Overview

The mitral valve was named by Versalius in the 16th century after it’s resemblance to a bishop’s “Mitre” hat with a geometrical appearance apparently similar.

Understanding the structure and function of the mitral valve in normality is crucial in order to identify and quantify the severity and location of any abnormalities using echo. Anatomically the mitral valve is not a simple planar structure with a pair of opening “lids” rather it exists as a complex structure involving three interconnected areas:

1. The annulus
2. The leaflets
3. The subvalvular apparatus

These will be described in more detail below.

The Annulus

First and foremost the annulus is not a discrete anatomical entity, it is fibrous only in part and is actually indistinguishable from the left ventricular wall in many individuals. Despite this it is useful to conceptually divide the annulus into discrete anatomical “zones” namely the anterior and posterior portions. The entire annulus forms a complex “pringle” shape which varies in its morphology throughout the cardiac cycle to ensure both adequate opening and coaptation in diastole and systole respectively.

The “annulus” consists of connective tissue of varying thickness and quality, in some individuals intertwining with the normal LV myocyte architecture when viewed histologically.

Posterior annulus

This portion of the annulus acts as a “hinge-point” or transition zone between the LA and LV section of the PML.

On the external surface of the heart superficial to the posterior annulus exists the “atrioventricular groove” in which lies the left circumflex (LCx) artery as well as the great cardiac vein which goes on to drain into the coronary sinus; located nearby draining into the right atrium.

The PML inserts 2mm below the annulus itself, this transitional region in between annulus and insertion point can be prone to dilatation in individuals with elevated LA pressure or mitral regurgitation.

Mitral annular calcification “MAC” is more commonly seen on the posterior annulus, possibly due to the greater mobility exhibited by this area of the annulus. This is a marker of other atherosclerotic processes and is also associated with coronary calcification and is more common in patients with renal failure who have abnormalities in calcium and phosphate handling. The greater mobility of the posterior annulus is a result of not being tethered in close proximity to the aortic valve like the anterior annulus.

Anterior Annulus

The anterior annulus also does not truly exist as a defined anatomical entity but it is useful to consider as a concept anatomically. It is also referred to as the “Intervalvular fibrosa” forming a transition zone between the fibrous portion of the aortic valve annulus and the anterior mitral leaflet.

The intervalvular fibrosa is avascular and therefore is commonly involved with endocarditis of the aortic valve, both via direct extension of infection and via infected regurgitant blood ejecting in a retrograde fashion against the anterior mitral leaflet and up towards the aorto-mitral junction (on the LA side)

This zone can be imaged in great detail using 3D TOE and looking “upwards” towards the aortic valve from the ventricular side “through” the LVOT. From here the NCC and LCC can be seen with the “interleaflet triangle” lying between these leaflets. This area is commonly affected by abscess and aneurysm formation, both as a consequence of endocarditis.

Leaflets

The two mitral leaflets (AML and PML) actually exist in continuity with one another, the anterolateral and posteromedial commissures not completely reaching the mitral annulus.

• Anterolateral commissure lies higher in the thorax and lies adjacent to P1/A1 scallops
• Posteromedial commissure exists lower down in the thorax and lies adjacent to P3/A3 scallops

Both commissures can be visualised via 3DTOE using the “top down” surgeons view to assess for mitro-annular dysjunction or stenosis of the commissures.

The leaflets themselves are not inert avascular structures, they are engineered in such a way as to maximise the efficacy of valve closure in normality.

The underside of the mitral leaflets consist of two distinct anatomical zones:

1. Pars rugosa “Rough zone” where the chordae insert into the valve
2. Pars Liscia “Translucent zone” which tends to be thinner and can prolapse into t he LA in normality

Histology

• Endothelium
• Atrial layer - lamellar collagen and elastin
• Spongiosa - Compressible central “cushion” layer containing glycosaminoglycans which absorb tension and friction forces
• Fibrosa (ventricularis) - Predominantly collagen providing strength and stiffness
• Endothelium

Normal leaflet thickness is 1mm, this tends to increase in degenerative mitral valve disease possibly as a secondary response to increased shear forces across the valve. Continued stretching and shear forces applied to the valve results in fibroblast activation, increased collagen deposition and increase in valve thickness. Further adaptations can occur as a result of LV dilatation and remodelling.

Anterior mitral leafelet

The AML is anchored to the fibrous portion of the aortic annulus via the intervalvular fibrosa to the aortic valve. In some books it is confusingly referred to as the “aortic leaflet”

• Trapezoidal in shape
• Has a higher tenting height than the PML
• 3cm circumferentially occupying one third of the annulus

Posterior Mitral Leaflet

The PML is usually divided into three clear scallops; P1, P2 and P3 via two indentation lines across its surface. P2 is frequently the largest scallop and also the most likely to prolapse. The scallops serve to “fold” the leaflet allowing for greater conformational change through the cardiac cycle.

• Trapeziodal in shape
• 5cm circumferentially extending around two thirds of the annulus

Leaflet Abnormalities

Secondary Mitral Regurgitation

Leaflets enlarge and thicken in patients with otherwise normal LV geometry and severe mitral regurgitation. Mechanical forces exerted on the valve are thought to activate fibroblasts resulting in cellular proliferation. This is thought to be a compensatory mechanism to maintain coaptation as mitral regurgitation progresses. Excessive remodelling is likely to make the leaflets stiffer and less compliant in a maladaptive cycle, paradoxically reducing coaptation.

Clefts

Clefts refer to indentations in the PML which extend all the way back from the coaptation surface to the hinge line of the annulus and are a leading cause of mitral regurgitation. These are commonly seen in degenerative mitral “Barlow’s” disease.

Chordae

These are tough, fibrous structures which exist in a “fan-like” configuration extending outwards from their respective papillary muscles to attach to the “Pars rugosa” portions of the mitral valve leaflets. They are anatomically subdivided into the following categories:

1st order “Marginal” chordae

• Insert on the free margin of the leaflet
• Rupture of these cause flail or severe prolapse

2nd order “ strut” or “stay” chordae

• Insert at the transition zone between the rough and translucent zones of the leaflets
• There are usually 2 on the AML subtending the valve surface at 1/3 intervals
• These chordae resist high pressure forces during systole although interestingly cutting them completely does NOT result in MR.
• Theory exists that these chordae serve to preserve favourable LV geometry
• These thicker chordae often contain blood vessels

3rd order “basal” chordae

• Originate from the LV wall and only insert into the PML
• Provide additional structural stability to the PML

Papillary Muscles

The papillary muscles serve as an interface between the chordae and the LV wall. They undergo active contraction during systole (along with the rest of the LV) resulting in chordae shortening, preventing eversion of the mitral leaflets. Both PM’s are orientated in the same direction as the LV chamber so that when systole occurs they pull the mitral leafelts downwards ensuring good coaptation.

Anterolateral Papillary Muscle

• ALPM has a dual blood supply from LAD and LCx
• Usually gives rise to 12x or so chordae which insert into the lateral and medial portions of the AML and PML fanning out from the AL-commissure

Posteromedial Papillary Muscle

• PMPM has a single blood supply derived from the PDA and is therefore more vulnerable to ischemic insult (With inferior STEMI)
• Arises from a network of trabeculations in the LV wall, arising in a pillar-like manner

Mitral Valve Function

Annular morphological changes

• In systole the annulus is “D-shaped” with the intercommisural dimension being larger than the “antero-posterior” dimension. This is ensures adequate coaptation of the AML and PML to prevent MR.
• In diastole the annulus becomes more circular facilitating blood to flow from the LA into the LV.
• The leaflets need to be able to stretch to 115% of their size in order to achieve adequate copatation. Elasticity and flexibility of the valve is essential to ensure this.

Annular motion

1. “Sphincter” contraction

This motion decreases the mitral valve area by 20-30% in systole preventing regurgitation of blood. It occurs as a result of contraction of the basal helical fibres of the heart which provide the “twisting” contribution towards systole.

2. Translational movement

This describes the “piston” type motion of the LV during systole where the overall height decreases and the mitral annulus moves towards the apex. Recall that the apex is usually fixed to the pericardium and diaphragm and the LV is therefore “pulled” towards the apex during systole. The opposite movement occurs in diastole and the upwards translational movement of the annulus at this phase of the cardiac cycle results in the column of blood which was present above the mitral valve being moved downwards into t he LV, contributing around 30% to filling and overall stroke volume. The overall translational motion is usually 5-10mm with disproportionally more movement occurring at the posterior annulus due to less tethering to adjacent structures.

3. Annular folding

This describes the accentuation of the “pringle” shape which occurs during systole. The end result of this increased folding is improved overlap and coaptation area between the AML and PML which prevents regurgitation.