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Revista Española de Cardiología (English Edition) Revista Española de Cardiología (English Edition)
Rev Esp Cardiol. 2011;64:1169-81 - Vol. 64 Num.12 DOI: 10.1016/j.rec.2011.06.023

Surgical Echocardiography of the Mitral Valve

Javier G. Castillo a,, Jorge Solís b, Ángel González-Pinto c, David H. Adams a

a Department of Cardiothoracic Surgery, The Mount Sinai Medical Center, New York, United States
b Departamento de Cardiología, Hospital General Universitario Gregorio Marañón, Madrid, Spain
c Departamento de Cirugía Cardiaca, Hospital General Universitario Gregorio Marañón, Madrid, Spain

Keywords

Mitral valve. Valvulopathy. Echocardiograhy. Surgery.

Abstract

In the western world, the prevalence of mitral regurgitation—particularly that due to degenerative disease—has gradually increased despite a substantial decrease in rheumatic disease. If present, secondary ventricular dysfunction, potentially irreversible when clinically diagnosed, requires close echocardiographic follow-up in order to establish a subclinical diagnosis. Thus, echocardiography has become an essential tool in managing patients with mitral valve regurgitation. As well as assessing parameters of ventricular geometry, in the hands of an expert echocardiography offers systematic documentation of lesion in each segment, which together with the dysfunction type should give an accurate idea of the complexity involved in the valve repair. This is increasingly relevant given the growing number of asymptomatic patients referred for mitral valve surgery. Consequently, the echocardiographic study performed prior to referral is crucial to successful mitral valve repair and cardiologists, cardiac imaging experts, and surgeons should be guided by results when referring patients to specialists with the skills necessary to undertake adequate repair of the lesions found.

Article

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INTRODUCTION

The prevalence of mitral regurgitation (MR) in the western world is on the increase1 despite the substantial reduction in rheumatic disease.2 Chronic organic MR (particularly when degenerative in origin) is the most common valvular disease: moderate or severe MR is found in 1.7% of the general population, 6.4% of patients aged 65-74 years, and 9.3% of those >75 years.3.

In the field of mitral valve repair surgery, Alain Carpentier radically changed the prognosis and clinical management of patients with MR.4 Since then, 2-dimensional, Doppler, and 3-dimensional echocardiography have gained much importance because they reveal the functional anatomy of the mitral valve (MV) and its dynamic structure. Today, an exhaustive echocardiographic study should always be the starting point when planning treatment of patients with MR. Echocardiography should provide precise data on the type and extent of valve lesions, the regurgitation mechanism, and its etiology, severity, and finally—the main objective of the present study–probability of repair.5.

SURGICAL ANATOMY OF THE MITRAL VALVE

The human MV is a complex 3-dimensional mechanism made of independent elements that constitute an anatomically dynamic structure.6 Functionally, it entails perfectly coordinated interaction between the valves or leaflets, mitral annulus, subvalvular apparatus (chordae tendineae and papillary muscles), and the left ventricle.

The Leaflets and Commissures

The MV has 2 leaflets, labeled anterior and posterior. They have similar surfaces and thickness (∼1mm), are separated by their respective commissures, and are anchored at the base to fibromuscular tissue of the annulus and at the free borders to the subvalvular apparatus by means of the chordae tendineae. Achieving an optimal coaptation line requires perfect adaptation between the free surfaces of the leaflets and the native MV orifice. The anterior leaflet is trapezoidal in shape, extends vertically, and is anchored to one third of the annular circumference. Thanks to its intimate relation with the aortomitral curtain, it is a continuation of the left ventricular outflow tract. The posterior leaflet is transversal to the MV orifice and, together with the commissures, is fixed to two thirds of the annular circumference. The posterior leaflet is closely related to the left ventricle wall base, the point of greatest systolic stress. Moreover, MVs have 2 clearly distinguished zones between the base and the free border: the atrial or membranous zone (smooth and translucent) and the coaptation zone (rough, nodular, and much thicker due to the fusion of numerous chordae tendineae). In histopathologic terms, we can discern 3 separate layers: the fibrous layer (a continuation of the chordae tendineae), the spongiosa (organized collagen fibers, proteoglycans, elastin, and other connective cells) and the fibroelastic layer, covering most of the leaflet surface (elastin and collagen). Moreover, as a surgical reference, the MV can be subdivided into 8 segments if the commissures are counted individually (Figure 1).7 Unlike the anterior leaflet, the posterior leaflet has 2 clefts in its free border that permit it to open fully during diastole or ventricular filling and which, in turn, separate the 3 segments. Of these, the middle one has much more redundancy and its thickness varies with the impact of greater systolic pressure, which would explain why it is more prone to prolapse and lesions.8, 9.

A, drawing of Carpentier's classification (adapted from Carpentier et al.<cross-ref><sup>7</sup></cross-ref> by permission of the author). B, surgical view of the mitral valve with signs of degenerative disease, seen from the left atrium. C, three-dimensional reconstruction of the saddle-shaped mitral annulus; the highest point corresponds to the anterior portion and the lowest to the trigones. D, three-dimensional reconstruction of mitral leaflets together with mitral annulus, showing anterior leaflet prolapse. AC, anterior commissure; AL, anterior leaflet; PC, posterior commissure; PL, posterior leaflet.

Figure 1. A, drawing of Carpentier's classification (adapted from Carpentier et al. 7 by permission of the author). B, surgical view of the mitral valve with signs of degenerative disease, seen from the left atrium. C, three-dimensional reconstruction of the saddle-shaped mitral annulus; the highest point corresponds to the anterior portion and the lowest to the trigones. D, three-dimensional reconstruction of mitral leaflets together with mitral annulus, showing anterior leaflet prolapse. AC, anterior commissure; AL, anterior leaflet; PC, posterior commissure; PL, posterior leaflet.

The commissures are triangular segments that establish continuity between the 2 leaflets. To identify them, we use the vertical axis of the papillary muscles and their corresponding chordae tendineae as a reference and thus obtain an anterior and posterior commissure.

The Mitral Annulus

The anatomic link between the left atrium and the left ventricle resembles a hinge of fibrous tissue and it is here that MV motion begins. This structure, labeled the mitral annulus, is an integral part of the fibrous skeleton of the human heart. The part of the annular zone where the posterior leaflet is inserted is 2mm from the fibrous tissue hinge and consists of a very thin band of connective tissue. As this segment of the annulus is not connected to any rigid structure, annular dilatation and calcification occur here in a great many patients.10 In contrast, the zone where the anterior leaflet is inserted is practically a continuation of the aortomitral curtain reinforced at the base by 2 rigid structures. These are both fibrous trigones: the right fibrous trigone (joining the membranous septum, mitral annulus, tricuspid annulus, and noncoronary cusp of the aortic annulus) and the left fibrous trigone, contiguous to the left coronary cusps of the aortic annulus and the left border of the mitral annulus. The normal mitral annulus is more or less elliptical (D-shaped) and shows greater eccentricity (is less circular) in systole than in diastole.11 Moreover, it presents a 3-dimensional saddle-shaped configuration with 2 lower points (trigones) and 1 peak at the midpoint of the anterior leaflet (Figure 1). This is always above the midpoint of the posterior leaflet. Annular area is 5cm2 to 11cm2 (mean, 7cm2) and is modified during the cardiac cycle. It increases in size at end-systole, continues to do so during isovolumic relaxation and reaches its maximum at end-diastole.12 Reduction in annular size begins with atrial contraction and reaches its maximum halfway through the systolic cycle, leading to optimal coaptation of both leaflets. It is worth noting that the changes in the annular surface occur practically at the will of the posterior annulus, as the anterior part of the annulus is virtually immobile. Finally, the mitral annulus also presents an oscillating or vertical movement towards the left atrium during diastole and towards the ventricular apex during systole. Normal annular contraction is estimated at 25%.13.

The Chordae Tendineae

The chordae tendineae are filament-like structures of connective fibrous tissue that join the ventricular surface and free border of the leaflets to the papillary muscles and, by default, the left ventricle posterior wall. Approximately 25 primary chordae begin in the papillary muscles and progressively subdivide to insert themselves into the leaflets. They are classified according to the point of insertion between the free border and the leaflet base. Marginal chordae are inserted in the free border of the leaflets and their function is to avoid leaflet prolapse. The intermediate or second-order chordae are inserted in the ventricular face of the leaflets and their principal function is to relieve excess tension in valve tissue. Basal or third order chordae are only found on the posterior leaflet and connect its base and the posterior mitral annulus to the papillary muscles (Figure 2).

Drawing of mitral subvalvular apparatus (left panel adapted from Carpentier et al.<cross-ref><sup>7</sup></cross-ref> by permission of the author). LCS, left coronary sinus; NCS, noncoronary sinus; RCS, right coronary sinus.

Figure 2. Drawing of mitral subvalvular apparatus (left panel adapted from Carpentier et al. 7 by permission of the author). LCS, left coronary sinus; NCS, noncoronary sinus; RCS, right coronary sinus.

Papillary Muscles

Two organized groups of papillary muscles exist. They are labeled with reference to their position in relation to the mitral commissures. The anterolateral papillary muscle has a single body, is larger, and is irrigated by the first obtuse marginal branch of the circumflex artery and the first diagonal branch of the anterior descending artery. The posteromedial papillary muscle has 2 bodies, is smaller in size, and is irrigated only by the posterior descending artery, a branch of the right descending coronary artery, in 90% of cases and by the circumflex artery in the other 10%.14 Hence, the posteromedial muscle is always much more vulnerable to ischemic episodes.

The Left Ventricle

The continuum from the papillary muscles to the left ventricle gives the latter a dominant role in mitral leaflet motion control, particularly in patients with ischemic disease. According to Starling's law, myocyte contractility would compensate for excess volume in the presence of MR, especially in its early stages.15 However, given that the left ventricle actively sustains all the mitral apparatus, any amount of pathologic dilatation—whether ischemic in origin or not—would lead to functional MR.16.

THE PATHOPHYSIOLOGIC TRIAD

MR is characterized by the existence of blood flow in systole from the left ventricle to the left atrium.17 Any minimal lesion can cause MR by reducing or eliminating mitral leaflet coaptation during systole. Hence, the study (localization and magnitude) and subsequent precise description of mitral lesions are essential to determine the chances of successful valve repair and proceed with an appropriate therapeutic plan, tailored to each individual patient.18 Carpentier established the “pathophysiologic triad” of MR to manage this particular group of patients in an ordered, systematic way.19 The triad highlights the importance of distinguishing between the condition causing MR (etiology), the resulting lesions, and finally how these lesions affect leaflet motion–ie, the type of dysfunction caused. With the passage of time, cardiovascular specialists have adopted this triad classification and today, although not yet in general use, it promotes clear mutual understanding between surgeons and cardiac imaging specialists.

Valve Dysfunction

It is vitally important that we identify the etiology and lesions that lead to clinical MR because choice of therapy and long-term results can differ substantially as a function of clinical context. It is also crucial to describe the valve dysfunction secondary to these lesions or the mechanism underlying MR, particularly when trying to establish the chances of successful repair. The classification of mitral dysfunction is based on the position of the leaflet margins with respect to the mitral annulus plane: a) type I dysfunction, normal leaflet motion with severe annular dilatation (central regurgitant jet) or perforation of one of the leaflets; b) type II dysfunction, excessive leaflet motion generally secondary to pathologic elongation or rupture of the chordae tendineae (in which case regurgitant jet is directed to the opposite side of the affected leaflet), and c) type III dysfunction, restricted leaflet motion due to retraction of the subvalvular apparatus (IIIa, frequent in rheumatic disease or inflammatory processes) or papillary muscle displacement (ischemic remodeling or dilated cardiomyopathy) causing apical displacement (tethering) of the valve (IIIb). Regurgitant jet is directed at the same side as the valve affected.

Etiologies and Lesions

Worldwide, rheumatic diseases are still the most frequent cause of MR but they have ceased to be its most common cause in the developed countries. Ischemic disease, currently responsible for 20% of MR, could soon lose importance thanks to the ever more aggressive treatment of coronary disease. However, degenerative disease is today the most frequent cause of MR.20.

Degenerative disease of the MV presents a spectrum of lesions21 from chordal rupture with prolapse of a single segment of an otherwise totally normal valve to multiple segment prolapse in both valves, accompanied by excess tissue and marked annular dilatation.22, 23 Moreover, the range of degenerative disease lesions gives rise to the distinction between 2 opposing clinical entities: fibroelastic deficiency (FD) and Barlow's disease (BD). All the etiologies and lesions implied in MR development are shown in Figure 3.

Pathophysiologic triad of mitral regurgitation. *Finding leaflet prolapse in the context of rheumatic disease only occurs if a type III dysfunction exists or pseudo-prolapse is identified.

Figure 3. Pathophysiologic triad of mitral regurgitation. *Finding leaflet prolapse in the context of rheumatic disease only occurs if a type III dysfunction exists or pseudo-prolapse is identified.

FD generally occurs in patients aged >60 years with a relatively short history of valvular disease and severe holosystolic MR.24 The term “fibroelastic” describes a pathologic condition associated with a deficit of the protein fibrillin25 that often leads to progressive weakening26 and elongation and rupture of the chordae tendineae,27 usually involving the posterior leaflet mid-segment.28 Chordal rupture is the most frequent lesion in FD.29 The leaflets are thin and translucent, although occasionally the prolapsing segment may present myxomatous characteristics and distension if disease has been present for a long time.30 The key to distinguishing FD from other entities is exhaustive analysis of segments contiguous to the one that has prolapsed.31 In this condition, the segments are usually totally normal, with no change in height, size, or tissue properties.32 Finally, annulus size,33 defined by anterior valve surface, is generally <32mm (Figure 4).

Spectrum of degenerative disease of the mitral valve. FD, fibroelastic deficiency; MR, mitral regurgitation.

Figure 4. Spectrum of degenerative disease of the mitral valve. FD, fibroelastic deficiency; MR, mitral regurgitation.

At the opposite end of the spectrum of degenerative diseases we find BD,34 primarily found in young patients, generally aged <60 years, when referred for surgery. These patients present a long history of cardiologic follow-up35, 36 for cardiac murmurs.37 In this context, the leaflets present much more diffuse, complex lesions. We often find prolapse and myxomatous degeneration38, 39 of many segments in one or both leaflets (Figure 4, Figure 5). The most common lesions are excess tissue and therefore leaflet thickening and distension, as well as elongation, thickening, and/or the rupture of many chordae tendineae.40 In these patients, annulus size is ≥36mm.41 Finally, it is not infrequent to find several degrees of calcification both in the annulus and subvalvular apparatus, in particular on the posterior face of the annulus and the anteromedial papillary muscle.42.

Surgical images of the lesions most frequently associated with degenerative disease of the mitral valve. A, posterior prolapse due to chordae tendineae rupture. B, anterior prolapse due to elongation, thinning and rupture of chordae tendineae. C, anterior and posterior prolapse secondary to elongation of the chordae tendineae and myxomatous degeneration of several segments; note the pathologic clefts in the posterior leaflet. D, Barlow's disease with myxomatous degeneration of both leaflets.

Figure 5. Surgical images of the lesions most frequently associated with degenerative disease of the mitral valve. A, posterior prolapse due to chordae tendineae rupture. B, anterior prolapse due to elongation, thinning and rupture of chordae tendineae. C, anterior and posterior prolapse secondary to elongation of the chordae tendineae and myxomatous degeneration of several segments; note the pathologic clefts in the posterior leaflet. D, Barlow's disease with myxomatous degeneration of both leaflets.

Ischemic MR can present acutely with papillary muscle rupture43 (organic ischemic MR) or as a consequence of left ventricular remodeling and apical and inferior displacement of the papillary muscles44 (functional ischemic MR), which pull the mitral leaflets and cause tethering of the leaflets and of their point of coaptation45 (Figure 6). Identifying this type of lesion in the echocardiographic study is of the greatest importance given that long-term survival following ischemic MR, even with mild ischemic lesions, is notably limited.46 When restricted leaflet movement occurs principally in systole,47 it gives rise to an asymmetric restrictive pattern, mainly observed in patients with posterior infarction and posterior leaflet restriction.48 In contrast, in patients with dilated cardiomyopathy or anterior and posterior infarctions, both leaflets present a restrictive deficit giving rise to a symmetric pattern49 (Figure 7).

Mechanism of functional mitral regurgitation. A, normal mitral valve. B, ischemic mitral valve with pronounced posterior restriction in P3 after an episode of ventricular ischemia. LV, left ventricle.

Figure 6. Mechanism of functional mitral regurgitation. A, normal mitral valve. B, ischemic mitral valve with pronounced posterior restriction in P3 after an episode of ventricular ischemia. LV, left ventricle.

Echocardiographic evaluation and surgical images of ischemic mitral regurgitation (A-C, symmetrical pattern; D-F, asymmetrical pattern). A, central regurgitant jet. B, symmetric restriction. C, note the symmetrical line of coaptation following repair. D, posterior regurgitant jet. E, asymmetric restriction. F, note the angle of the line of coaptation following annular repair.

Figure 7. Echocardiographic evaluation and surgical images of ischemic mitral regurgitation (A-C, symmetrical pattern; D-F, asymmetrical pattern). A, central regurgitant jet. B, symmetric restriction. C, note the symmetrical line of coaptation following repair. D, posterior regurgitant jet. E, asymmetric restriction. F, note the angle of the line of coaptation following annular repair.

ECHOCARDIOGRAPHIC EVALUATION

When conducted by an expert, systematic examination of the MV using transthoracic echocardiography (TTE) should reliably predict repair.50 However, more and more centers now opt for transesophageal echocardiography (TEE), particularly in complex cases, prior to referring patients for surgical evaluation.51 An echocardiographic representation of the MV should provide information that is both general52 (previous illness, posterior or bilateral) and specific to leaflet segments (individual analysis of each segment); it should identify an excess or scarcity of tissue in the leaflets (etiologic differentiation),53 evaluate annular dimensions, detail subvalvular apparatus status, and estimate ventricular resistance.54 To do so, the systematic examination should include 4 transesophageal projections (4-chamber, commissure, 2-chamber and long-axis), as well as a gastric projection (short-axis) (Figure 8).

Echocardiographic distinction between fibroelastic deficiency (A-C) and Barlow's disease (D-F). A-C, note the presence of fine nonmyxomatous leaflets, only one affected segment and prolapse generally due to chordae tendineae rupture. C-E, thickened leaflets with marked myxomatous degeneration of several segments or both leaflets affected and atrial displacement of the posterior leaflet fibrous tissue hinge.

Figure 8. Echocardiographic distinction between fibroelastic deficiency (A-C) and Barlow's disease (D-F). A-C, note the presence of fine nonmyxomatous leaflets, only one affected segment and prolapse generally due to chordae tendineae rupture. C-E, thickened leaflets with marked myxomatous degeneration of several segments or both leaflets affected and atrial displacement of the posterior leaflet fibrous tissue hinge.

Four-Chamber View

If we use TTE, the classic apical 4-chamber view will enable us to analyze the anterior leaflet, especially A2 and A3, as well as the lateral segment of the P1 posterior leaflet. In contrast, TEE enables us to observe practically all segments as a function of the degree of rotation of the transducer. At 0°, the transducer shows both leaflets’ mid-segments (A2 and P2). If the probe rotates 20°, it cuts the line of coaptation obliquely and obtains detailed information for the most lateral segments, such as A2, A1, and P1.

View of Both Commissures

This can be obtained with an apical 2-chamber plane in TTE or by rotating the transesophageal probe approximately 60° so that the image plane cuts perpendicularly through that which delimits both commissures, thus cutting through both valves to facilitate analysis of P3 (to the left of the image), A2 (in the center of the image), and P1 (to the right of the image). In this plane, the papillary muscles can normally be seen. Moreover, this view is of great value in determining which segment is pathologic because if the regurgitant jet begins to the left of the line of coaptation, we deduce it is secondary to a lesion in P3 or A3; if the regurgitant jet starts to the right of the line of coaptation, the segments involved will be P1 or A1. The height of P1 and P3 can be calculated from this plane, which is highly important when predicting repair complexity. If these segments are >1.5cm in height, we can assume anterior systolic movement is more likely following repair; consequently, under these circumstances, the repair will be more complex as it requires partial resectioning of the leaflets.55.

Two-Chamber View

If we continue rotating the transducer to 90°, we obtain a 2-chamber view. In this plane, P3 can be seen to the left of the image and all the anterior leaflet segments are located to the right. This view is crucial to analysis of the anterior leaflet and complete evaluation of the posteromedial part of the line of coaptation (A3 and P3), as well as its corresponding commissure.

Parasternal or Sagittal Long-Axis View

The long axis of the parasternal plane, using TTE, or the sagittal view with the probe rotated to 120°, using TEE, will cut the line of coaptation perpendicularly, through P2 (to the left of the image) and A2 (to the right of the image). This view is especially important as prolapse of P2 is the most frequent, particularly in patients with degenerative disease. Moreover, this view enables us to evaluate the annular surface, extrapolating annular diameter from the anterior leaflet surface. Pathologic annular dilatation is considered present when the annulus:anterior leaflet ratio is >1.3 or annular diameter is >35mm. Moreover, the surgeon should know of any substantial calcification in the annulus or subvalvular apparatus, as surgical strategy changes radically when facing calcified segments or extremely rigid tissue.

Parasternal Short-Axis or Transgastric View

This view, although requiring an experienced operator, can be obtained by TTE (classic parasternal view) or TEE (0° transgastric view). In diastole, it enables us to evaluate all segments and both commissures. In systole, we can deduce the localization of the pathologic segment by analyzing regurgitant jet. Moreover, we can obtain information about the subvalvular apparatus and the distance between the head of the papillary muscle and mitral annulus.

THREE-DIMENSIONAL ECHOCARDIOGRAPHY

The latest technological advances in 3-dimensional echocardiography have enabled us to obtain real-time images of the MV and much greater detail, which significantly adds to our knowledge of MV anatomy and functioning.56 This is particularly the case in geometric evaluation of the mitral annulus.57 It has been shown that the mitral annulus is saddle-shaped.58 The highest points, ie, those furthest from the cardiac apex, correspond to the anterior region closest to the aortic root and the posterior region closest to the left ventricle posterior wall.59 In contrast, the lowest points correspond to the mitral commissures. In healthy individuals, the saddle shape is more marked in mid-systole, when annular area is at its minimum. At the end of both phases, the annulus presents a much flatter, more extended shape.60 These variables gain greater clinical interest when we analyze the anatomy of patients with functional MR. In this context, we can observe marked dilatation of the intercommissural diameter and anteroposterior diameter, because of which the annulus takes on a flattened, circular shape.61 If the infarction is anterior, the annulus becomes flatter than if it is inferior.

Three-dimensional echocardiographic analysis of the mitral leaflets (together with the annulus) provides the surgeon with the most important data. Currently, we can trace the exact location of the mitral leaflets and measure their area using special computer software. Due to the saddle shape of the annulus, 2-dimensional echocardiography can overestimate the existence of prolapse due to apparent leaflet displacement towards the left atrium. During 3-dimensional reconstruction, the prolapsing segment becomes convex when viewed from the atrium, and concave when viewed from the ventricle. Moreover, this correlates exactly with the anatomic examination the surgeon conducts during the intervention (superior orientation of the anterior leaflet and inferior orientation of the posterior leaflet), with >96% localization of the prolapse.62 Three-dimensional echocardiography can also locate all the points of surgical interest: a) annular area and possible size of the mitral ring that will be implanted; b) leaflet surface; c) prolapsed segment and volume of prolapse; d) tenting volume (volume between the annulus and the mitral leaflets); e) tethering distance (between any point on the mitral annulus and the papillary muscles), and f) interpapillary distance63 (Figure 9).

Correlation of conventional preoperative echocardiography and 3-dimensional echocardiography with intraoperative images. A, anterior; AL, anterolateral; Ao, aorta; P, posterior; PM, posteromedial.

Figure 9. Correlation of conventional preoperative echocardiography and 3-dimensional echocardiography with intraoperative images. A, anterior; AL, anterolateral; Ao, aorta; P, posterior; PM, posteromedial.

MITRAL SURGERY

The echocardiographic study prior to patient referral is decisive in achieving effective mitral valve repair and should inform patients, cardiologists, and surgeons preparing the optimal route-map for each patient with MR.64, 65 In this context, it is increasingly important to evaluate mitral valve disease exhaustively to refer each patient to the surgeon with the skills necessary to repair each of the observed lesions.66 The systematic documentation of the disease found in each segment, together with leaflet dysfunction type, should provide a precise idea of the complexity of repairing the valve in question.67.

Several echocardiographic parameters are identified in the literature as possible predictors of failure in MV repair68 (Table 1). They include severe central regurgitation jet, major annular dilatation (≥50mm), 3 or more affected segments, anterior leaflet lesions, or intense calcification, among others.69 Moreover, the scarcity of leaflet tissue is also an important risk factor both in rheumatic disease and in patients with infective endocarditis or degenerative disease with advanced FD.70 In ischemic disease, TEE findings of ≥37mm diastolic annular diameter, ≥1.6cm2 tenting area, and severe MR can lead to mitral valve repair failure in 50% of patients during clinical follow-up.71 In contrast, with transthoracic transducer echocardiography,72 >1cm coaptation distance, >2.5cm2 systolic tenting area, >45° posterior leaflet angle (posterior leaflet restriction), central regurgitation jet (indicating substantial restriction of both leaflets), central or posteromedial regurgitant jet, and significant ventricular hypertrophy (ventricular remodeling following repair) increase the risk of repair failure.73.

Table 1. Echocardiographic Predictors of Failed Mitral Valve Repair.

Organic MR Functional MR
Severe central jet Coaptation distance ≥1 cm
Annular dilatation ≥50 mm Tenting area >2.5cm2
Lesions in 3 or more segments Posterolateral angle >45°
Lesions of the anterior leaflet Interpapillary distance >20 mm
Severe calcification Ventricular akinesia
Scarcity of tissue in the leaflets EDD >65mm or ESD >51 mm
Opposite dysfunction Sphericity index >0.7

EDD, end-diastolic diameter; ESD, end-systolic diameter; MR, mitral regurgitation.

Surgical Referral

The decision to operate in a patient with MR is the result of a complex process entailing the evaluation of many variables,74, 75 including MR severity, its impact on atrial and ventricular remodeling, ventricular function, pulmonary pressures, the chances of successful repair, comorbidities, operative risk, and the state of the patient's symptoms.76, 77 If we analyze each parameter individually, it would be no exaggeration to say that any variation in current treatment of severe MR depends entirely on the echocardiographic study. In fact, increasingly less importance is given to the patient's symptoms and correspondingly more importance to ventricular geometry data.78 In this respect, opinions differ as to the right time for surgery.79 The first, more traditional, widely agreed view recommends careful follow-up (echocardiography every 6 or 12 months) until the appearance of symptoms or clear indicators of ventricular dysfunction such as left ventricular ejection fraction <60% or end-systolic diameter >40mm (>45mm in European guidelines).80, 81, 82 Moreover, when ventricular function is normal, surgery is recommended in the presence of pulmonary hypertension (>50mmHg) or atrial fibrillation.83 In contrast, the second view,84 which is much more up-to-date and recommends surgical intervention in asymptomatic patients with conserved systolic function, is much more controversial.85 Thus, surgery would always be recommended in asymptomatic patients if we have echocardiographic data that confirm the severity of MR,86 analysis indicates >95% chances of repair, and operative mortality is <1%.87 These requirements presuppose the closest possible collaboration between a cardiologist experienced in echocardiographic quantification, a surgeon who performs around 50 mitral valve repair interventions a year,88 and an experienced intensive care unit89 (Table 2). Although a range of opinions and approaches to management is important, we believe the individualized treatment of each patient should not exclude any alternatives if these are appropriately employed (Figure 10). Moreover, individualized treatment should mean choosing the appropriate surgical technique90, 91, 92, 93 for each of the lesions found.

Table 2. Echocardiographic Pattern of Referral for Surgery to Optimize the Probability of Mitral Valve Repair (Approximate Stratification by Number of Cases per Year Performed by a Single Surgeon).

Etiology Dysfunction Calcification Lesions Probability of repair
        <50 cases/year ≥50 cases/year
Fibroelastic II No/annular Posterior localized prolapse (P2) Feasible Feasible
  II No/annular Anterior prolapse Probable Feasible
Barlow II No/annular Posterior localized prolapse (P2) Feasible Feasible
  II No/annular Prolapse of 3 or more segments Probable Feasible
  II Leaflets Prolapse of 3 or more segments Improbable Probable
  II No/annular Anterior prolapse Improbable Probable
Endocarditis I No Perforation Probable Feasible
  II No Prolapse Probable Feasible
  II No Destructive lesions Improbable Probable
Rheumatic IIIA Annular Malleable anterior leaflet Probable Feasible
  IIIA Leaflets (Rigid) calcified anterior leaflet Improbable Improbable
(Functional) ischemic I No Dilatation or annular deformation Feasible Feasible
  IIIB No Tethering Feasible Feasible
  IIIB No Predictors of repair failure Improbable Probable

Proposed algorithm for treatment of mitral regurgitation. EF, ejection fraction; ERO, effective regurgitant orifice; ESD, end-systolic diameter; M, moderate; NYHA, New York Heart Association; RVol, regurgitant volume; S, severe.

Figure 10. Proposed algorithm for treatment of mitral regurgitation. EF, ejection fraction; ERO, effective regurgitant orifice; ESD, end-systolic diameter; M, moderate; NYHA, New York Heart Association; RVol, regurgitant volume; S, severe.

When dealing with patients with ischemic MR, the risk of papillary muscle or even ventricular muscle rupture is high and surgery should be immediate. However, surgical risk is greater and although symptoms may improve following restrictive annuloplasty,94 the long-term benefit to survival has not been proven. Moreover, implantation of a restrictive ring (2 sizes smaller than measured) can cause postoperative mitral valve stenosis and not correct the underlying problem of papillary muscle displacement.95 Hence surgical studies are being conducted into posterior leaflet extension in P3 with pericardial tissue, to relieve tension on the leaflets without the need for restrictive annuloplasty. Current trends suggest that in mild or moderate ischemic MR (effective regurgitation orifice [ERO] <0.2cm2), we should consider surgical correction using annuloplasty but if ERO is >0.2cm2 (severe ischemic MR), valve replacement and myocardial revascularization can be equally feasible alternatives to mitral valve repair.

CONCLUSIONS

Without doubt, imaging studies are becoming increasingly important in the management of patients with MR, particularly given the trend for early interventions in patients with severe asymptomatic MR. Precise follow-up of changes in geometry and volume is possible and this facilitates establishing surgical indications for patients with a tendency towards ventricular dysfunction before ejection fraction declines. Three-dimensional echocardiography gives a perfect “surgeon's-eye view” of the MV, enabling preoperative identification of complex lesions that require referral to a specialized center. The incessant training of future generations of specialists is clearly crucial in avoiding unnecessary replacements. Multidisciplinary evaluation of the patient with MR should become standard practice when choosing the appropriate therapeutic strategy.

FUNDING

This project was financed by The Mount Sinai Medical Center, New York, United States.

CONFLICTS OF INTEREST

None declared.

Corresponding author: The Mount Sinai Medical Center, 1190 Fifth Avenue GP2W, New York, NY 10029, United States. javier.castillo@mountsinai.org

Bibliography

1. Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez-Sarano M. Burden of valvular heart diseases: a population-based study. Lancet. 2006;368:1005-11.
Medline
2. Essop MR, Nkomo VT. Rheumatic and nonrheumatic valvular heart disease: epidemiology, management, and prevention in Africa. Circulation. 2005;112:3584-91.
Medline
3. Iung B, Vahanian A. Epidemiology of valvular heart disease in the adult. Nat Rev Cardiol. 2011;8:162-72.
Medline
4. Carpentier A. Cardiac valve surgery—the “French correction”J Thorac Cardiovasc Surg. 1983;86:323-37.
Medline
5. Adams DH, Anyanwu AC, Sugeng L, Lang RM. Degenerative mitral valve regurgitation: surgical echocardiography. Curr Cardiol Rep. 2008;10:226-32.
Medline
6. Perloff JK, Roberts WC. The mitral apparatus. Functional anatomy of mitral regurgitation. Circulation. 1972;46:227-39.
Medline
7. Carpentier A, Adams DH, Filsoufi F. Carpentier's reconstructive valve surgery. Maryland Heights: Saunders-Elsevier;2010.
8. Okamoto H, Itoh Y, Nara Y. Geometric analysis of the anterior mitral leaflet and mitral valve orifice in cadaveric hearts. Circ J. 2007;71:1794-9.
Medline
9. Pomerance A. Ballooning deformity (mucoid degeneration) of atrioventricular valves. Br Heart J. 1969;31:343-51.
Medline
10. Nguyen TC, Itoh A, Carlhall CJ, Bothe W, Timek TA, Ennis DB, et al. The effect of pure mitral regurgitation on mitral annular geometry and three-dimensional saddle shape. J Thorac Cardiovasc Surg. 2008;136:557-65.
Medline
11. Levine RA. Dynamic mitral regurgitation —more than meets the eye. N Engl J Med. 2004;351:1681-4.
Medline
12. Levine RA, Handschumacher MD, Sanfilippo AJ, Hagege AA, Harrigan P, Marshall JE, et al. Three-dimensional echocardiographic reconstruction of the mitral valve, with implications for the diagnosis of mitral valve prolapse. Circulation. 1989;80:589-98.
Medline
13. Eriksson MJ, Bitkover CY, Omran AS, David TE, Ivanov J, Ali MJ, et al. Mitral annular disjunction in advanced myxomatous mitral valve disease: echocardiographic detection and surgical correction. J Am Soc Echocardiogr. 2005;18:1014-22.
Medline
14. Godley RW, Wann LS, Rogers EW, Feigenbaum H, Weyman AE. Incomplete mitral leaflet closure in patients with papillary muscle dysfunction. Circulation. 1981;63:565-71.
Medline
15. Dell’italia LJ. The forgotten left ventricle in right ventricular pressure overload. J Am Coll Cardiol. 2011;57:929-30.
Medline
16. Kono T, Sabbah HN, Stein PD, Brymer JF, Khaja F. Left ventricular shape as a determinant of functional mitral regurgitation in patients with severe heart failure secondary to either coronary artery disease or idiopathic dilated cardiomyopathy. Am J Cardiol. 1991;68:355-9.
Medline
17. Enriquez-Sarano M, Miller FA, Hayes SN, Bailey KR, Tajik AJ, Seward JB. Effective mitral regurgitant orifice area: clinical use and pitfalls of the proximal isovelocity surface area method. J Am Coll Cardiol. 1995;25:703-9.
Medline
18. Adams DH, Anyanwu AC, Rahmanian PB, Filsoufi F. Current concepts in mitral valve repair for degenerative disease. Heart Fail Rev. 2006;11:241-57.
Medline
19. Carpentier A, Chauvaud S, Fabiani JN, Deloche A, Relland J, Lessana A, et al. Reconstructive surgery of mitral valve incompetence: ten-year appraisal. J Thorac Cardiovasc Surg. 1980;79:338-48.
Medline
20. Freed LA, Levy D, Levine RA, Larson MG, Evans JC, Fuller DL, et al. Prevalence and clinical outcome of mitral-valve prolapse. N Engl J Med. 1999;341:1-7.
Medline
21. Nesta F, Leyne M, Yosefy C, Simpson C, Dai D, Marshall JE, et al. New locus for autosomal dominant mitral valve prolapse on chromosome 13: clinical insights from genetic studies. Circulation. 2005;112:2022-30.
Medline
22. Anyanwu AC, Adams DH. Etiologic classification of degenerative mitral valve disease: Barlow's disease and fibroelastic deficiency. Semin Thorac Cardiovasc Surg. 2007;19:90-6.
Medline
23. Fornes P, Heudes D, Fuzellier JF, Tixier D, Bruneval P, Carpentier A. Correlation between clinical and histologic patterns of degenerative mitral valve insufficiency: a histomorphometric study of 130 excised segments. Cardiovasc Pathol. 1999;8:81-92.
Medline
24. Carpentier A, Lacour-Gayet F, Camilleri J. Fibroelastic dysplasia of the mitral valve: an anatomical and clinical entity. Circulation. 1982;3:307.
25. Disse S, Abergel E, Berrebi A, Houot AM, Le Heuzey JY, Diebold B, et al. Mapping of a first locus for autosomal dominant myxomatous mitral-valve prolapse to chromosome 16p11.2-p12.1. Am J Hum Genet. 1999;65:1242-51.
Medline
26. Chou HT, Shi YR, Hsu Y, Tsai FJ. Association between fibrillin-1 gene exon 15 and 27 polymorphisms and risk of mitral valve prolapse. J Heart Valve Dis. 2003;12:475-81.
Medline
27. Barber JE, Ratliff NB, Cosgrove DM, Griffin BP, Vesely I. Myxomatous mitral valve chordae. I: Mechanical properties. J Heart Valve Dis. 2001;10:320-4.
Medline
28. Grande-Allen KJ, Borowski AG, Troughton RW, Houghtaling PL, Dipaola NR, Moravec CS, et al. Apparently normal mitral valves in patients with heart failure demonstrate biochemical and structural derangements: an extracellular matrix and echocardiographic study. J Am Coll Cardiol. 2005;45:54-61.
Medline
29. Rabkin E, Aikawa M, Stone JR, Fukumoto Y, Libby P, Schoen FJ. Activated interstitial myofibroblasts express catabolic enzymes and mediate matrix remodeling in myxomatous heart valves. Circulation. 2001;104:2525-32.
Medline
30. Barlow JB, Pocock WA. Billowing, floppy, prolapsed or flail mitral valves?. Am J Cardiol. 1985;55:501-2.
Medline
31. St John Sutton M, Weyman AE. Mitral valve prolapse prevalence and complications: an ongoing dialogue. Circulation. 2002;106:1305-7.
Medline
32. Briffa N. Surgery for degenerative mitral valve disease. BMJ. 2010;341:c5339.
Medline
33. DiBardino DJ, ElBardissi AW, McClure RS, Razo-Vasquez OA, Kelly NE, Cohn LH. Four decades of experience with mitral valve repair: analysis of differential indications, technical evolution, and long-term outcome. J Thorac Cardiovasc Surg. 2010;139:76-83.
Medline
34. Barlow JB, Bosman CK. Aneurysmal protrusion of the posterior leaflet of the mitral valve. An auscultatory-electrocardiographic syndrome. Am Heart J. 1966;71:166-78.
Medline
35. Gulotta SJ, Gulco L, Padmanabhan V, Miller S. The syndrome of systolic click, murmur, and mitral valve prolapse—a cardiomyopathy?. Circulation. 1974;49:717-28.
Medline
36. Reduto LA, Gulotta SJ. Cardiology: prolapsed mitral valve syndrome. Postgrad Med. 1976;60:171-6.
Medline
37. Barlow JB, Pocock WA. The significance of late systolic murmurs and mid-late systolic clicks. Md State Med J. 1963;12:76-7.
Medline
38. Allen H, Harris A, Leatham A. Significance and prognosis of an isolated late systolic murmur: a 9- to 22-year follow-up. Br Heart J. 1974;36:525-32.
Medline
39. Angelini A, Ho SY, Anderson RH, Becker AE, Davies MJ. Disjunction of the mitral annulus in floppy mitral valve. N Engl J Med. 1988;318:188-9.
Medline
40. Adams DH, Anyanwu AC, Rahmanian PB, Abascal V, Salzberg SP, Filsoufi F. Large annuloplasty rings facilitate mitral valve repair in Barlow's disease. Ann Thorac Surg. 2006;82:2096-100.
Medline
41. Ng CM, Cheng A, Myers LA, Martinez-Murillo F, Jie C, Bedja D, et al. TGF-beta-dependent pathogenesis of mitral valve prolapse in a mouse model of Marfan syndrome. J Clin Invest. 2004;114:1586-92.
Medline
42. David TE, Omran A, Armstrong S, Sun Z, Ivanov J. Long-term results of mitral valve repair for myxomatous disease with and without chordal replacement with expanded polytetrafluoroethylene sutures. J Thorac Cardiovasc Surg. 1998;115:1279-85.
Medline
43. Horstkotte D, Schulte HD, Niehues R, Klein RM, Piper C, Strauer BE. Diagnostic and therapeutic considerations in acute, severe mitral regurgitation: experience in 42 consecutive patients entering the intensive care unit with pulmonary edema. J Heart Valve Dis. 1993;2:512-22.
Medline
44. Hueb AC, Jatene FB, Moreira LF, Pomerantzeff PM, Kallas E, De Oliveira SA. Ventricular remodeling and mitral valve modifications in dilated cardiomyopathy: new insights from anatomic study. J Thorac Cardiovasc Surg. 2002;124:1216-24.
Medline
45. McCully RB, Enriquez-Sarano M, Tajik AJ, Seward JB. Overestimation of severity of ischemic/functional mitral regurgitation by color Doppler jet area. Am J Cardiol. 1994;74:790-3.
Medline
46. Mihaljevic T, Lam BK, Rajeswaran J, Takagaki M, Lauer MS, Gillinov AM, et al. Impact of mitral valve annuloplasty combined with revascularization in patients with functional ischemic mitral regurgitation. J Am Coll Cardiol. 2007;49:2191-201.
Medline
47. Watanabe N, Ogasawara Y, Yamaura Y, Yamamoto K, Wada N, Kawamoto T, et al. Geometric differences of the mitral valve tenting between anterior and inferior myocardial infarction with significant ischemic mitral regurgitation: quantitation by novel software system with transthoracic real-time three-dimensional echocardiography. J Am Soc Echocardiogr. 2006;19:71-5.
Medline
48. Magne J, Girerd N, Senechal M, Mathieu P, Dagenais F, Dumesnil JG, et al. Mitral repair versus replacement for ischemic mitral regurgitation: comparison of short-term and long-term survival. Circulation. 2009;120(Suppl 11):S104-11.
Medline
49. Glower DD, Tuttle RH, Shaw LK, Orozco RE, Rankin JS. Patient survival characteristics after routine mitral valve repair for ischemic mitral regurgitation. J Thorac Cardiovasc Surg. 2005;129:860-8.
Medline
50. Kirkpatrick JN, Lang RM. Surgical echocardiography of heart valves: a primer for the cardiovascular surgeon. Semin Thorac Cardiovasc Surg. 2010;22:200.e1-200.e22.
51. Chandra S, Salgo IS, Sugeng L, Weinert L, Tsang W, Takeuchi M, et al. Characterization of degenerative mitral valve disease using morphologic analysis of real-time three-dimensional echocardiographic images: objective insight into complexity and planning of mitral valve repair. Circ Cardiovasc Imaging. 2011;4:24-32.
Medline
52. Pepi M, Tamborini G, Maltagliati A, Galli CA, Sisillo E, Salvi L, et al. Head-to-head comparison of two- and three-dimensional transthoracic and transesophageal echocardiography in the localization of mitral valve prolapse. J Am Coll Cardiol. 2006;48:2524-30.
Medline
53. Ray S. The echocardiographic assessment of functional mitral regurgitation. Eur J Echocardiogr. 2010;11:i11-7.
Medline
54. Cameli M, Lisi M, Giacomin E, Caputo M, Navarri R, Malandrino A, et al. Chronic mitral regurgitation: left atrial deformation analysis by two-dimensional speckle tracking echocardiography. Echocardiography. 2011;28:327-34.
Medline
55. Jebara VA, Mihaileanu S, Acar C, Brizard C, Grare P, Latremouille C, et al. Left ventricular outflow tract obstruction after mitral valve repair. Results of the sliding leaflet technique. Circulation. 1993;88(5 Pt 2):II30-4.
Medline
56. Altiok E, Hamada S, Van Hall S, Hanenberg M, Dohmen G, Almalla M, et al. Comparison of direct planimetry of mitral valve regurgitation orifice area by three-dimensional transesophageal echocardiography to effective regurgitant orifice area obtained by proximal flow convergence method and vena contracta area determined by color Doppler echocardiography. Am J Cardiol. 2011;107:452-8.
Medline
57. Itoh A, Ennis DB, Bothe W, Swanson JC, Krishnamurthy G, Nguyen TC, et al. Mitral annular hinge motion contribution to changes in mitral septal-lateral dimension and annular area. J Thorac Cardiovasc Surg. 2009;138:1090-9.
Medline
58. Salgo IS, Gorman JH, Gorman RC, Jackson BM, Bowen FW, Plappert T, et al. Effect of annular shape on leaflet curvature in reducing mitral leaflet stress. Circulation. 2002;106:711-7.
Medline
59. Ormiston JA, Shah PM, Tei C, Wong M. Size and motion of the mitral valve annulus in man. II. Abnormalities in mitral valve prolapse. Circulation. 1982;65:713-9.
Medline
60. Solis J, Sitges M, Levine RA, Hung J. Ecocardiografía tridimensional. Nuevas perspectivas sobre la caracterización de la válvula mitral. Rev Esp Cardiol. 2009;62:188-98.
Medline
61. Grigioni F, Enriquez-Sarano M, Zehr KJ, Bailey KR, Tajik AJ. Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment. Circulation. 2001;103:1759-64.
Medline
62. Sugeng L, Chandra S, Lang RM. Three-dimensional echocardiography for assessment of mitral valve regurgitation. Curr Opin Cardiol. 2009;24:420-5.
Medline
63. Kronzon I, Sugeng L, Perk G, Hirsh D, Weinert L, Garcia Fernandez MA, et al. Real-time 3-dimensional transesophageal echocardiography in the evaluation of post-operative mitral annuloplasty ring and prosthetic valve dehiscence. J Am Coll Cardiol. 2009;53:1543-7.
Medline
64. Adams DH, Anyanwu AC. The cardiologist's role in increasing the rate of mitral valve repair in degenerative disease. Curr Opin Cardiol. 2008;23:105-10.
Medline
65. McCarthy PM. When is your surgeon good enough? When do you need a “referent surgeon”?. Curr Cardiol Rep. 2009;11:107-13.
Medline
66. Lancellotti P, Moura L, Pierard LA, Agricola E, Popescu BA, Tribouilloy C, et al. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr. 2010;11:307-32.
Medline
67. Michelena HI, Bichara VM, Margaryan E, Forde I, Topilsky Y, Suri R, et al. Avances en el tratamiento de la insuficiencia mitral grave. Rev Esp Cardiol. 2010;63:820-31.
Medline
68. Omran AS, Woo A, David TE, Feindel CM, Rakowski H, Siu SC. Intraoperative transesophageal echocardiography accurately predicts mitral valve anatomy and suitability for repair. J Am Soc Echocardiogr. 2002;15:950-7.
Medline
69. Bolling SF, Li S, O’Brien SM, Brennan JM, Prager RL, Gammie JS. Predictors of mitral valve repair: clinical and surgeon factors. Ann Thorac Surg. 2010;90:1904-11.
Medline
70. Gillinov AM, Blackstone EH, Nowicki ER, Slisatkorn W, Al-Dossari G, Johnston DR, et al. Valve repair versus valve replacement for degenerative mitral valve disease. J Thorac Cardiovasc Surg. 2008;135:885-93. 893.e1–2
Medline
71. Kongsaerepong V, Shiota M, Gillinov AM, Song JM, Fukuda S, McCarthy PM, et al. Echocardiographic predictors of successful versus unsuccessful mitral valve repair in ischemic mitral regurgitation. Am J Cardiol. 2006;98:504-8.
Medline
72. Magne J, Pibarot P, Dumesnil JG, Senechal M. Continued global left ventricular remodeling is not the sole mechanism responsible for the late recurrence of ischemic mitral regurgitation after restrictive annuloplasty. J Am Soc Echocardiogr. 2009;22:1256-64.
Medline
73. Lancellotti P, Marwick T, Pierard LA. How to manage ischaemic mitral regurgitation. Heart. 2008;94:1497-502.
Medline
74. Anyanwu AC, Bridgewater B, Adams DH. The lottery of mitral valve repair surgery. Heart. 2010;96:1964-7.
Medline
75. Bridgewater B, Hooper T, Munsch C, Hunter S, Von Oppell U, Livesey S, et al. Mitral repair best practice: proposed standards. Heart. 2006;92:939-44.
Medline
76. Mirabel M, Iung B, Baron G, Messika-Zeitoun D, Detaint D, Vanoverschelde JL, et al. What are the characteristics of patients with severe, symptomatic, mitral regurgitation who are denied surgery?. Eur Heart J. 2007;28:1358-65.
Medline
77. Toledano K, Rudski LG, Huynh T, Beique F, Sampalis J, Morin JF. Mitral regurgitation: determinants of referral for cardiac surgery by Canadian cardiologists. Can J Cardiol. 2007;23:209-14.
Medline
78. Tribouilloy CM, Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, et al. Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications. Circulation. 1999;99:400-5.
Medline
79. Suri RM, Schaff HV, Dearani JA, Sundt TM, Daly RC, Mullany CJ, et al. Recovery of left ventricular function after surgical correction of mitral regurgitation caused by leaflet prolapse. J Thorac Cardiovasc Surg. 2009;137:1071-6.
Medline
80. Detaint D, Sundt TM, Nkomo VT, Scott CG, Tajik AJ, Schaff HV, et al. Surgical correction of mitral regurgitation in the elderly: outcomes and recent improvements. Circulation. 2006;114:265-72.
Medline
81. Ling LH, Enriquez-Sarano M, Seward JB, Orszulak TA, Schaff HV, Bailey KR, et al. Early surgery in patients with mitral regurgitation due to flail leaflets: a long-term outcome study. Circulation. 1997;96:1819-25.
Medline
82. Rosenhek R, Rader F, Klaar U, Gabriel H, Krejc M, Kalbeck D, et al. Outcome of watchful waiting in asymptomatic severe mitral regurgitation. Circulation. 2006;113:2238-44.
Medline
83. Tribouilloy C, Grigioni F, Avierinos JF, Barbieri A, Rusinaru D, Szymanski C, et al. Survival implication of left ventricular end-systolic diameter in mitral regurgitation due to flail leaflets a long-term follow-up multicenter study. J Am Coll Cardiol. 2009;54:1961-8.
Medline
84. Topilsky Y, Suri R, Schaff HV, Enriquez-Sarano M. When to intervene for asymptomatic mitral valve regurgitation. Semin Thorac Cardiovasc Surg. 2010;22:216-24.
Medline
85. Adams DH, Anyanwu AC. Valve Disease: Asymptomatic mitral regurgitation: does surgery save lives?. Nat Rev Cardiol. 2009;6:330-2.
Medline
86. Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, Detaint D, Capps M, Nkomo V, et al. Quantitative determinants of the outcome of asymptomatic mitral regurgitation. N Engl J Med. 2005;352:875-83.
Medline
87. Kang DH, Kim JH, Rim JH, Kim MJ, Yun SC, Song JM, et al. Comparison of early surgery versus conventional treatment in asymptomatic severe mitral regurgitation. Circulation. 2009;119:797-804.
Medline
88. Gammie JS, Sheng S, Griffith BP, Peterson ED, Rankin JS, O’Brien SM, et al. Trends in mitral valve surgery in the United States: results from the Society of Thoracic Surgeons Adult Cardiac Surgery Database. Ann Thorac Surg. 2009;87:1431-7.
Medline
89. Gammie JS, O’Brien SM, Griffith BP, Ferguson TB, Peterson ED. Influence of hospital procedural volume on care process and mortality for patients undergoing elective surgery for mitral regurgitation. Circulation. 2007;115:881-7.
Medline
90. Casselman FP, Van Slycke S, Dom H, Lambrechts DL, Vermeulen Y, Vanermen H. Endoscopic mitral valve repair: feasible, reproducible, and durable. J Thorac Cardiovasc Surg. 2003;125:273-82.
Medline
91. Chitwood WR, Rodriguez E, Chu MW, Hassan A, Ferguson TB, Vos PW, et al. Robotic mitral valve repairs in 300 patients: a single-center experience. J Thorac Cardiovasc Surg. 2008;136:436-41.
Medline
92. Seeburger J, Borger MA, Doll N, Walther T, Passage J, Falk V, et al. Comparison of outcomes of minimally invasive mitral valve surgery for posterior, anterior and bileaflet prolapse. Eur J Cardiothorac Surg. 2009;36:532-8.
Medline
93. Seeburger J, Kuntze T, Mohr FW. Gore-tex chordoplasty in degenerative mitral valve repair. Semin Thorac Cardiovasc Surg. 2007;19:111-5.
Medline
94. Bax JJ, Braun J, Somer ST, Klautz R, Holman ER, Versteegh MI, et al. Restrictive annuloplasty and coronary revascularization in ischemic mitral regurgitation results in reverse left ventricular remodeling. Circulation. 2004;110(11 Suppl 1):II103-8.
Medline
95. Magne J, Senechal M, Mathieu P, Dumesnil JG, Dagenais F, Pibarot P. Restrictive annuloplasty for ischemic mitral regurgitation may induce functional mitral stenosis. J Am Coll Cardiol. 2008;51:1692-701.
Medline

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