Mitral Valve Anatomy: Leaflets, Annulus, and Subvalvular Apparatus

The mitral valve is a complex three-dimensional left atrioventricular valve apparatus, not simply a pair of leaflets. Normal mitral competence depends on the coordinated interaction of the mitral annulus, anterior leaflet, posterior leaflet, commissures, chordae tendineae, papillary muscles, adjacent left ventricular geometry, and the aorto-mitral fibrous continuity [1, 2].

This concept is clinically fundamental. The mitral valve apparatus functions as an integrated geometric and mechanical unit: the leaflets provide the coaptation surface, the annulus provides a dynamic frame, the chordae regulate leaflet motion, the papillary muscles transmit ventricular geometry to the valve, and the left ventricle provides the closing force required for systolic competence [2, 3].

Mitral regurgitation develops when this balanced system loses sufficient leaflet coaptation. The responsible abnormality may be structural, functional, or mixed, and may involve the leaflets, chordae, papillary muscles, annulus, left atrium, or left ventricle [3, 4].

2. Leaflet Anatomy

The mitral valve has two principal leaflets:

1. Anterior leaflet
2. Posterior leaflet

The anterior leaflet is also called the aortic leaflet because it is in fibrous continuity with the aortic valve. It occupies a smaller portion of the annular circumference but contributes a large proportion of the coaptation surface.

The posterior leaflet is also called the mural leaflet because it is attached along the posterior left ventricular wall. It occupies a larger portion of the annular circumference and is typically divided into three scallops [1, 2].

Although the traditional description uses “two leaflets,” surgically the mitral valve should be analyzed in a segmental manner. Segmental anatomy allows precise communication of prolapse, restriction, cleft-like deficiency, chordal rupture, commissural pathology, and repair strategy.

3. Segmental Nomenclature: A1–A3 and P1–P3

The posterior leaflet is divided into three scallops:

• P1: lateral posterior scallop
• P2: middle posterior scallop
• P3: medial posterior scallop

The anterior leaflet does not have true scallops in the same anatomic sense, but it is commonly described by corresponding opposing segments:

• A1 opposite P1
• A2 opposite P2
• A3 opposite P3

This nomenclature is essential for surgical planning and echocardiographic communication. For example, P2 prolapse suggests excess motion of the central posterior scallop, whereas A3 restriction suggests impaired systolic excursion of the medial anterior leaflet segment. These two lesions may both produce mitral regurgitation, but their mechanisms and repair strategies differ substantially [3, 5].

4. Commissures and Commissural Leaflets

The mitral valve has two commissures:

1. Anterolateral commissure
2. Posteromedial commissure

Each commissural region contains a small commissural leaflet or commissural bridging tissue between the anterior and posterior leaflets. These commissural zones are not passive junctions. They contribute to coaptation and can become important sites of localized regurgitation.

Commissural pathology may include:

• Commissural prolapse
• Commissural restriction
• Commissural fusion
• Abnormal commissural chordae
• Cleft-like separation near the commissural zone
• Residual regurgitation after incomplete repair

For this reason, intraoperative valve analysis should include commissural inspection in addition to simple anterior-versus-posterior leaflet assessment.

5. Mitral Annulus

The mitral annulus is a dynamic three-dimensional structure rather than a flat circular ring. It has a characteristic saddle-shaped configuration, with higher points anteriorly and posteriorly and lower points near the commissural regions [2, 6].

This saddle shape is mechanically important because it helps reduce leaflet stress and supports efficient coaptation. During the cardiac cycle, the annulus changes in size and shape, contributing to normal valve competence. Loss of annular dynamics, annular dilatation, or flattening of the saddle configuration can impair leaflet coaptation and contribute to mitral regurgitation [4, 6].

Surgically, annular assessment is important for:

• Annuloplasty sizing
• Restoring leaflet coaptation
• Reducing recurrent annular dilatation
• Avoiding excessive leaflet tension
• Preserving the aorto-mitral curtain
• Avoiding distortion near the fibrous trigones

In degenerative mitral regurgitation, annular stabilization is often required to support the reconstructed leaflet geometry. In functional mitral regurgitation, annular dilatation is frequently accompanied by ventricular remodeling and papillary muscle displacement, so annuloplasty alone may not fully address the tethering mechanism [4, 7].

6. Aorto-Mitral Continuity and Fibrous Trigones

Anteriorly, the mitral annulus is in fibrous continuity with the aortic valve through the aorto-mitral curtain, also called the intervalvular fibrosa. This region is anchored by the:

1. Right fibrous trigone
2. Left fibrous trigone

The aorto-mitral curtain is part of the central fibrous skeleton of the heart and forms an important anatomic bridge between the mitral valve and the left ventricular outflow tract [1, 2].

This relationship is surgically relevant in:

• Mitral valve repair
• Mitral valve replacement
• Aortic valve surgery
• Double-valve surgery
• Endocarditis involving the intervalvular fibrosa
• Aorto-mitral curtain reconstruction
• Complex left ventricular outflow tract reconstruction

The anterior mitral annulus should therefore not be viewed as an isolated mitral structure. It is part of a shared fibrous architecture linking the left atrioventricular valve, the aortic valve, and the left ventricular outflow tract.

7. Chordae Tendineae

The chordae tendineae connect the mitral leaflets to the papillary muscles and ventricular wall. Their primary role is to prevent systolic leaflet prolapse into the left atrium while maintaining a stable coaptation surface during ventricular contraction [1, 2].

Functionally, chordae can be divided into two major groups:

7.1 Primary Chordae

Primary chordae attach near the free edge of the leaflet. They prevent leaflet edge prolapse during systole.

Failure of primary chordae may produce:

• Leaflet prolapse
• Flail leaflet segment
• Eccentric mitral regurgitation jet
• Segment-specific regurgitation, such as P2 flail or A2 prolapse

Primary chordal rupture or elongation is a typical mechanism of degenerative or structural mitral regurgitation. In this setting, the primary abnormality is excessive leaflet motion due to loss of restraint [3, 5].

7.2 Secondary Chordae

Secondary chordae attach to the ventricular surface or body of the leaflet, particularly the anterior leaflet. They couple the leaflet to left ventricular geometry and distribute systolic load across the valve apparatus.

Secondary chordae are especially important in functional mitral regurgitation. When the left ventricle dilates or remodels, papillary muscles may be displaced apically, laterally, or posteriorly. This displacement increases leaflet tethering, restricts systolic closure, and reduces coaptation despite structurally normal leaflet tissue [4, 7].

Thus, primary chordal pathology tends to produce excess leaflet motion, whereas secondary chordal tethering tends to produce restricted leaflet motion.

8. Papillary Muscles

The mitral valve is supported by two major papillary muscle groups:

1. Anterolateral papillary muscle
2. Posteromedial papillary muscle

Each papillary muscle sends chordae to both the anterior and posterior leaflets. This dual distribution helps stabilize the coaptation line and distribute systolic forces across the valve [1, 2].

Papillary muscle dysfunction may cause mitral regurgitation through several mechanisms:

• Papillary muscle rupture
• Papillary muscle ischemia
• Papillary muscle displacement from ventricular remodeling
• Congenital papillary muscle malposition
• Parachute mitral valve morphology
• Arcade-like mitral valve morphology
• Shortened or abnormally inserted chordae

The anterolateral papillary muscle often has dual coronary supply, whereas the posteromedial papillary muscle more commonly has a single dominant blood supply. This difference helps explain the clinical vulnerability of the posteromedial papillary muscle to ischemic injury.

In secondary mitral regurgitation, papillary muscle displacement is a central mechanism. The papillary muscles are pulled away from the annular plane by ventricular dilatation or regional remodeling, increasing tethering forces and preventing adequate leaflet closure [4, 7].

9. Force Balance and Mechanisms of Mitral Regurgitation

Mitral competence depends on the balance between:

1. Closing forces
2. Tethering forces
3. Available leaflet tissue for coaptation

Closing forces are generated by left ventricular systolic pressure, which pushes the leaflets toward the left atrium and promotes coaptation. Tethering forces are generated by the chordae, papillary muscles, and ventricular geometry. These forces prevent prolapse but can also restrict leaflet motion if the subvalvular apparatus is displaced.

Mitral regurgitation occurs when structural or functional impairment exhausts the valve’s coaptation reserve [4].

9.1 Primary Mitral Regurgitation

In primary mitral regurgitation, the main abnormality is intrinsic to the valve apparatus. Examples include:

• Leaflet prolapse
• Flail leaflet
• Chordal rupture
• Leaflet thickening
• Rheumatic restriction
• Cleft-like leaflet deficiency
• Commissural abnormality

The surgical objective is usually to correct the structural lesion, restore segmental coaptation, and stabilize the annulus.

9.2 Secondary Mitral Regurgitation

In secondary mitral regurgitation, the leaflets may be structurally normal, but ventricular or atrial remodeling prevents effective coaptation. Mechanisms include:

• Left ventricular dilatation
• Papillary muscle displacement
• Leaflet tethering
• Annular dilatation
• Loss of annular contraction
• Left atrial enlargement in atrial functional mitral regurgitation

In this setting, the valve is abnormal because the surrounding geometry is abnormal. Durable treatment requires understanding the interaction between annular remodeling, papillary muscle position, leaflet tethering, and ventricular function [4, 7].

10. Surgical Relevance

A precise anatomic analysis of the mitral valve is essential before and during repair. The surgeon should define:

• Which leaflet segment is abnormal
• Whether the lesion is prolapse, restriction, cleft-like deficiency, or commissural pathology
• Whether the annulus is dilated, flattened, calcified, or distorted
• Whether chordae are ruptured, elongated, shortened, fused, or tethered
• Whether papillary muscle position and morphology are normal
• Whether ventricular geometry is contributing to regurgitation
• Whether the aorto-mitral curtain or fibrous trigones are involved
• Whether the pathology is primary, secondary, or mixed

Mitral valve repair is therefore an anatomic and physiologic reconstruction. Durable repair requires restoration of adequate leaflet coaptation, annular geometry, chordal balance, papillary muscle alignment, and valve–ventricle interaction [2–5].

11. Key Concept

The mitral valve should be understood as a dynamic valve–ventricle complex.

The leaflets create the coaptation surface.

The annulus provides a three-dimensional saddle-shaped frame.

The chordae regulate leaflet motion and distribute systolic load.

The papillary muscles transmit ventricular geometry to the valve.

The aorto-mitral curtain links the mitral valve to the left ventricular outflow tract.

Mitral regurgitation occurs when this integrated system loses geometric and mechanical balance.

References

[1] Ho SY. Anatomy of the mitral valve. Heart. 2002;88 Suppl 4(Suppl 4):iv5-iv10.

[2] Dal-Bianco JP, Levine RA. Anatomy of the mitral valve apparatus: role of 2D and 3D echocardiography. Cardiol Clin. 2013;31(2):151-164.

[3] Topilsky Y. Mitral regurgitation: anatomy, physiology, and pathophysiology—lessons learned from surgery and cardiac imaging. Front Cardiovasc Med. 2020;7:84.

[4] Dal-Bianco JP, Beaudoin J, Handschumacher MD, Levine RA. Basic mechanisms of mitral regurgitation. Can J Cardiol. 2014;30(9):971-981.

[5] Karagodin I, Singh A, Lang RM. Pathoanatomy of mitral regurgitation. Struct Heart. 2020;4(4):254-263.

[6] Watanabe N. The mitral valve complex: divine perfection. Circ Cardiovasc Imaging. 2016;9(1):e004353.

[7] Nogara A, Minacapelli A, Zambelli G, Lo Coco V, Fattouch K. Functional anatomy and echocardiographic assessment in secondary mitral regurgitation. J Card Surg. 2022;37(12):4103-4111.