Surgical Considerations in Mitral and Tricuspid Valve Surgery
Erik A.K. Beyer
Gonzalo Gonzalez-Stawinski
A. Marc Gillinov
PRIMARY MITRAL VALVE DISEASE
The most common cause of mitral regurgitation in North America is degenerative mitral valve disease (1,2,3,4). In recent surgical series, myxomatous degeneration of the mitral valve accounted for more than 50% of the cases (5). Rheumatic heart disease, though rare in industrialized nations, is still a frequent cause of mitral regurgitation and stenosis, requiring surgical correction in developing countries (4). Mitral regurgitation caused by coronary artery disease, termed ischemic mitral regurgitation, is increasingly common. Of patients evaluated for surgery for coronary artery disease, approximately one-third will have some degree of mitral regurgitation (6). Infective endocarditis remains a problem and is the etiology of pure mitral regurgitation in 2% to 8% of patients presenting for surgical correction of mitral regurgitation (7). Severe endocarditic mitral regurgitation is related to ruptured chordae and/or leaflet perforation (8). Other diseases that can affect the mitral valve include idiopathic calcification of the mitral annulus, systemic diseases, such as Marfan’s and Ehlers-Danlos syndromes, and hypertrophic cardiomyopathy.
Preoperative evaluation of mitral valve pathology is performed with transthoracic echo. Doppler echocardiography is the primary tool for assessing mitral valve disease. It identifies the morphologic lesions, the degree of mitral regurgitation/stenosis, and quantifies ventricular function. During mitral valve surgery, transesophageal echocardiography (TEE) is essential. It allows identification of the lesion and mechanisms of mitral valve dysfunction (Tables 27.1 and 27.2). It also determines whether the valve is regurgitant, stenotic, or a combination of both. TEE is valuable in determining the likelihood of repair versus replacement. Intraoperative TEE delineates dynamic abnormalities related to valve opening and closing. It also characterizes leaflet abnormalities and regurgitant jet size and duration. Characteristics of the regurgitant jet help clarify the nature of the mitral valve dysfunction. Usually, leaflet flail directs the regurgitant jet in the opposite direction of the flail segment, whereas restricted leaflets generally cause jets on the ipsilateral side of the pathologic segment. TEE therefore, guides the surgeon’s approach to reestablish effective coaptation in regurgitant valves and to improve opening in stenotic ones (9). Echocardiography is also necessary to assess the other valves and quantify ventricular function. Finally, TEE assesses the results of surgical intervention. Late durability of MV repair in degenerative disease is enhanced by TEE (10). Technical errors at surgery are identified accurately in the operating room, thereby allowing immediate correction.
PROSTHETIC MITRAL DISEASE
Since the first prosthetic heart valve was placed in 1960, millions of valves have been implanted. Although most patients do well following mitral valve replacement, they are subject to a variety of complications (11,12). These complications include prosthetic valve endocarditis (PVE), periprosthetic leak, structural valve degeneration (SVD), valve thrombosis, and thromboembolism. PVE most frequently occurs in the first several months postoperatively, with an early incidence of up to 2% (13). The incidence then decreases to 0.17% to 1% per patient year (14). Periprosthetic leaks occur when the seal between the sewing ring and the host tissue is inadequate. The incidence of periprosthetic leaks ranges between 0.3 and 2.2% per year (15,16). Structural failure related to valve design or material selection is rare with currently available mechanical valves. However, bioprosthetic valves have limited durability due to SVD (17).
TRICUSPID VALVE
Tricuspid regurgitation is most commonly caused by volume overload attributable to chronic left-sided valvular lesions (Table 27.3). Right ventricular and atrial volume overload causes annular dilatation and tricuspid regurgitation. Ten to fifty percent of patients with severe mitral valve dysfunction have significant tricuspid regurgitation (18). Functional tricuspid regurgitation is frequently accompanied by pulmonary hypertension and right ventricular dilatation and dysfunction (19). Organic involvement of the tricuspid valve by rheumatic disease can also result in tricuspid regurgitation. Another major etiology of tricuspid regurgitation is endocarditis. Endocarditis of the tricuspid valve is prevalent in IV drug abusers and patients with chronic indwelling venous catheters. Other less common causes of tricuspid regurgitation include fibrosis secondary to carcinoid disease and degenerative disease.
TABLE 27.1. Mitral Regurgitation Etiology and Pathological Changes | ||||||||||||||
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TABLE 27.2. Mitral Stenosis Etiology and Pathological Changes | ||||||||||||||
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TABLE 27.3. Tricuspid Valve Disease Etiology and Pathological Changes | ||||||||||
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STRUCTURE AND ANATOMY
Mitral Valve
The components of the mitral valve include the annulus, leaflets, chordae, and papillary muscles. A review of the anatomic and functional aspects as they pertain to mitral valve surgery will be presented. The mitral annulus is composed of muscular and fibrous tissue that anchors the base of the mitral valve leaflets (20,21). The annular ring extends between the endocardium of the left atrium and the endocardium of the left ventricle and incorporates within its boundaries the valve tissue itself. In an average adult, the orifice area of the mitral valve at the level of the annulus is approximately 6.5 cm2 for women and 8 cm2 for men (22). Diastolic and systolic annulus sizes differ by 23% to 40% (23). The annulus itself is extremely dynamic and changes in size, shape, and position throughout the cardiac cycle. During diastole, the annulus moves outward with the posterior wall of the left ventricle, allowing the shape of the annulus to become more circular (22).
Leaflets
The mitral valve has two leaflets, the anterior and posterior. The anterior leaflet is triangular and the posterior leaflet is rectangular. The length of the basal attachments of the posterior leaflet is 0.5 cm longer than the basal attachment of the anterior leaflet (22). The posterior leaflet edge has multiple indentations or clefts, which are connected by fanlike cords. The commissures separate the anterior and posterior leaflets. Commissural cusps (leaflets) are also present and can vary in size with the posterior commissural cusp being more prominent. During diastole the combined surface area of the two leaflets is 1.5 to 2 times the surface area of the functional mitral orifice. During systole, the anterior leaflet alone could cover the mitral orifice.
The Chords
The chordae are tendinous, stringlike structures connecting the valvular tissue to the papillary muscles or the myocardium. The chords do not stretch more than 10% under physiologic conditions. They vary in length from approximately 3 to 0.2 cm from the valvular to the ventricular insertion (20). Chords arise as single projections from the ventricle and then divide in succession until attaching to the valve as small chords. The chords insert into the papillary muscle in a semicircular fashion. Chords arising from the lowest portion of the papillary muscle are known as strut chords because they support the central portion of the leaflets. Chords are further divided anatomically into marginal, intermediate, and basal chords based on their attachment to the ventricular surface of the leaflets in a perpendicular plane to the edge of the valve leaflet. Marginal or first-order chordae attach to the edge of the valve leaflet and thereby prevent eversion of the free marginal component of the valve. The intermediate or second-order (“strut”) chordae attach to the midsection/rough zone of the ventricular leaflet and prevent billowing or doming of the cusp. Finally, the basal, or third-order chordae, which represent the largest chords morphologically, insert at the annulus and help maintain ventricular geometry (22).
Papillary Muscles
There are two distinct papillary muscles arising from the free wall of the left ventricle. The anterolateral papillary muscle is single and usually larger than the posteromedial muscle. It is located posterior and to the left on the left ventricle. The posteromedial papillary muscle is U-shaped and located near the septal border of the posterior wall. It can have two or more subheads. The posteromedial papillary muscle usually derives its blood supply from the right coronary artery, whereas the anterolateral papillary muscle has dual blood supply from the left anterior descending and circumflex coronary arteries (24). Therefore the posterior papillary muscle is more susceptible to ischemic insults, which can directly affect valvular competence.
Tricuspid Valve
The tricuspid valve is composed of an annulus, leaflets, chordae, and papillary muscles. The tricuspid valve does not have a well-formed collagenous annulus. The normal annulus circumference is 10 cm in women and 11.2 cm in men (25). The atrioventricular groove folds into the tricuspid valve leaflets. There are three leaflets of the tricuspid valve named based on their anatomic locations: anterior, posterior, and septal. The leaflets are separated at the
commissures and are tethered by chordae tendineae. The anterior leaflet is usually the longest, measuring on average 2.2 cm in length. The posterior leaflet typically has two or three scallops separated by cleft or indentations at its free edge (26). Chordae arise from three papillary muscles and consist of five different types, the fan-shaped, rough zone, basal, free-edge, and deep (26). On average there are 25 chordae to the tricuspid valve.
commissures and are tethered by chordae tendineae. The anterior leaflet is usually the longest, measuring on average 2.2 cm in length. The posterior leaflet typically has two or three scallops separated by cleft or indentations at its free edge (26). Chordae arise from three papillary muscles and consist of five different types, the fan-shaped, rough zone, basal, free-edge, and deep (26). On average there are 25 chordae to the tricuspid valve.
PATHOLOGY
Mitral Valve
Degenerative Myxomatous Disease of the Mitral Valve
Dilatation of the mitral annulus is a major factor in mitral insufficiency caused by degenerative disease. It is the sole cause of mitral insufficiency in 15% of degenerative cases (27). The dilatation is asymmetric, causing the anterior to posterior diameter to become greater than the transverse diameter. Dilatation only affects the posterior two-thirds of the annulus, which corresponds to the area of the posterior leaflet.
The most commonly encountered lesion in degenerative mitral valve disease is posterior chordal rupture (5). Prolapse of the posterior leaflet because of elongated or ruptured chords is the cause of mitral regurgitation in the majority of cases (4). Of degenerative mitral valves operated on in one surgical series, 41% had ruptured posterior chords, 30% had elongated chords and 10% had ruptured anterior chords (27). Other features of myxomatous mitral valves found on echocardiogram include billowing and redundant leaflets. The leaflet tissue is thinned and increased in size. In 16% of patients annular and leaflet calcification is seen in myxomatous disease of the mitral valve. Prolapse of the mitral valve leaflets is generally present in myxomatous mitral valve disease. Intraoperative TEE determines the site of leaflet involvement and therefore dictates techniques of repair.
Left ventricular outflow tract obstruction (LVOTO) caused by abnormal systolic anterior motion (SAM) of the anterior leaflet of the mitral valve occurs in 4%-10% of patients having mitral valve repair for myxomatous disease (28). Intraoperative transesophageal echocardiography is essential in diagnosing this complication following repair. TEE can also help determine valvular pathology that would lend to the potential for SAM and thereby guide surgical decision making. Excess valvular tissue is associated with a higher risk of LVOTO. A posterior leaflet with a significant redundant central portion pushes the anterior leaflet against the septum after correction of the mitral regurgitation (3). Therefore, a sliding leaflet repair is applied to floppy valves with large posterior leaflets in order to restore a more normal ratio of the anterior to posterior leaflet surface area. The incidence of SAM has been reduced in several recent surgical series to as low as 0%-2% (28).
Rheumatic Disease of the Mitral Valve
Rheumatic mitral valve disease remains a surgical challenge because of the progressive nature of its pathology and the young patient population affected. It is not repaired as frequently as myxomatous disease due to the very nature of the disease. Rheumatic mitral valve disease can result in stenosis, regurgitation, or a combination of the two.
The cardinal anatomic changes of mitral valve stenosis are leaflet thickening and fibrosis, commissural fusion, and chordal fusion and shortening (29). Chordae tendineae can become shortened to the point that they appear to insert directly into the papillary muscle. As the disease progresses a stenosed, slitlike orifice, termed “fishmouth” is produced. Surgical candidates for valve repair or replacement have valve areas less than 1.4 cm2.
Isolated mitral valve regurgitation secondary to rheumatic valvular disease is the result of leaflet shortening caused by scarring. Often the posterior leaflet is affected when the clefts are obliterated and the scallops become fused. In long-standing regurgitation the leaflet free margin becomes thickened and folded in the direction of regurgitant flow. However, rheumatic mitral regurgitation is more often associated with valve stenosis caused by commissural fusion. Leaflet and annular calcification are also seen in long- standing rheumatic heart disease. This is readily seen on TEE as echodense areas. Also, annular dilatation in rheumatic disease is asymmetric and is often greatest toward the posteriormedial commissure (30).
Intraoperative TEE helps establish repairability or the need for valve replacement in rheumatic heart disease. Some centers report a 65% repair rate for rheumatic mitral disease (31). For mitral stenosis, commissurotomy and valve debridement are often used. Generally it is unnecessary to place an annuloplasty ring following a commissurotomy. However, when a central leak is observed and when the annulus is dilated, as shown by a circular rather than an oval shape, an annuloplasty ring should be considered. The ability to repair a stenotic rheumatic mitral valve rests on the thickness of the valve leaflets and the presence of chordae tendineae. Patients with anterior leaflet and chordal pliability should be considered for repair (32). A regurgitant rheumatic mitral valve should likewise be considered for repair if there is annular dilatation and the leaflets are thickened but mobile and the chords are thickened and elongated. Severe commissural fusion and subvalvular fibrosis are a contraindication to repair (32).
Ischemic Disease of the Mitral Valve
Ischemic mitral valve disease represents approximately 11%-27% of patients undergoing surgery for mitral valve disease. Compared to other etiologies of mitral valve disease, surgery for ischemic mitral valve disease is associated with higher mortality rates, ranging between 10% and 48% (33). This is clearly related to the underlying cause of mitral regurgitation—coronary artery disease.
Ischemic mitral valve disease lacks a widely accepted classification scheme. This makes comparing studies difficult. For our purposes, ischemic mitral valve disease will be divided into the three categories based on the mechanisms causing regurgitation. These categories include functional, infarcted but unruptured papillary muscle, and ruptured papillary muscle (34).
The most common cause of regurgitation in ischemic disease is functional. In a recent review by Gillinov, 76% of patients undergoing surgery for ischemic mitral regurgitation had functional impairment. In these patients the leaflets and subvalvular apparatus appear morphologically normal at echo and upon direct inspection. The cause of regurgitation is failure of leaflet coaptation during ventricular systole. This produces a regurgitant jet on echo that is usually central but can be eccentric or complex (34).
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