4 The Mitral Valve

The mitral valve is a large (4.5–6 cm²), anatomically complex three-dimensional structure; hence it is more of an “apparatus” than a valve. It is not circular; hence, even its simplest geometry is not well described in terms of diameter. Maintaining its competence requires that all the components be in ongoing adequate spatial position throughout systole, as the ventricular volume reduces by half, as the ventricular diameter and length reduce, and as the annular area reduces. Some components of the mitral apparatus have fixed dimensions (leaflets and chordae), some actively shorten in systole to preserve the length–tension apparatus (papillary muscles and the left ventricle myocardium between the papillary muscle and the annulus), and some passively shorten (mitral annulus)

Through its lifetime, the mitral valve moves twice per cardiac cycle (in the absence of atrial fibrillation, marked first-degree atrioventricular block, or marked tachycardia), and thus opens and closes through an average of 210,000 cardiac cycles daily, or about 7 billion times in a lifetime of 80 years. Like the aortic valve, it is subjected to systemic pressures, but over a pressure gradient twice as high.

Each component of the mitral valve is susceptible to disease, and, as with aortic insufficiency, not only the severity, but also the cause of the insufficiency, must be sought in all cases of mitral insufficiency. Determining the basis of mitral dysfunction is important, because it may guide the approach to the disease (e.g., emergency surgery for papillary rupture, antibiotics for endocarditis, repair for many myxomatous lesions) and determine the feasibility of surgical repair versus replacement.

Disease may involve a single component of the valve (e.g., endocarditis perforating a leaflet), or several components of the valve (e.g., myxomatous disease lengthening leaflet components, chordae, and the annulus). Disease processes may result in competing effects on valve competence: for example, prolapse may reduce coaptation and displace the valve basally while cavitary dilation secondary to the mitral regurgitation (MR) from the prolapse offsets the prolapse by displacing the papillary muscle anchoring point of the apparatus apically. Some regurgitant orifices are relatively fixed (e.g., flail chordae/leaflets and perforations), and some are dynamic (e.g., mitral valve prolapse, in which the regurgitant orifice may vary in time and severity through systole, and MR due to dilation/remodeling of the left ventricle). The mitral valve is complex, and, as a result, so is mitral insufficiency. Better understanding of the inherent complexity of the mitral valve has improved surgical approaches and, especially, surgical results.

Anatomic Components

Two leaflets

The anterior mitral leaflet

The posterior mitral leaflet

An oblique commissure

Anterolateral portion

Posteromedial portion

Two papillary muscles

Anterolateral

• Typically with one trunk/one head

Posteromedial

• Typically with two trunks/two heads

Chordae tendineae

Primary, secondary, and tertiary

Inserting into

• The free edge of the mitral leaflets

• The body of the mitral leaflets

Ventricular myocardium

Under (“subtending”) the papillary muscles, situating the papillary muscle

In longitudinal relation to the leaflets

In radial relation to the leaflets

Mitral Leaflets

The surface area of the two mitral leaflets is nearly the same, but their shape is very different.

The annular length of the posterior leaflet is about twice that of the anterior leaflet, but the height of the anterior leaflet is more than twice that of the posterior leaflet. The area of the leaflets is about 2.5 times the area of the mitral valve annulus. The leaflets are in continuity with each other, apposing over several millimeters, to achieve coaptation and competence and a reserve of coaptation.

The posterior mitral leaflet is formed of three scallops: anterior, middle, and posterior. The distinction among these leaflets is somewhat arbitrary.

The leaflets are lined by atrialis tissue on the atrial side and ventricularis tissue on the ventricular side, and contain the spongiosa and fibrosa layers in between. Different disease processes affect the leaflets differently; for example, rheumatic heart disease affects primarily the fibrosa, whereas myxomatous degeneration affects primarily the spongiosa.

The Commissures

Anatomically, there is only a single commissure, but by convention, the lateral portion is referred to as the anterolateral commissure, and the medial portion is referred to as the medial commissure.

The commissure is the site of systolic apposition of opposing leaflet surfaces, and the site of diastolic separation of the leaflets.

Rheumatic mitral stenosis results from fusion of the commissure from the outside in toward the center, resulting is a small residual central orifice. The treatment for mitral stenosis is to restore motion (separation) of the leaflets by “splitting” the commissure, allowing for a larger diastolic orifice. Rheumatic calcification of the commissures diminishes the probability of a good split from catheter balloon valvuloplasty, and increases the probability that the split will occur through the body of the leaflet (following the path of least resistance), rather than along the commissures, resulting in MR.

The best operation for mitral valve repair of myxomatous disease is the quadrangular resection of the central P2 component of the posterior leaflet, with reapposition of the leaflet margins and insertion of an annular ring to avoid tension on the sutured leaflet margins. Surgical resection of the lateral (P1) or medial (P3) leaflets has a greater chance of compromising the commissure.

Chordae

Three generations (primary, secondary, and tertiary) of chordae insert onto the undersurface (ventricular surface) of the leaflets via branching arcades. An average of 12 chordae arise from each papillary muscle, and 120 insert into the mitral valve leaflets.

The leaflets are suspended optimally by the chordae. Chordae insert into the free edge of the mitral valve and also one third to halfway back along the leaflet body.

Rheumatic disease and myxomatous disease may involve the chordae:

Rheumatic disease results in shortening, thickening, stiffening, and fusion of the chordae.

Myxomatous disease may result in elongation, stretching, weakening, and rupture of chordae.

Papillary Muscles

The two papillary muscles are deemed anterolateral and posteromedial, although their position, morphology, and number are prone to variation. Both are located one third of the distance from the base of the left ventricle toward the apex.

The Anterolateral Papillary Muscle

The anterolateral papillary muscle is the more constant of the two, usually consisting of a single trunk that protrudes well into the ventricular cavity.

The anterolateral papillary muscle is imaged by

Transthoracic echocardiography

• apical four-chamber view

Transesophageal echocardiography

• Lower esophageal horizontal view

• Transgastric long- and short-axis views

The Posteromedial Papillary Muscle

The posteromedial papillary muscle usually is smaller, and often consists of multiple insertions into the left ventricle, and sometimes even of multiple separate trunks.

Most patients have either two “heads” or two adjacent “trunks” of the posteromedial papillary muscle.

Rupture of the posteromedial papillary muscle has the chance of involving one head or trunk, leaving the other intact, and resulting in less fulminant MR than would complete rupture of both heads or trunks, or of a solitary (e.g., anterolateral) papillary muscle.

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Related posts:

1. The Aortic Valve
2. Aortic Insufficiency
3. Coronary Artery Disease: Stress Echocardiography
4. Mitral Insufficiency

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