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Surgical mitral valve repair and replacement
Key points
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The mitral valve is a complex, three-dimensional assembly of independent anatomic components, including the annulus, leaflets and commissures, chordae tendineae, papillary muscles, and left ventricle. Abnormalities (lesions with etiologic implications) in any of these components may cause alteration in closure (i.e., dysfunction) against left ventricular (LV) pressure and consequently mitral regurgitation (MR) or mitral stenosis (MS).
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Although rheumatic disease remains the most common cause of MR worldwide, it is no longer a frequent cause of mitral valve disease in developed countries. In Western countries, degenerative disease is the leading cause of mitral valve disease and MR. Ischemic MR (i.e., secondary MR) accounts for 10% to 20% of cases, but early percutaneous intervention in acute coronary syndromes will progressively limit this disease prevalence.
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Several variables have been identified that significantly affect the natural history of MR in the setting of mitral valve prolapse and can serve as surgical triggers. They include LV dysfunction with an ejection fraction of less than 60%, New York Heart Association functional class III or IV, regurgitant orifice area of 40 mm 2 or larger, LV end-systolic dimension greater than 40 mm, left atrial index of 60 mL/m 2 or less, left atrial dimension greater than 55 mm, pulmonary hypertension at rest or during exercise, and atrial fibrillation.
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Mitral valve repair is the gold standard treatment for patients with degenerative mitral valve disease. The literature demonstrates that it is possible to repair almost all prolapsing degenerative mitral valves with a very low perioperative risk and absence of residual MR when the procedure is performed in reference centers. This is crucial because of the increasing number of asymptomatic patients referred for surgery. The latest practice guidelines introduced the referral to reference centers as an algorithm variable.
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Whereas mitral valve replacement (MVR) is rare in patients with degenerative disease, it is prevalent among patients with rheumatic disease and may be considered a viable option for selected patients with ischemic MR. In cases of ischemic MR, MVR may provide a good alternative because prosthetic valve function is not affected by the degree of LV dysfunction, although there is the early risk of prosthesis-related complications.
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If the decision to proceed with MVR is made, a chordal-sparing approach should be employed to preserve chordal-ventricular-annular continuity, which is important to maintain long-term LV shape and performance.
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Use of a mechanical prosthesis is reasonable in middle-aged patients if there are no contraindications to anticoagulation and if there is a clear risk of accelerated structural valve deterioration. However, there is a significant trend toward the use of bioprostheses. Bioprostheses should be recommended when good-quality anticoagulation is unlikely (due to compliance problems or contraindication), for reoperation for mechanical thrombosis despite excellent anticoagulant control, in women contemplating pregnancy, and in patients wishing to avoid anticoagulation.
The normal mitral valve is in the left atrioventricular groove and allows unidirectional flow of oxygenated blood from the left atrium into the left ventricle (LV) in a near-frictionless fashion during diastole. The valve is a complex, three-dimensional assembly of independent anatomic components: the annulus, the leaflets and commissures, the chordae tendineae, the papillary muscles, and the LV. During systole, a coordinated interaction of these anatomic components seals the valve against LV pressure. Even a normal, competent valve may permit a physiologically trivial amount of reversed flow into the left atrium; more than a trace of mitral regurgitation (MR) is considered pathologic.
Although mild to moderate MR may be tolerated indefinitely, severe MR eventually leads to LV remodeling, heart failure, and death. In this context, the natural history of MR depends intimately on its cause, the severity of LV volume overload, LV contractile performance, and the appearance of overlapping clinical conditions due to reversal of flow, such as atrial fibrillation and pulmonary hypertension.
Primary degenerative mitral valve disease is the most prevalent cause of isolated severe MR in the United States. Distinct pathologic features of the disease include mitral valve billowing (i.e., intact valve coaptation) and prolapse (i.e., deficient valve coaptation) caused by myxomatous degeneration of the mitral leaflets, chordal elongation or rupture, or papillary muscle elongation or rupture.
In the setting of severe MR, even in the absence of symptoms, mitral valve repair is the gold standard procedure for patients who require surgery for degenerative MR. For this subset of patients, mitral valve repair has become feasible and safe, and repair techniques have demonstrated an excellent durability, especially when performed in high-volume institutions.
The latest guidelines for managing valvular heart disease suggest targeted referral to reference centers with experienced surgeons to ensure a repair rate greater than 90% and a mortality rate of 1% or less. Although these new standards have triggered a more liberal referral of asymptomatic patients, mitral valve repair is still underused in the United States. A data analysis from the Society of Thoracic Surgeons (STS) observed an average mitral valve repair rate of only 70%.
Simple lesions such as posterior leaflet prolapse are associated with very high mitral valve repair rates in many centers, but the overall repair rate for more complex scenarios, as defined by leaflet involvement (e.g., isolated anterior leaflet or bileaflet prolapse), lesion complexity (e.g., significant annular calcification, significant excess tissue), or patient comorbidities (e.g., older age, reoperations), remains uncertain and seems to be well below guideline recommendations.
Surgical anatomy of the mitral valve
The normal mitral valve is a dynamic complex of independent anatomic structures. Abnormalities (i.e., lesions) in any of these components may lead to altered closure against LV pressure (i.e., dysfunction) and, consequently, MR. Structural abnormalities of the mitral valve are referred to as primary mitral valve disease , whereas valve dysfunction due to perturbations in LV geometry is called ischemic MR in ischemic cardiomyopathy and functional MR in dilated cardiomyopathy.
Mitral annulus
The mitral annulus is a discontinuous, fibromuscular, D-shaped ring located in the left atrioventricular groove (between the LV and the left atrium) that serves as an anchor and hinge point for the mitral valve leaflets. The mitral annulus can be subjectively divided into anterior and posterior segments according to the attachments of the anterior and posterior mitral leaflets. It can also be segmented by location into septal and lateral components. The anterior part of the mitral annulus is in continuity with the fibrous skeleton of the heart and is limited by the right and left fibrous trigones and the aortic mitral curtain (i.e., continuity at the level of the left and noncoronary aortic valve cusps). The posterior part of the mitral annulus lacks a fibrous skeleton and is more prone to dilation and calcification.
The resultant changes in annular dimensions lead to a more circular annulus compared with its normal kidney-bean shape, and this compromises the coaptation of the mitral leaflets. The normal mitral annulus also has a three-dimensional saddle shape with two lower points at the level of both trigones and one peak at the midpoint of the anterior leaflet. The peak point is always above the midpoint of the posterior leaflet, allowing bulging during systole to accommodate the aortic root and optimize stress distribution over both leaflets.
The overall circumference of the annulus may decrease by as much as 20% during systole (i.e., less eccentricity), promoting central leaflet coaptation. Reduction in annular size begins with atrial contraction and reaches its maximum halfway through the systolic cycle.
Mitral leaflets and commissures
The mitral valve has two leaflets (anterior and posterior) with similar surface areas and thicknesses (≈1 mm) but significantly different shapes. The anterior leaflet is taller and has a shorter base than the posterior leaflet; it extends vertically and is anchored to one third of the annular circumference between the right and left fibrous trigones. The posterior leaflet is broader based and has a shorter height than the anterior leaflet; it lies transverse to the mitral valve orifice, and together with the commissures, it is fixed to the remaining two thirds of the annulus. The posterior leaflet is closely related to the LV wall base, the point of greatest systolic stress.
The different orientations of the two leaflets ensures a competent closure line of the mitral valve during systole. The closure line is located in the posterior one third of the valve orifice, which naturally prevents systolic anterior motion. Both leaflets have two zones from the base to the free border or margin: the atrial or membranous zone, which is smooth and translucent, and the coaptation zone, which is rough, nodular, and thicker due to the attachment and fusion of chordae tendineae.
As a surgical reference, the leaflets of the mitral valve can be distinguished by location of the clefts or indentations in the posterior leaflet. If both commissures are counted as individual segments, a total of eight segments can be identified. Unlike the anterior leaflet, the posterior leaflet has two clefts in its free margin that allow full opening during LV filling and demarcate three segments or scallops. The middle scallop of the posterior leaflet is designated P2 , and the adjacent medial and lateral scallops are designated P1 and P3, respectively. The corresponding areas of the anterior leaflet are designated by their opposition to the segments in the posterior leaflet as A1, A2, and A3 ( Fig. 19.1 ).
In addition to the anterior and posterior leaflet scallops or segments, the mitral valve has two triangular segments (i.e., commissures) that establish continuity between the two leaflets. These distinct areas of leaflet tissue are supported by chordal fans and are critical to achieving a good surface of coaptation at the junctions of the two leaflets. For their identification, the vertical axis of the papillary muscles and their corresponding chordae tendineae is used as a reference point, thereby obtaining an anterior commissure and a posterior commissure ( Fig. 19.2 ).
Chordae tendineae
The chordate tendineae are filament-like structures of fibrous connective tissue that join the LV surface and free border of the mitral leaflets to the papillary muscles and, by default, to the posterior wall of the LV. They create a suspension system that allows full opening of the leaflets during diastole and prevents excursion of the leaflets above the annular plane during systole.
About 25 primary chordae begin in the papillary muscles and progressively subdivide to insert into the leaflets. Chordae tendineae are classified according to their insertion point between the free border and the base of the mitral leaflets. Primary or marginal chordae attach along the margin (every 3 to 5 mm) of the leaflets and are critical to prevent leaflet prolapse and to align the rough zones of the anterior and posterior leaflets during systole. Secondary or intermediate chordae, which are inserted in the ventricular side of the body of the leaflets, relieve excess tension during systole. Tertiary or basal chordae are found only on the posterior leaflet; they connect its base and the posterior annulus to the papillary muscles, providing additional linkage to the ventricle (see Fig. 19.2 ).
Papillary muscles and the left ventricle
The mitral valve leaflets are attached by the chordae tendineae to the papillary muscles, which are considered an extension of the LV. The papillary muscles vary in number of heads and exact position in the ventricle, but two organized groups usually can be identified. Each papillary muscle is designated according to the relationship to the valve commissures, and each provides a fan chord to its corresponding commissure and to the anterior and posterior leaflets.
The anterior papillary muscle has a single body, is larger, and is perfused by the first obtuse marginal branch of the circumflex artery and the first diagonal branch of the left anterior descending artery (see Fig. 19.1 ). The posterior papillary muscle has two bodies, is smaller, and is supplied blood only by the posterior descending artery, a branch of the right coronary artery, in 90% of cases or by the circumflex artery in the other 10%. This arrangement explains the relative vulnerability of the posterior papillary muscle to ischemia and its subsequent involvement in localized remodeling in the setting of ischemic MR.
The LV supports the entire mitral apparatus due to its continuation with the papillary muscles. LV dimensional changes in the setting of volume overload and remodeling, whether ischemic or not, can lead to leaflet tethering and MR.
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