave Doppler for quantification, and a systematic structural evaluation of the tricuspid valve and RV. Right atrial and ventricular dimensions and cardiothoracic area ratio help quantify hemodynamic impact. Composite tools such as the cardiovascular profile score (10-point score) integrate multiple echocardiographic parameters to estimate heart failure risk; scores of 10 indicate no heart failure, whereas values below 7 are associated with higher perinatal mortality (29). Serial examinations are often necessary to document temporal evolution and to distinguish transient, self-limited TR from patterns that progress towards decompensation.

Physiological TR is typically described as a small, narrow jet confined to the immediate vicinity of the tricuspid valve, with peak velocity below 2.0–2.5 m/s, brief early-systolic duration, normal valve morphology, preserved right ventricular size and function and spontaneous resolution during gestation (2). Pathological TR, in contrast, is suspected when Doppler demonstrates a holosystolic, turbulent jet extending ≥3–5 mm into the right atrium, with peak velocity ≥2.5–3.0 m/s, and when this is accompanied by valve dysplasia, apical displacement of the septal leaflet, annular dilation, right atrial or ventricular enlargement, abnormal DV flow or signs of fetal heart failure (15-17). Table 4 illustrates the main characteristics of physiological and pathological TR Doppler flow.

Integration of evidence

When the data from the included studies are interpreted against the background of known fetal physiology and the broader screening literature, a coherent picture emerges. In fetuses with structurally normal hearts from low-risk pregnancies, the TR described in our four included studies behaves as a functional phenomenon rather than an early sign of disease. The Doppler characteristics such as short regurgitant jets, low velocities, normal chamber dimensions and absence of downstream Doppler abnormalities, are consistent with the concept of normal right-sided volume dynamics in utero. Importantly, none of the included studies reported progression to clinically relevant cardiac dysfunction, perinatal compromise or need for neonatal intervention. At the same time, first-trimester screening studies remind us that TR cannot be interpreted in isolation from gestational age and global risk profile. In high-risk or unselected screening populations, TR in early gestation integrates with NT and DV Doppler as a marker of aneuploidy and major CHD (3,4,11,12). In late gestation, TR may signal increased PASP or evolving right heart failure in specific settings (8), or may simply reflect physiological hemodynamic shifts, as suggested by Tague et al. (9) and by studies demonstrating lower TR velocities in physiologic right atrial enlargement compared with true volume-overload states (13). Observations by Respondek-Liberska et al. (14) and de Melo Lopes et al. (10) add nuance by showing that functional TR in structurally normal hearts can coexist with subtle perinatal findings (such as elevated neonatal bilirubin) but rarely implies major structural disease or need for intervention (10,14). Altogether, this framework helps reconcile the apparently divergent roles of TR: a meaningful risk marker in the first-trimester screening algorithms when combined with other abnormal findings, and a largely benign, self-limited Doppler observation when mild, isolated TR is identified in structurally normal hearts, particularly in the third trimester.

Implications for clinical practice

For clinicians evaluating low-risk pregnancies, the presence of isolated TR, whether detected in the first trimester or later, should always be interpreted within the context of a complete structural and functional assessment. Once cardiac anatomy is confirmed as normal and there are no signs of altered hemodynamics, mild, low-velocity TR with typical “physiological” features should not, on its own, prompt concern or invasive investigation. Serial examinations, when performed, tend to show stability or spontaneous resolution, as documented in the studies included in this review and reinforced by third-trimester cohorts (2,7,10,14).

Conversely, TR with atypical characteristics, a holosystolic, turbulent jet with high velocity, associated chamber enlargement, abnormal DV or ductal Doppler, or systemic signs of fetal compromise, demands a different level of vigilance. In these scenarios, clinicians should actively investigate structural valve disease (including the spectrum of EA and non-Ebstein tricuspid dysplasia), ductal constriction, or other conditions that increase right-sided afterload, and should consider closer surveillance or early delivery depending on gestational age and global risk.

The collective evidence supports the interpretation that, in structurally normal fetuses from low-risk pregnancies, mild isolated TR is usually a benign, self-limited variation of fetal cardiac physiology rather than a marker of occult disease. At the same time, standardized Doppler criteria and trimester-specific interpretation are essential to avoid both underestimation of truly pathological TR and overestimation of benign findings. For prenatal counseling, this distinction is crucial: it helps prevent unnecessary anxiety and overuse of specialized fetal echocardiography in low-risk settings, while still preserving the sensitivity of TR as part of multi-parametric screening and hemodynamic assessment in higher-risk scenarios.

Conclusions

The broader literature describes well-established criteria for pathological TR: holosystolic turbulent jets, high Doppler velocities, chamber enlargement, or associated abnormal Doppler patterns. In fetuses with structurally normal hearts, TR is consistently characterized as a mild transient, and clinically benign finding. Across the available studies, it was not associated with structural heart disease or adverse perinatal outcomes. These findings support the interpretation that isolated TR reflects physiological hemodynamic variation rather than pathology. Based on the available evidence, isolated TR should be interpreted as a benign variation of fetal cardiac physiology. Although further prospective studies are warranted, current evidence supports a conservative approach and reassurance in low-risk pregnancies.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the PRISMA reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0202/rc

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0202/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0202/coif). E.A.J. serves as an unpaid editorial board member of Translational Pediatrics from October 2025 to December 2027. 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.

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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