Conotruncal Rotation (TGA-Type) — False Taussig–Bing
In this conotruncal-rotation framework, “False Taussig–Bing” refers to a TGA-type great-artery relationship produced by coupled lateral shifts of the great arteries together with a characteristic re-orientation of the outflow septal complex—most practically recognized as a specific behavior of the infundibular fold / infundibular septum (IF). As emphasized in classic morphologic work, “Taussig–Bing” itself is best understood as a spectrum unified by a juxtapulmonary (subpulmonary) VSD and malalignment of the infundibular/outlet septal structures, spanning forms that look like DORV at one end and discordant VA connection (TGA physiology) at the other. [1]
“False Taussig–Bing” is therefore not a “new diagnosis,” but a geometric subtype within that spectrum—defined by how the great arteries shift and how the IF aligns relative to the interventricular septum (IVS). [1,2]
1) Core morphologic signature
1. Great-artery relationship: TGA-type
- Pulmonary artery (PA) behaves as the posterior great artery.
- Aorta (Ao) behaves as the anterior great artery.
This “macro-pattern” (posterior PA / anterior Ao) sets the reference geometry for the subtype.
2. Great-artery “shift” pattern (lateral translation superimposed on rotation)
- Posterior PA → rightward shift (+)
- Anterior Ao → mild leftward shift
This paired translation narrows and re-centers the outflow corridor, altering which ventricular outlet is most directly “committed” to each great artery (a key concept across DORV/TGA variants). [3]
3. IF behavior: septalization
Two coupled features define the subtype:
- IF attaches to the tricuspid-side ventriculo-infundibular fold (Rt VIF).
- IF runs parallel to the IVS (rather than forming an oblique, “offset” wedge between the outflows).
This IF–IVS parallelism is the critical geometric clue that the outflow septal complex has become functionally aligned with the ventricular septum—a concept strongly grounded in surgical-anatomic descriptions of the infundibular septum/IF in TGA/VSD morphologies (including discussion of “false Taussig–Bing” configurations). [2]
4. VSD commitment: subpulmonary
- VSD is subpulmonary, located beneath the posterior PA.
Practically: the defect is pulmonary-committed, even though the PA sits posteriorly in this TGA-type arrangement.
2) Structural logic in the conotruncal-rotation model
This pattern can be described as a late-stage TGA-type rotation outcome in which rotation + translation + IF anchoring converge:
- Rotation establishes the TGA-type macro-relationship (posterior PA / anterior Ao).
- Lateral shifts (posterior rightward, anterior leftward) reshape the outlet geometry and redefine the “closest” outflow to the VSD plane.
- The IF rotates/anchors toward the tricuspid side (Rt VIF) and becomes IVS-parallel, effectively “septalizing” the outflow septal complex.
When the IF is septal-parallel, the subpulmonary outlet is preferentially aligned with the VSD plane, explaining why the VSD is subpulmonary by commitment in this subtype. [2,3]
3) Hemodynamic phenotype: what it tends to behave like
Because the VSD is subpulmonary, physiology often resembles TGA-with-VSD streaming/mixing, where:
- LV outflow preferentially streams through the VSD toward the pulmonary outflow, promoting pulmonary overcirculation when PVR falls.
- RV aligns more directly with the anterior outflow (Ao), supporting systemic output.
- The clinical phenotype is strongly modified by associated anatomy that is common in the Taussig–Bing spectrum:
- Aortic arch obstruction, subaortic narrowing, RVOT/LVOT geometry, and especially coronary patterns (which heavily influence operative strategy and risk). [1,4,8]
4) Practical recognition points (echo/CT and intraoperative “pattern recognition”)
When you suspect “False Taussig–Bing,” actively confirm three layers—macro, micro, and commitment:
- Macro (great arteries)
- Posterior PA with rightward displacement
- Anterior Ao with mild leftward shift
- Micro (outflow septal complex)
- IF attached toward Rt VIF
- IF parallel to IVS (the most discriminating geometric sign). [2]
- Commitment (VSD to outflow)
- A subpulmonary VSD whose “exit direction” points toward the PA outflow, even when the PA is posterior.
These observations mirror the broader message from morphologic series: internal geometry and outlet septal relationships often matter more than labels when determining surgical options. [1]
5) Why the distinction matters: concept → operative thinking
Across the Taussig–Bing spectrum, the operative question is rarely “What is it called?” and almost always:
- Which outlet is committed to the VSD?
- How is the IF aligned relative to the IVS (offset vs septal-parallel)? [2]
- Can the LV be routed to the systemic outflow without obstruction or distortion?
- What are the coronary and arch modifiers? [1,8]
Historically and in modern series, definitive repair strategies for Taussig–Bing–type anatomies include:
- Arterial switch operation (ASO) + VSD closure (frequently favored when geometry supports it). [6,8,9]
- Intraventricular rerouting (when arterial-level repair is not ideal due to internal geometry, distances, or obstructive risks). [4,6]
- Broader DORV classification frameworks can help keep decision-making consistent by describing the lesion according to VSD–great artery relationships and outflow obstruction, rather than relying on a single eponym. [7]
In this sense, “False Taussig–Bing” is best used as a high-yield anatomic logic statement:
TGA-type great arteries + (posterior PA right shift / anterior Ao mild left shift) + IF septalization (Rt VIF attachment, IF ‖ IVS) → subpulmonary VSD commitment, with predictable implications for streaming and repair planning. [1,2,6]
References
[1] Stellin G, Ho SY, Anderson RH, Zuberbuhler JR, Siewers RD. The surgical anatomy of the Taussig-Bing malformation. J Thorac Cardiovasc Surg. 1987;93(4):560-569.
[2] Kurosawa H, Becker AE. Surgical anatomy of the infundibular septum in transposition of the great arteries with ventricular septal defect. J Thorac Cardiovasc Surg. 1986;91(1):123-132.
[3] Sridaromont S, Feldt RH, Ritter DG, Davis GD, Edwards JE. Double outlet right ventricle: hemodynamic and anatomic correlations. Am J Cardiol. 1976;38(1):85-94.
[4] Yacoub MH, Radley-Smith R. Anatomic correction of the Taussig-Bing anomaly. J Thorac Cardiovasc Surg. 1984;88(3):380-388.
[5] Kanter K, Anderson RH, Lincoln C, Firmin R, Rigby ML. Anatomic correction of double-outlet right ventricle with subpulmonary ventricular septal defect (the “Taussig-Bing” anomaly). Ann Thorac Surg. 1986;41(3):287-292.
[6] Serraf A, Lacour-Gayet F, Bruniaux J, Losay J, Petit J, Touchot-Kone A, Bouchart F, Planche C. Anatomic repair of Taussig-Bing hearts. Circulation. 1991;84(5 Suppl):III200-III205.
[7] Artrip JH, Sauer H, Campbell DN, Mitchell MB, Haun C, Almodovar MC, Hraska V, Lacour-Gayet F. Biventricular repair in double outlet right ventricle: surgical results based on the STS-EACTS international nomenclature classification. Eur J Cardiothorac Surg. 2006;29(4):545-550.
[8] Griselli M, McGuirk SP, Ko CS, Clarke A, Barron DJ, Brawn WJ. Arterial switch operation in patients with Taussig-Bing anomaly--influence of staged repair and coronary anatomy on outcome. Eur J Cardiothorac Surg. 2007;31(2):229-235.
[9] Rodefeld MD, Ruzmetov M, Vijay P, Fiore AC, Turrentine MW, Brown JW. Surgical results of arterial switch operation for Taussig-Bing anomaly: is position of the great arteries a risk factor? Ann Thorac Surg. 2007;83(4):1451-1457.
[10] Pigula FA. The Taussig-Bing anomaly turns 65: What we have learned in a lifetime. J Thorac Cardiovasc Surg. 2015;149(4):1132-1133.