Tricuspid Valve #2: Papillary Muscle

1) Why the papillary muscles matter

The tricuspid valve (TV) is an integrated annulus–leaflet–subvalvular–ventricular system rather than “three leaflets on an annulus” [1, 2]. Valve competence depends on the papillary muscles (PMs) and chordae, which:

Distribute systolic load across leaflet tissue and commissures, limiting focal stress concentrations [1, 2].
Stabilize coaptation geometry by maintaining leaflet position relative to the right ventricular (RV) wall, preserving an effective coaptation surface [1].
Determine whether regurgitation is primarily due to intrinsic leaflet/chordal pathology versus secondary tethering from RV remodeling (functional TR) [2].

A key practical point is that the TV subvalvular apparatus is highly variable, and this variability has direct implications for exposure, mechanism assessment, and repair durability [1].

2) Core papillary muscle groups and nomenclature (what you should expect to find)

Because TV terminology has historically been inconsistent, a functional framework and standardized descriptors are useful for communication across surgery and echocardiography [3]. Morphologic studies also emphasize that “papillary muscle groups” are often clusters rather than single discrete muscles, with multiple heads being common [3].

A pragmatic “workhorse” surgical map is:

Anterior papillary muscle (often dominant)

Frequently the largest PM and a reliable RV orientation landmark (often near/linked to the moderator band in many hearts) [1].
Typically provides chordae to the anterior leaflet and may contribute to adjacent leaflet support depending on chordal distribution [1, 2].

Posterior papillary muscle (often dominant)

Often substantial, supporting the posterior leaflet and adjacent commissural regions [1, 2].

Septal papillary muscle group (most variable)

Commonly small, multiple, fragmented, or occasionally rudimentary/absent; septal leaflet support may instead be achieved by short chordae and/or direct septal attachments [1].

Take-home: In many hearts, anterior + posterior PMs act as the dominant “pillars,” while the septal apparatus is the most variable element—particularly relevant to septal leaflet tethering patterns and repair mechanics [1, 3].

3) Chordal architecture and the “variable septal leaflet” problem

Compared with the mitral valve, the TV chordal network is less stereotyped and more heterogeneous [1, 2]. Clinically important variability includes:

Septal leaflet support via multiple small septal PMs versus direct septal attachments (short chordae/attachment points along the septum) [1].
Additional chordae that may arise from RV trabeculations, which can change how the septal leaflet behaves with RV dilation or device interaction [1, 2].

This explains why the septal leaflet can behave very differently among patients even with similar degrees of annular dilation.

4) Functional TR as a 3D geometric disease: PM displacement and tethering are not “secondary details”

Contemporary functional TR is best conceptualized as a 3D geometric disorder of the RV–annulus–subvalvular complex [2]:

RV dilation/shape change → papillary muscle displacement (often apical and/or lateral)
PM displacement → leaflet tethering (restricted systolic excursion toward the annular plane)
Tethering + annular dilation → coaptation gap → TR progression

Two complementary lines of evidence support PM displacement as a key mechanistic driver:

In vitro (mechanistic) data: In a right-heart simulator, isolated PM displacement increased TR even with a normal annular area, demonstrating that PM displacement alone can produce functional TR physiology [4].
Clinical 3D echo (in vivo) data: In patients studied with 3D echocardiography, TR severity correlated not only with pulmonary arterial pressure and annular area, but also with apical/lateral PM displacement and tenting measures (tenting height/area) [5].

Surgical pitfall: When tethering is dominant, annuloplasty alone may be insufficient, because the subvalvular tether vectors remain uncorrected [6, 7].

5) Surgical implications: intraoperative checklist (surgeon-facing)

A durable repair starts with correctly defining the mechanism and mapping the subvalvular geometry.

Step 1 — Identify the dominant PM pillars

Confirm the anterior and posterior PMs and their chordal territories [1, 2].

Step 2 — Interrogate septal leaflet support

Determine whether the septal leaflet is supported mainly by:

small/multiple septal PMs, or
direct septal attachments/short chordae [1].

Step 3 — Define the mechanism

Primary lesion: leaflet/chordal abnormality (prolapse/flail, chordal rupture, tissue deficiency)
Secondary mechanism: RV remodeling → PM displacement → tethering and coaptation gap (functional TR) [2, 4, 5]

Step 4 — Predict repair durability (tethering is a red flag)

Classic clinical data show that tethering predicts residual TR after annuloplasty, with quantitative thresholds (e.g., tethering distance/area) associated with postoperative residual TR risk [6].
Contemporary commentary and series continue to report residual/recurrent TR in the ~10–20% range after repair in functional TR cohorts, particularly when tethering is not addressed [7].

6) Subvalvular strategies: why they exist and what the early data show

Because functional TR is frequently driven by subvalvular geometry, several approaches aim to reduce tethering by modifying PM position and leaflet closing angles:

Papillary muscle septalization (concept + early experience): Approximating the PM toward the septum (typically combined with restrictive annuloplasty) is intended to reduce leaflet tenting and restore coaptation geometry [7, 8].
Composite subvalvular procedures for tethering-dominant TR: In a feasibility study of patients with severe tethering, combining subvalvular techniques with ring annuloplasty improved TR grade and reduced tethering height (e.g., from ~9.9 mm to ~5.5 mm, p<0.001), with higher freedom from moderate TR at follow-up in composite vs single-technique approaches [9].

Interpretation: The emerging theme is consistent—annular correction is necessary but not always sufficient in tethering-dominant functional TR; adjunct subvalvular strategies are rational and may improve durability, though longer-term and larger comparative datasets remain important [7–9].

References

[1] Dahou A, Levin D, Reisman M, Hahn RT. Anatomy and Physiology of the Tricuspid Valve. JACC Cardiovasc Imaging. 2019;12(3):458-468.

[2] Buzzatti N, De Bonis M, Moat N. Anatomy of the Tricuspid Valve, Pathophysiology of Functional Tricuspid Regurgitation, and Implications for Percutaneous Therapies. Interv Cardiol Clin. 2018;7(1):1-11.

[3] Joudinaud TM, Flecher EM, Duran CMG. Functional terminology for the tricuspid valve. J Heart Valve Dis. 2006;15(3):382-388.

[4] Spinner EM, Shannon P, Buice D, Jimenez JH, Veledar E, del Nido PJ, Adams DH, Yoganathan AP. In vitro characterization of the mechanisms responsible for functional tricuspid regurgitation. Circulation. 2011;124(8):920-929.

[5] Spinner EM, Lerakis S, Higginson J, Pernetz M, Howell S, Veledar E, Yoganathan AP. Correlates of tricuspid regurgitation as determined by 3D echocardiography: pulmonary arterial pressure, ventricle geometry, annular dilatation, and papillary muscle displacement. Circ Cardiovasc Imaging. 2012;5(1):43-50.

[6] Fukuda S, Song JM, Gillinov AM, McCarthy PM, Daimon M, Kongsaerepong V, Thomas JD, Shiota T. Tricuspid valve tethering predicts residual tricuspid regurgitation after tricuspid annuloplasty. Circulation. 2005;111(8):975-979.

[7] Hirji SA, Seese L, Sabe AA. Commentary: Addition of papillary muscle septalization to tricuspid valve repair: Boom or bust? JTCVS Tech. 2021;10:289-290.

[8] Couetil JP, Nappi F, Spadaccio C, Fiore A. Papillary muscle septalization for functional tricuspid regurgitation: Proof of concept and preliminary clinical experience. JTCVS Tech. 2021;10:282-288.

[9] Takeshita M, Arai H, Nagaoka E, Oi K, Yashima M, Fujiwara T, Oishi K, Mizuno T. Efficacy of singular and composite annular repositioning and subvalvular surgical techniques to treat functional tricuspid regurgitation due to leaflet tethering: Early results of a feasibility study. Eur J Cardiothorac Surg. 2022;62(3):ezac101.