Congenital Total Pulmonary Venous Return Anomaly

1. Disease Information

1.1 Overview (current understanding)

TAPVC/TAPVR is a rare cyanotic congenital heart disease in which oxygenated pulmonary venous blood returns to the right-sided circulation/systemic veins rather than the left atrium, causing systemic desaturation and abnormal pulmonary/systemic blood flow patterns. (cheng2024clinicaldiagnosisand pages 1-4, xue2023prenataldiagnosisand pages 1-2)

A major determinant of early clinical deterioration is pulmonary venous obstruction (PVO) along the anomalous venous pathway, which increases pulmonary venous pressure, drives pulmonary edema, and worsens hypoxemia/hemodynamic compromise. (xue2023prenataldiagnosisand pages 2-3, cheng2024clinicaldiagnosisand pages 4-6)

1.2 Key identifiers and coding systems

• ICD-10 (registry definition): Q262 / Q26.2 “Total anomalous pulmonary venous connection” used to identify TAPVC in a nationwide registry study. (henningsen2025nationwideregistrystudy pages 2-3)
• Prenatal classification system: Commonly described using the historical Darling classification into four anatomic types: supracardiac, intracardiac/cardiac, infracardiac, and mixed. (cheng2024clinicaldiagnosisand pages 4-6, xue2023prenataldiagnosisand pages 1-2)
• MONDO / Orphanet / OMIM / MeSH: Not retrievable from the currently available full-text corpus in this run; therefore not reported here.

1.3 Common synonyms and alternative names

• Total anomalous pulmonary venous connection (TAPVC)
• Total anomalous pulmonary venous return (TAPVR)
• Total anomalous pulmonary venous drainage (TAPVD) (terminology varies across fetal imaging literature) (azab2022tbx5variantwith pages 1-2)

1.4 Evidence provenance (patient-level vs aggregated)

Most information below is derived from aggregated cohorts (fetal cohorts and surgical cohorts), retrospective registries, and review-level synthesis, supplemented by smaller case series. (xue2023prenataldiagnosisand pages 1-2, li2023totalanomalouspulmonary pages 1-2, henningsen2025nationwideregistrystudy pages 2-3)

2. Etiology

2.1 Primary causal factors (mechanistic)

Clinical and surgical literature describes TAPVC/TAPVR as arising from abnormal embryologic development/remodeling of pulmonary venous connections and venous pole structures, with contributions from genetic variation in some patients. (cheng2024clinicaldiagnosisand pages 4-6, xue2023prenataldiagnosisand pages 1-2)

2.2 Genetic risk factors (genes and syndromic associations)

TBX5 (Holt–Oram syndrome expansion): - A pathogenic TBX5 nonsense variant (c.577G>T; p.Gly193) was reported in a family where the proband had mixed-type TAPVR, and subsequent phenotyping supported Holt–Oram syndrome. This report is described as the first genetic investigation* reporting this association. (azab2022tbx5variantwith pages 1-2)

ANKRD1 (candidate gene; gain-of-function signal; mechanistic animal model): - A mechanistic study reports that increased ANKRD1 levels (including gain-of-function contexts) have been associated in humans with TAPVR and motivated creation of a myocardial ANKRD1 overexpression mouse model. In transgenic mice, myocardial ANKRD1 overexpression caused sinus venosus/venous pole remodeling defects with abnormal pulmonary vein–systemic venous communications, linking a plausible developmental mechanism to anomalous venous return phenotypes. (piroddi2020myocardialoverexpressionof pages 1-3, piroddi2020myocardialoverexpressionof pages 7-9, piroddi2020myocardialoverexpressionof pages 3-4)

Associated laterality/heterotaxy context (clinical association): In fetal cohorts, TAPVC frequently co-occurs with complex congenital heart disease and laterality disorders such as right atrial isomerism (a heterotaxy phenotype). (xue2023prenataldiagnosisand pages 7-7, xue2023prenataldiagnosisand pages 8-10)

2.3 Environmental risk/protective factors; GxE

No TAPVC-specific, well-supported protective factors or gene–environment interaction evidence was identified in the retrieved corpus. Environmental teratogen evidence is not established in the extracted TAPVC-focused texts.

3. Phenotypes

3.1 Core clinical presentation (typical)

Neonatal/infant presentations in clinical series commonly include respiratory distress/shortness of breath, cyanosis, recurrent respiratory infections/pneumonia, and heart failure/poor growth—particularly in obstructed forms. (cheng2024clinicaldiagnosisand pages 1-4, cheng2024clinicaldiagnosisand pages 4-6)

3.2 Fetal imaging phenotypes and prenatal “suspicious signs”

A structured fetal echocardiography approach highlighted suspicious ultrasound findings such as: - “a small LA,” “an increased distance from the LA to the descending aorta,” “a smooth posterior wall of the LA,” “unobservable orifices of the PV,” “evident extra vessels and centrifugal venous flow,” and “an abnormal dilated vein (e.g., SVC, INN, AZV, IVC, or CS).” (xue2023prenataldiagnosisand pages 2-3)

3.3 Suggested HPO terms (examples)

Note: HPO IDs are suggested based on phenotype labels; they were not retrieved from an ontology database in this run. - Cyanosis (HP:0000969) - Respiratory distress (HP:0002098) - Tachypnea (HP:0002789) - Recurrent pneumonia (HP:0006532) - Pulmonary venous obstruction/stenosis (concept; may map to Pulmonary vein stenosis (HP:0012728)) - Failure to thrive (HP:0001508)

3.4 Quality of life impact

No TAPVC-specific validated QoL instrument results (e.g., PedsQL, SF-36) were found in the retrieved TAPVC-focused corpus.

4. Genetic / Molecular Information

4.1 Causal genes and pathogenic variants (evidence-supported in retrieved corpus)

• TBX5: c.577G>T; p.Gly193* (nonsense; loss-of-function) associated with mixed-type TAPVR in a Holt–Oram syndrome context (family-based trio exome sequencing). (azab2022tbx5variantwith pages 1-2)

4.2 Candidate genes / functional mechanisms

• ANKRD1: gain-of-function/dysregulation implicated as a candidate driver of venous pole remodeling defects relevant to anomalous pulmonary venous return; transgenic overexpression produces congenital sinus venosus defects and later diastolic dysfunction. (piroddi2020myocardialoverexpressionof pages 1-3, piroddi2020myocardialoverexpressionof pages 7-9)

4.3 Variant class and origin

• TBX5 variant reported: nonsense (likely pathogenic in the report’s interpretation). (azab2022tbx5variantwith pages 1-2)
• ANKRD1 evidence in retrieved corpus: gain-of-function/dysregulation signal and experimental overexpression model; specific human variant nomenclature is not fully extractable from the limited snippets provided. (piroddi2020myocardialoverexpressionof pages 3-4, piroddi2020myocardialoverexpressionof pages 1-3)

4.4 Modifier genes, epigenetics, chromosomal abnormalities

No specific, TAPVC-focused modifier gene sets, epigenetic signatures, or recurrent CNVs could be extracted from the retrieved full-text corpus in this run.

5. Environmental Information

No TAPVC-specific environmental, lifestyle, occupational, or infectious causal triggers were identified in the retrieved TAPVC-focused literature.

6. Mechanism / Pathophysiology

6.1 Causal chain (integrated clinical + developmental model)

1. Developmental misconnection/remodeling failure results in absent direct pulmonary vein–left atrium connection and anomalous drainage to systemic venous pathways/right atrium. (xue2023prenataldiagnosisand pages 1-2, cheng2024clinicaldiagnosisand pages 1-4)
2. Mixing of oxygenated pulmonary venous blood with systemic venous blood in the right atrium leads to cyanosis/hypoxemia and abnormal loading conditions. (cheng2024clinicaldiagnosisand pages 1-4)
3. Pulmonary venous obstruction (when present) increases pulmonary venous pressure, aggravating pulmonary congestion and worsening hypoxemia and hemodynamics; obstruction status strongly influences prognosis and urgency of intervention. (xue2023prenataldiagnosisand pages 2-3, cheng2024clinicaldiagnosisand pages 4-6)
4. Post-repair, some patients develop pulmonary vein stenosis (PVS)/recurrent obstruction, a major driver of reintervention, morbidity, and mortality. (wen2024insightintothe pages 12-14, alifu2024assessingtherisk pages 3-5)

6.2 Molecular/cellular processes (evidence-linked)

ANKRD1 gain-of-function model (mouse): myocardial overexpression causes sinus venosus defects originating from impaired embryonic remodeling, with early transcriptional perturbations involving GATA4 and NKX2-5 and downstream sarcomeric/titin modulation; embryos show abnormal venous pole connections, and adults develop progressive diastolic dysfunction. (piroddi2020myocardialoverexpressionof pages 1-3, piroddi2020myocardialoverexpressionof pages 7-9)

6.3 Suggested ontology mappings

GO (Biological Process) suggestions: - Heart morphogenesis (GO:0003007) - Cardiovascular system development (GO:0072358) - Pulmonary vein development (term exists conceptually; exact GO ID not retrieved in this run) - Blood vessel morphogenesis (GO:0048514)

CL (Cell Ontology) suggestions: - Cardiomyocyte (CL:0000746) - Endothelial cell (CL:0000115) - Cardiac fibroblast (CL term exists; exact ID not retrieved in this run)

UBERON (Anatomy) suggestions: - Pulmonary vein (UBERON term) - Left atrium (UBERON term) - Sinus venosus / venous pole region (UBERON term)

7. Anatomical Structures Affected

7.1 Organ/system level

• Primary: pulmonary veins and their confluence, left atrium (failed connection), right atrium/systemic venous pathways receiving pulmonary venous return. (xue2023prenataldiagnosisand pages 1-2, cheng2024clinicaldiagnosisand pages 1-4)
• Secondary functional involvement: lungs (pulmonary congestion/edema, especially with obstruction), pulmonary vasculature (risk of pulmonary hypertension), and systemic oxygen delivery (cyanosis). (cheng2024clinicaldiagnosisand pages 4-6, cheng2024clinicaldiagnosisand pages 1-4)

8. Temporal Development

• Onset: congenital; often clinically apparent in the neonatal period, especially in obstructed TAPVC. (cheng2024clinicaldiagnosisand pages 4-6)
• Course: without surgery, high early mortality is reported; after repair, risk of postoperative pulmonary vein stenosis/obstruction often appears within months and can progress rapidly. (cheng2024clinicaldiagnosisand pages 4-6, wen2024insightintothe pages 12-14)

9. Inheritance and Population

9.1 Epidemiology (selected recent/representative statistics)

• TAPVC is described as approximately 2% of congenital heart disease in a recent clinical summary. (cheng2024clinicaldiagnosisand pages 4-6)
• In a TBX5-associated report, TAPVR is described as ~7 per 100,000 live births (and ~1–3% of CHD). (azab2022tbx5variantwith pages 1-2)

9.2 Sex ratio / demographics

A clinical summary notes TAPVC is reported more frequently in males than females. (cheng2024clinicaldiagnosisand pages 4-6)

9.3 Inheritance

The retrieved corpus supports heterogeneous genetic architecture: sporadic cases predominate, but rare monogenic syndromic associations (e.g., TBX5 in Holt–Oram) and candidate gene mechanisms (ANKRD1 gain-of-function contexts) exist. (azab2022tbx5variantwith pages 1-2, piroddi2020myocardialoverexpressionof pages 1-3)

10. Diagnostics

10.1 Prenatal diagnosis (real-world implementation)

A fetal cohort describes a four-step prenatal ultrasonography workflow: 1) demonstrate absent PV–LA connections; 2) identify common pulmonary vein and drainage route for subtype classification; 3) assess obstruction (turbulence and max velocity >50 cm/s suggested); 4) assess associated malformations. (xue2023prenataldiagnosisand pages 2-3)

Performance (2023 fetal cohort): diagnostic accuracy by type was reported as 95% (supracardiac), 75% (intracardiac), 95% (infracardiac), 77% (mixed); among isolated TAPVC (n=21), 6 were missed and 1 misclassified prenatally. (xue2023prenataldiagnosisand pages 8-10, xue2023prenataldiagnosisand pages 1-2)

Figure/Table evidence (classification + drainage routes + obstruction): Table 5 from the fetal cohort provides structured subtype and drainage-route detail along with obstruction findings. (xue2023prenataldiagnosisand media 1a8f0ae4)

10.2 Postnatal diagnosis

• Transthoracic echocardiography (TTE) is typically first-line but can have mis-/underdiagnosis in some settings.
• Computed tomographic angiography (CTA) can increase anatomic diagnostic clarity and can also be used for surgical planning, but introduces radiation/contrast considerations. (cheng2024clinicaldiagnosisand pages 4-6, matsuhisa2020computedtomographybasedsurgical pages 1-2)

10.3 Differential diagnosis (not exhaustively captured in retrieved corpus)

Differentials for cyanotic neonatal CHD with pulmonary overcirculation/respiratory distress may include transposition physiology, obstructed left-sided lesions, and other complex CHD; specific differential algorithms were not retrievable from society guidelines in the current corpus.

11. Outcome / Prognosis

11.1 Natural history without intervention

A clinical summary reports very poor natural prognosis without timely surgical intervention (e.g., mortality up to 48.8% in infancy and high mortality in the first year in severe physiologic circumstances). (cheng2024clinicaldiagnosisand pages 4-6)

11.2 Contemporary surgical outcomes and complications

• Review-level synthesis describes early postoperative mortality in published series commonly ranging from <10% to ~20%, with postoperative pulmonary vein stenosis (PVS) as the most common complication and an incidence often cited around 10–20%. (wen2024insightintothe pages 12-14)
• In a single-center 2023 series using primary sutureless repair (n=80), there were 2 early deaths and 1 late death, and 2 patients developed postoperative PVO with no reintervention required. (li2023totalanomalouspulmonary pages 1-2)

11.3 Reoperation risk stratification (2024 evidence)

A 2024 cohort found that pre-discharge mild PVO (Doppler velocity >1.2 m/s) was associated with substantially higher reoperation rates; in the fully adjusted model, HR 13.90 (95% CI 1.16–166.5) for reoperation within 1 year. (alifu2024assessingtherisk pages 3-5, alifu2024assessingtherisk pages 5-6)

12. Treatment

12.1 Surgical/interventional treatment (current practice)

Definitive management is surgical repair, typically in the neonatal period when clinically indicated. (cheng2024clinicaldiagnosisand pages 4-6)

Primary sutureless repair (2023 outcomes): In a single-center series (2015–2020), primary sutureless repair across all Darling subtypes showed low postoperative PVO incidence (2/80) and no reintervention, supporting the view that sutureless approaches may reduce anastomotic-level restenosis risk across subtypes. (li2023totalanomalouspulmonary pages 1-2)

Imaging-guided surgical planning (CTA era effect): A 112-patient era comparison reported marked improvement in 5-year survival with a CTA-based strategy (biventricular: 69%→97%; single-ventricle: 21%→70%) and reduced/managed PVS burden with aggressive reintervention. (matsuhisa2020computedtomographybasedsurgical pages 1-2)

Technique comparisons: For supracardiac TAPVC, a modified L-shaped incision approach was associated with improved freedom from death/postoperative PVO versus the posterior technique, especially in those with preoperative obstruction. (feng2020midtermresultsof pages 1-2)

12.2 Supportive perioperative management

Postoperative management may include intensive care strategies and pulmonary hypertension-directed therapies (e.g., inhaled nitric oxide, endothelin receptor antagonists, PDE-5 inhibitors, prostacyclin) as adjuncts when pulmonary hypertension is present. (cheng2024clinicaldiagnosisand pages 4-6)

12.3 Pharmacotherapy / advanced therapeutics

No TAPVC-specific disease-modifying pharmacotherapy trials, gene therapy, or RNA therapeutics were identified in the retrieved corpus.

12.4 Suggested MAXO terms (examples)

Note: MAXO IDs not retrieved in this run; terms suggested as labels. - Surgical repair of congenital heart defect (e.g., “TAPVC repair”) - Sutureless pulmonary venous anastomosis - Computed tomography angiography for preoperative planning - Echocardiographic surveillance / follow-up

13. Prevention

Primary prevention of TAPVC is not established. Practical prevention focuses on: - Secondary prevention via prenatal detection and perinatal planning (delivery at tertiary center; timely neonatal stabilization/surgery). (xue2023prenataldiagnosisand pages 8-10) - Genetic counseling/testing when syndromic features or familial recurrence is suspected (e.g., TBX5/Holt–Oram context). (azab2022tbx5variantwith pages 1-2)

14. Other Species / Natural Disease

No naturally occurring veterinary TAPVC disease series were identified in the retrieved corpus.

15. Model Organisms

A transgenic mouse model with myocardial ANKRD1 overexpression demonstrates congenital venous pole defects (sinus venosus defects; abnormal PV–systemic venous communications) and progressive functional deterioration, providing a mechanistic model relevant to anomalous pulmonary venous return. (piroddi2020myocardialoverexpressionof pages 1-3, piroddi2020myocardialoverexpressionof pages 7-9)

Recent developments (2023–2024 highlights)

• Structured fetal diagnostic protocols with quantified type-specific accuracy and documentation that isolated TAPVC is more likely to be missed than syndromic/heterotaxy-associated TAPVC. (xue2023prenataldiagnosisand pages 8-10, xue2023prenataldiagnosisand pages 1-2)
• Expansion of sutureless repair evidence showing low postoperative obstruction rates in a 2023 single-center cohort. (li2023totalanomalouspulmonary pages 1-2)
• Quantitative echocardiographic risk stratification immediately prior to discharge (1.2 m/s threshold) associated with markedly increased reoperation risk within 1 year. (alifu2024assessingtherisk pages 3-5)

Evidence map of key studies

Table: This table condenses high-value recent and foundational studies on TAPVC/TAPVR across prenatal diagnosis, operative strategy, postoperative obstruction risk, and genetics. It is useful as a quick-reference evidence map for building a disease knowledge base entry.

Key visual evidence

The following table image (from a 2023 fetal cohort) summarizes TAPVC anatomic subtypes, drainage routes, and obstruction findings, supporting the classification and prenatal evaluation sections. (xue2023prenataldiagnosisand media 1a8f0ae4)

Limitations of this report (data availability)

• MONDO/Orphanet/OMIM/MeSH identifiers, formal guideline documents, and TAPVC-specific QoL datasets were not retrievable in the accessible corpus for this run; therefore, these elements are flagged as unavailable rather than inferred.
• Some epidemiology estimates are study-/setting-specific; population-level prevalence estimates vary by ascertainment method and inclusion criteria.

References

1. (cheng2024clinicaldiagnosisand pages 1-4): Weiping Cheng, Junzhao Zhu, Youbo Xu, Yingqiang Guo, and Lexiang Shi. Clinical diagnosis and treatment of 5 cases of tapcv in infants. Unknown journal, Oct 2024. URL: https://doi.org/10.21203/rs.3.rs-3480976/v1, doi:10.21203/rs.3.rs-3480976/v1.

2. (xue2023prenataldiagnosisand pages 1-2): Xiaoying Xue, Qiumei Wu, Mingtao Xiong, Wen Ling, Shan Guo, Hong Ma, Biying Huang, Min Liu, Xiuqing Qiu, and Zongjie Weng. Prenatal diagnosis and postnatal verification in fetuses with total anomalous pulmonary venous connection. Frontiers in Pediatrics, Jun 2023. URL: https://doi.org/10.3389/fped.2023.1206032, doi:10.3389/fped.2023.1206032. This article has 6 citations.

3. (xue2023prenataldiagnosisand pages 2-3): Xiaoying Xue, Qiumei Wu, Mingtao Xiong, Wen Ling, Shan Guo, Hong Ma, Biying Huang, Min Liu, Xiuqing Qiu, and Zongjie Weng. Prenatal diagnosis and postnatal verification in fetuses with total anomalous pulmonary venous connection. Frontiers in Pediatrics, Jun 2023. URL: https://doi.org/10.3389/fped.2023.1206032, doi:10.3389/fped.2023.1206032. This article has 6 citations.

4. (cheng2024clinicaldiagnosisand pages 4-6): Weiping Cheng, Junzhao Zhu, Youbo Xu, Yingqiang Guo, and Lexiang Shi. Clinical diagnosis and treatment of 5 cases of tapcv in infants. Unknown journal, Oct 2024. URL: https://doi.org/10.21203/rs.3.rs-3480976/v1, doi:10.21203/rs.3.rs-3480976/v1.

5. (henningsen2025nationwideregistrystudy pages 2-3): Maj Beldring Henningsen, Cathrine Bohnstedt, Therese Risom Vestergaard, Morten Holdgaard Smerup, Pi Vejsig Madsen, and Lone Graff Stensballe. Nationwide registry study of long term survival and comorbidities in total anomalous pulmonary venous connection in denmark. Scientific Reports, Aug 2025. URL: https://doi.org/10.1038/s41598-025-15769-0, doi:10.1038/s41598-025-15769-0. This article has 3 citations and is from a peer-reviewed journal.

6. (azab2022tbx5variantwith pages 1-2): Bilal Azab, Dunia Aburizeg, Weizhen Ji, Lauren Jeffries, Nooredeen Isbeih, Amal Al‑Akily, Hashim Mohammad, Yousef Osba, Mohammad Shahin, Zain Dardas, Ma'mon Hatmal, Iyad Al‑Ammouri, and Saquib Lakhani. Tbx5 variant with the novel phenotype of mixed-type total anomalous pulmonary venous return in holt-oram syndrome and variable intrafamilial heart defects. Molecular Medicine Reports, May 2022. URL: https://doi.org/10.3892/mmr.2022.12726, doi:10.3892/mmr.2022.12726. This article has 11 citations and is from a peer-reviewed journal.

7. (li2023totalanomalouspulmonary pages 1-2): Gefei Li, Baoying Meng, Cheng Zhang, Weimin Zhang, Xiaodong Zhou, Qing Zhang, and Yiqun Ding. Total anomalous pulmonary venous connection in 80 patients: primary sutureless repair and outcomes. Frontiers in Surgery, Jan 2023. URL: https://doi.org/10.3389/fsurg.2022.1086596, doi:10.3389/fsurg.2022.1086596. This article has 5 citations.

8. (piroddi2020myocardialoverexpressionof pages 1-3): Nicoletta Piroddi, Paola Pesce, Beatrice Scellini, Stefano Manzini, Giulia S Ganzetti, Ileana Badi, Michela Menegollo, Virginia Cora, Simone Tiso, Raffaella Cinquetti, Laura Monti, Giulia Chiesa, Steven B Bleyl, Marco Busnelli, Federica Dellera, Daniele Bruno, Federico Caicci, Annalisa Grimaldi, Roberto Taramelli, Lucia Manni, David Sacerdoti, Chiara Tesi, Corrado Poggesi, Simonetta Ausoni, Francesco Acquati, and Marina Campione. Myocardial overexpression of ankrd1 causes sinus venosus defects and progressive diastolic dysfunction. Cardiovascular research, 116:1458-1472, Nov 2020. URL: https://doi.org/10.1093/cvr/cvz291, doi:10.1093/cvr/cvz291. This article has 40 citations and is from a domain leading peer-reviewed journal.

9. (piroddi2020myocardialoverexpressionof pages 7-9): Nicoletta Piroddi, Paola Pesce, Beatrice Scellini, Stefano Manzini, Giulia S Ganzetti, Ileana Badi, Michela Menegollo, Virginia Cora, Simone Tiso, Raffaella Cinquetti, Laura Monti, Giulia Chiesa, Steven B Bleyl, Marco Busnelli, Federica Dellera, Daniele Bruno, Federico Caicci, Annalisa Grimaldi, Roberto Taramelli, Lucia Manni, David Sacerdoti, Chiara Tesi, Corrado Poggesi, Simonetta Ausoni, Francesco Acquati, and Marina Campione. Myocardial overexpression of ankrd1 causes sinus venosus defects and progressive diastolic dysfunction. Cardiovascular research, 116:1458-1472, Nov 2020. URL: https://doi.org/10.1093/cvr/cvz291, doi:10.1093/cvr/cvz291. This article has 40 citations and is from a domain leading peer-reviewed journal.

10. (piroddi2020myocardialoverexpressionof pages 3-4): Nicoletta Piroddi, Paola Pesce, Beatrice Scellini, Stefano Manzini, Giulia S Ganzetti, Ileana Badi, Michela Menegollo, Virginia Cora, Simone Tiso, Raffaella Cinquetti, Laura Monti, Giulia Chiesa, Steven B Bleyl, Marco Busnelli, Federica Dellera, Daniele Bruno, Federico Caicci, Annalisa Grimaldi, Roberto Taramelli, Lucia Manni, David Sacerdoti, Chiara Tesi, Corrado Poggesi, Simonetta Ausoni, Francesco Acquati, and Marina Campione. Myocardial overexpression of ankrd1 causes sinus venosus defects and progressive diastolic dysfunction. Cardiovascular research, 116:1458-1472, Nov 2020. URL: https://doi.org/10.1093/cvr/cvz291, doi:10.1093/cvr/cvz291. This article has 40 citations and is from a domain leading peer-reviewed journal.

11. (xue2023prenataldiagnosisand pages 7-7): Xiaoying Xue, Qiumei Wu, Mingtao Xiong, Wen Ling, Shan Guo, Hong Ma, Biying Huang, Min Liu, Xiuqing Qiu, and Zongjie Weng. Prenatal diagnosis and postnatal verification in fetuses with total anomalous pulmonary venous connection. Frontiers in Pediatrics, Jun 2023. URL: https://doi.org/10.3389/fped.2023.1206032, doi:10.3389/fped.2023.1206032. This article has 6 citations.

12. (xue2023prenataldiagnosisand pages 8-10): Xiaoying Xue, Qiumei Wu, Mingtao Xiong, Wen Ling, Shan Guo, Hong Ma, Biying Huang, Min Liu, Xiuqing Qiu, and Zongjie Weng. Prenatal diagnosis and postnatal verification in fetuses with total anomalous pulmonary venous connection. Frontiers in Pediatrics, Jun 2023. URL: https://doi.org/10.3389/fped.2023.1206032, doi:10.3389/fped.2023.1206032. This article has 6 citations.

13. (wen2024insightintothe pages 12-14): Chen Wen, Geng Shen, Chenhao Fang, and Lan Tian. Insight into the research history and trends of total anomalous pulmonary venous connection: a bibliometric analysis. Journal of Cardiothoracic Surgery, May 2024. URL: https://doi.org/10.1186/s13019-024-02787-8, doi:10.1186/s13019-024-02787-8. This article has 6 citations and is from a peer-reviewed journal.

14. (alifu2024assessingtherisk pages 3-5): Ailixiati Alifu, Haifan Wang, and Renwei Chen. Assessing the risk of reoperation for mild pulmonary vein obstruction post-tapvc repair: a retrospective cohort study. Frontiers in Cardiovascular Medicine, Jun 2024. URL: https://doi.org/10.3389/fcvm.2024.1399659, doi:10.3389/fcvm.2024.1399659. This article has 2 citations and is from a peer-reviewed journal.

15. (xue2023prenataldiagnosisand media 1a8f0ae4): Xiaoying Xue, Qiumei Wu, Mingtao Xiong, Wen Ling, Shan Guo, Hong Ma, Biying Huang, Min Liu, Xiuqing Qiu, and Zongjie Weng. Prenatal diagnosis and postnatal verification in fetuses with total anomalous pulmonary venous connection. Frontiers in Pediatrics, Jun 2023. URL: https://doi.org/10.3389/fped.2023.1206032, doi:10.3389/fped.2023.1206032. This article has 6 citations.

16. (matsuhisa2020computedtomographybasedsurgical pages 1-2): Hironori Matsuhisa, Yoshihiro Oshima, Tomonori Higuma, Shunsuke Matsushima, Shota Hasegawa, Yuson Wada, Michio Matsuoka, and Toshikatsu Tanaka. Computed tomography-based surgical strategy for total anomalous pulmonary venous connection. European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery, 58:237-245, Feb 2020. URL: https://doi.org/10.1093/ejcts/ezaa028, doi:10.1093/ejcts/ezaa028. This article has 8 citations.

17. (alifu2024assessingtherisk pages 5-6): Ailixiati Alifu, Haifan Wang, and Renwei Chen. Assessing the risk of reoperation for mild pulmonary vein obstruction post-tapvc repair: a retrospective cohort study. Frontiers in Cardiovascular Medicine, Jun 2024. URL: https://doi.org/10.3389/fcvm.2024.1399659, doi:10.3389/fcvm.2024.1399659. This article has 2 citations and is from a peer-reviewed journal.

18. (feng2020midtermresultsof pages 1-2): Zicong Feng, Yang Yang, Fengpu He, Kunjing Pang, Kai Ma, Sen Zhang, Lei Qi, Guanxi Wang, Fengqun Mao, Jianhui Yuan, and Shoujun Li. Mid-term results of modified l-shaped incision technique for supracardiac total anomalous pulmonary venous connection. European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery, 58:1261-1268, Sep 2020. URL: https://doi.org/10.1093/ejcts/ezaa264, doi:10.1093/ejcts/ezaa264. This article has 9 citations.

19. (alifu2024assessingtherisk pages 1-2): Ailixiati Alifu, Haifan Wang, and Renwei Chen. Assessing the risk of reoperation for mild pulmonary vein obstruction post-tapvc repair: a retrospective cohort study. Frontiers in Cardiovascular Medicine, Jun 2024. URL: https://doi.org/10.3389/fcvm.2024.1399659, doi:10.3389/fcvm.2024.1399659. This article has 2 citations and is from a peer-reviewed journal.

20. (alifu2024assessingtherisk pages 2-3): Ailixiati Alifu, Haifan Wang, and Renwei Chen. Assessing the risk of reoperation for mild pulmonary vein obstruction post-tapvc repair: a retrospective cohort study. Frontiers in Cardiovascular Medicine, Jun 2024. URL: https://doi.org/10.3389/fcvm.2024.1399659, doi:10.3389/fcvm.2024.1399659. This article has 2 citations and is from a peer-reviewed journal.

21. (piroddi2020myocardialoverexpressionof pages 12-13): Nicoletta Piroddi, Paola Pesce, Beatrice Scellini, Stefano Manzini, Giulia S Ganzetti, Ileana Badi, Michela Menegollo, Virginia Cora, Simone Tiso, Raffaella Cinquetti, Laura Monti, Giulia Chiesa, Steven B Bleyl, Marco Busnelli, Federica Dellera, Daniele Bruno, Federico Caicci, Annalisa Grimaldi, Roberto Taramelli, Lucia Manni, David Sacerdoti, Chiara Tesi, Corrado Poggesi, Simonetta Ausoni, Francesco Acquati, and Marina Campione. Myocardial overexpression of ankrd1 causes sinus venosus defects and progressive diastolic dysfunction. Cardiovascular research, 116:1458-1472, Nov 2020. URL: https://doi.org/10.1093/cvr/cvz291, doi:10.1093/cvr/cvz291. This article has 40 citations and is from a domain leading peer-reviewed journal.