(Chest. 2003;124:1929-1936.)
© 2003
American College of Chest Physicians
The Subvalvular Apparatus in Rheumatic Mitral Stenosis*
Methods of Assessment and Therapeutic Implications
Yoav Turgeman, MD;
Shaul Atar, MD and
Tiberio Rosenfeld, MD
* From the Department of Cardiology, Ha’Emek Medical Center, Afula, Israel.
Correspondence to: Yoav Turgeman, MD, Director, Invasive Cardiology Unit, Ha’Emek Medical Center, Afula, 18101, Israel; e-mail: yoav_t{at}clalit.org.il
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Abstract
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The assessment of the structure and function of the subvalvular apparatus (SVA) in patients with rheumatic mitral stenosis (MS) is complex, yet is of major importance prior to therapeutic decision making. Currently available methods of assessment are neither sufficiently accurate nor feasible. We review anatomic and functional aspects of the SVA and define SVA involvement in rheumatic MS. The role of various noninvasive and invasive methods for evaluating the integrity and function of SVA in rheumatic MS, as well as clinical implications and pitfalls in assessment of SVA are also discussed.
Key Words: chordae tendineae • mitral stenosis • rheumatic • subvalvar
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Introduction
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The diagnosis, evaluation, and treatment of patients with rheumatic mitral stenosis (MS) may involve pediatricians, family practitioners, interventional and noninterventional cardiologists, as well as cardiac surgeons. Treatment of patients with MS should optimally be based on an integration of subjective as well as objective parameters such as functional capacity, compliance, patient age, pulmonary hypertension, cardiac function, and associated valvular abnormalities. However, in common clinical practice, the functional anatomy of the mitral valve is the main parameter that effects the selection of the therapeutic modality.
The subvalvar apparatus (SVA) is an integral part of the mitral valve structural complex and includes the left ventricular free wall, two papillary muscles, and chordae tendinae. Subvalvar deformity was noted in 40% of autopsy specimens of patients with rheumatic MS and in two thirds of patients undergoing open mitral commissurotomy.1
2
3
It has previously been demonstrated that both immediate and long-term results of percutaneous balloon mitral valvuloplasty (PBMV) are adversely influenced by severe subvalvular deformity.4
5
Proper assessment of SVA morphology and function in patients with rheumatic MS is therefore essential for therapeutic decision making—surgery vs palliative PBMV. Several methods and parameters for assessment of SVA are currently available, yet none are easy to use and can be readily used as a "gold standard." Current methods are mainly limited due to difficulties in assessment of the different degrees of pathologic involvement of the various valvular structural components. Moreover, there is no linear correlation between the observed anatomic abnormality and the functional abnormality of the mitral valve components.
The aims of this review are to describe anatomic and functional aspects of the SVA, and to define SVA involvement in rheumatic MS. The role of noninvasive and invasive methods for evaluating both the integrity and function of SVA in rheumatic disease, as well as clinical implications and pitfalls in assessment of SVA, will also be discussed.
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Anatomy and Function of the SVA
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Normal mitral valve function results from a complex of synchronized interactions between the valve components: left atrial and ventricular walls, valvular annulus, valve leaflets, papillary muscles, and chordae tendineae. MS is almost invariably the result of rheumatic fever. The functional and anatomic derangement in rheumatic MS results from three processes that may occur concomitantly: commissural fusion, leaflet abnormalities, and subvalvar disease.6
Anatomy of the SVA
Left ventricular free wall, two papillary muscles, and chordae tendineae constitute the SVA.
Papillary Muscles:
Both the anterolateral and posteromedial papillary muscles are attached to the left ventricular free wall near the apex and its mid third. The anterolateral papillary muscle consists of a single large trunk, whereas the posteromedial papillary muscle consists of one to three columns.7
8
They have the same muscular volume and are innervated by the left His bundle network. The posteromedial papillary muscle receives its blood supply from the posterior descending branch of the right coronary artery, and the anterolateral papillary muscle receives its blood supply from the diagonal branches of the left anterior descending artery and often by marginal branches of the left circumflex artery as well.8
Chordae Tendineae:
Although the chordae tendineae system has been extensively investigated, its physiologic and functional assessment remains controversial, mainly due to large variations in number, origin, length, direction, and point of insertion to the mitral leaflets. From each papillary muscle head, chordae tendineae originate and insert into the corresponding half of the two mitral leaflets. After a variable course and division each chordae tendineae branches into two to four small digits termed the functional unit that are attached to the ventricular aspect of the leaflet. Points of chordal insertion vary among the two leaflets. Most of the chordae tendineae directed to the anterior mitral leaflet terminate at the edge of the ventricular aspect (called the rough zone), whereas chordae tendineae directed to the posterior leaflet are inserted from the edge back along the leaflet body (called the clear zone) to the annular area.
Until 1970, the most commonly used classifications of chordae tendineae were those suggested by Tandler9
and later by Quain.10
This classification divides the chordae tendineae into three orders: the first-order chordae tendineae insert into the leaflet’s edge, the second-order chordae tendineae insert 6 to 8 mm beyond the free margins, and the third-order chordae tendineae insert into the basal portion of the ventricular aspect of the posterior leaflet. Although the classification of Tandler9
and Quain10
is simple to use, it neither emphasizes the morphologic differences between chordae tendineae nor relates their sites of insertion to their function.
In 1970, Lam et al11
introduced a new chordae tendineae classification that distinguish commissural and leaflet chordae tendineae and relates chordae tendineae function to their morphology and location. As presented in Figure 1
, according to the classification of Lam et al,11
four types of chordae tendineae terminate at the rough zone of each half of the anterior mitral leaflet: strut (main), commissural, paracommissural, and paramedian. The strut chordae tendineae are the thickest and constitute the "skeleton" of the chordal system directed to the anterior leaflet. The average length and thickness (± SD) of chordae tendineae of the anterior leaflet are 17.5 ± 2.5 mm and 0.84 ± 0.28 mm, respectively.11
The posterior mitral leaflet has three types of chordae tendineae: the basal (annular region), the cleft (indentations between scallops), and the rough zone. The average length and thickness of the rough zone chordae tendineae of the posterior leaflet is 14 ± 0.8 mm and 0.65 ± 0.24 mm, respectively.11
Table 1
compares the classification of Lam et al11
with the classification of Tandler9
and Quain.10
From a practical point of view, a classification based on point of insertion has a greater advantage for both the surgeon and the interventional cardiologist.
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Figure 1.. A schematic of the classification of Lam et al11
showing course and point of insertion of chordae tendinae directed to the anterior and posterior mitral leaflets. Top left, A, and top right, C present a ventricular view of the anterior and posterior mitral leaflets, respectively. Bottom left, B, and bottom right, D, present a lateral view, respectively. An = annulus; Cz = clear zone; Rz = rough zone; Pm = papillary muscle; Ct = chordae tendinae; C = commissural; P = paracommissural; Pam = paramedian; S = strut.
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Function of the SVA
Until 2 decades ago, the closure and opening of the atrioventricular valves were considered to be a passive consequence of dynamic pressure gradients between the atria and ventricles throughout the cardiac cycle; however, it has been shown by Marzilli et al12
that opening and closing of the atrioventricular valves is an active process involving a synchronous function of all mitral structural components including the SVA. In fact, all subvalvar structures, including left ventricular free wall, papillary muscles, and chordae tendineae have an important role in opening and closure of the mitral valve leaflets.13
During ventricular systole, the main role of papillary muscles and chordae tendineae is to prevent mitral leaflets prolapse into the left atrium. Maximal shortening and elongation of the papillary muscles occurs 65 ± 6 ms after peak shortening and elongation of the muscular wall fibers.12
This time delay leads to active separation of both mitral leaflets during early diastole and approximation between left ventricular free wall and mitral leaflets during early systole, enabling the "keystone" mechanism of the mitral valve to be undertaken.14
The major contribution of the chordae tendineae to the closure of the mitral valve is by ensuring proper position of the rough zones of the two leaflets in order to maintain valve competence. Rough zone chordae tendineae are more important in preventing mitral valve prolapse than commissural chordae tendineae, whereas the strut (main) chordae tendineae are particularly the pillars of the keystone mechanism of the mitral valve.6
In 1983, Hetzer et al15
revived the concept that preservation of chordae tendineae integrity contributes to preservation of left ventricular contractility after mitral valve surgery. Studies15
16
have shown that left ventricular function was higher in patients who underwent mitral valve replacement without resection of chordae tendineae compared to the classic operation with chordae tendineae resection. This is most probably related to preservation of left ventricular geometry.13
15
SVA Involvement in Rheumatic Heart Disease
Subvalvular rheumatic deformity is a result of two closely related mechanisms: (1) a late manifestation of healed inflammation following acute rheumatic valvulitis, and (2) superimposed turbulence that induces fibrosis.17
Although papillary muscle hypertrophy has been noted by left ventriculography in patients with valvular rheumatic MS more often than in subvalvular MS,18
it is unusual to find any pathologic involvement of the papillary muscles in rheumatic heart disease.19
We believe that finding papillary muscle hypertrophy on angiography represents an angiographic pitfall, most probably due to an inability to distinguish between papillary muscle head and the agglutinated bundle of chordae tendineae. However, chordae tendineae involvement in the rheumatic process is not uncommon. Pathologic macroscopic findings such as fusion (agglutination), thickening, retraction, shortening, and calcification are frequently noted. Figure 2
presents normal chordae tendineae and abnormal chordae tendineae with rheumatic involvement. As a consequence of the rheumatic process, the free interchordal space diminishes and the opened "leaflet - chordae tendineae tunnel" available for diastolic flow is limited. This pathologic subtype may be called subvalvular MS.20
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Figure 2.. Left, A: An excised posterior mitral leaflet obtained from a patient with severe nonpliable MS prior to mitral valve replacement, showing thickened and fused (agglutinated) chordae tendineae (white arrow) attached to the tip of the papillary muscle (broken white arrow). Right, B: Anterior mitral leaflet with normal chordae tendinae (white arrow) attached to papillary muscle (broken white arrow).
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Methods of Assessment of the SVA
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Noninvasive Methods
Cardiac Auscultation:
The classical auscultatory features of rheumatic MS indicating preserved pliability are a loud first heart sound, high-pitch opening snap, and presystolic accentuation of the diastolic rumbling murmur. The auscultatory findings are influenced by the anatomy of the valve, the pressure gradient across the valve, as well as the atrioventricular electrical activation (ie, PR interval length in sinus rhythm or the presence of atrial fibrillation).21
22
Preserved anterior leaflet mobility and normal chordae tendineae length directed to the anterior leaflet are essential to produce these auscultatory findings23
; however, in the adult Western population, stenotic mitral valves are neither purely pliable nor totally rigid, and a wide range of auscultatory findings representing various levels of pliability may be found.24
It is well documented that patients with predominant subvalvular deformity and open commissures (eg, restenosis after surgical mitral commissurotomy) may have auscultatory findings indicating preserved pliability.6
Thus, the utility of cardiac auscultation for assessment of SVA involvement in rheumatic MS is limited.
Echocardiography:
Since the early 1980s, both M-mode and two-dimensional echocardiography are the main noninvasive methods for evaluating subvalvar rheumatic deformity25
; however, careful scanning of the subvalvular region in multiple views allows only a qualitative assessment of SVA structural components such as chordal thickening, fusion, and calcification. Moreover, measuring chordal length, differentiating chordae tendineae subgroups, and determining point of insertion in each leaflet are extremely limited by two-dimensional echocardiography.26
As presented in Table 2
, several echocardiographic scoring systems have been suggested to evaluate mitral valve anatomy and function and predict immediate and late results of PBMV.27
28
29
Most authors use the score of Wilkins et al,27
in which four parameters are semiquantitatively assessed: leaflet mobility, valvular thickening, subvalvular thickening, and valvular calcification.27
The score of Padial et al28
for the prediction of appearance of mitral regurgitation after PBMV uses the same criteria as in the score of Wilkins et al27
for the assessment of SVA. Only the classification of Iung et al29
is more quantitative regarding SVA evaluation, where direct measurements of chordal length are performed. Based on this classification, patients with pliable noncalcified anterior mitral leaflet with thin chordae (10 mm) have the best chances of achieving optimal immediate and long-term results after PBMV; however, none of the echocardiographic scoring systems have been found to be superior. All scoring systems are limited due to technical factors, difficulty of reproducibility, as they are only semiquantitative, as well as underestimation of severity, especially regarding the assessment of the SVA.
The advantage of transesophageal echocardiography (TEE) over transthoracic echocardiography (TTE) for SVA evaluation is still controversial. In a study by Hausmann et al, 30
thickening of SVA was graded lower by monoplane TEE than by TTE due to acoustic shadowing of the mitral valve, whereas results of biplane TEE were similar to TTE; the authors conclude that TEE has no clear advantage over TTE for the assessment of the subvalvular apparatus. Levin et al31
compared the value of monoplane TEE to TTE to predict outcome after PBMV. They found that except for leaflet mobility, TTE scores (according to the criteria of Wilkins et al27
) intended to be higher than TEE scores, particularly in the categories of subvalvular disease and valve thickening. Nevertheless, Levin et al31
conclude that both TEE and TTE have limited ability to accurately identify and evaluate the specific valvular features that influence PBMV outcome, especially subvalvular disease. The additional value of multiplane TEE for the assessment of the mitral valve has been documented by Stewart et al,32
and is currently the imaging method of choice for the evaluation of the SVA.
Invasive Methods
Fluoroscopy and Left Ventriculography:
Cardiac fluoroscopy and left ventriculography performed in the right and left anterior oblique projections were the first invasive methods in use for evaluation of both mitral valve morphology and function.33
34
Chordal calcification is easily determined by fluoroscopy. In 1979, Akins et al35
described the "mitral subvalvar distance ratio" by left ventriculography, in order to identify preoperatively patients with significant subvalvar fibrosis who may require valve replacement instead of palliative commissurotomy. This angiographic index compared the maximal length of the chordae tendineae from papillary muscle tip to the mitral valve level in systole with the long axis of the left ventricle (from the apex to the aortic valve) during diastole. An index < 0.14 precluded a good long-term result of mitral commissurotomy alone. Pitfalls in cardiac axis measurements, cardiac rotation due to right ventricular enlargement, electrical instability including the presence of atrial fibrillation, together with the development of echocardiography, have led to abandonment of this index. Fluoroscopy and left ventriculography are currently rarely in use for the assessment of the SVA.
Left Atrial Pressure-Wave Analysis:
At the early phase of systole, after the pressure crossing point between the left ventricular and atrial pressure curves, the coapted mitral leaflets continue to ascend into the left atrial cavity, leading to the formation of the left atrial C wave (Fig 3 ). At the peak of the C wave, the chordae tendineae are fully tensed and elongated while the anterior mitral leaflet is billowing toward the left atrial cavity.3
19
The absence of left atrial C wave is commonly associated with rigid, short, and thickened chordae tendineae directed to the anterior mitral leaflet36
; therefore, the presence of left atrial C wave in patients with rheumatic MS indicates a reasonably preserved chordae tendineae length and function.
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Figure 3.. Left atrial pressure-wave recording (A, C, and V waves) in a patient with severe pliable MS prior to performing PBMV. The presence of left atrial C wave is a marker for the absence of subvalvular deformity.
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During PBMV
During the performance of PBMV, two indirect signs have been suggested to indicate the presence of significant subvalvular disease. The "balloon impasse," which, albeit rare, indicates crossing and propagation difficulties of the deflated balloon catheter into the left ventricular apex due to high resistance at the submitral region.37
The "balloon compression" sign is a result of the distorted inflated balloon configuration at the subvalvular level. As shown in Figure 4
, the inflated balloon has a distorted contour due to the presence of significant subvalvular deformity, instead of having the typical "hourglass" appearance.38
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The Impact of SVA Deformity on the Results of PBMV
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The results of PBMV as well as of surgical closed mitral commissurotomy are mainly determined by the morphologic characteristics of the diseased valve and its supportive structures27
39
; however, the currently available data and medical literature on PBMV results do not differentiate between deformed mitral valves as a whole, in contrast to valves with fibrosed and distorted SVA only. Palacios et al40
found the postdilatation valve area to be significantly lower in patients with greater valve deformity, whereas Feldman and Carroll41
concluded that valve deformity does not significantly effect the acute results of PBMV. These conflicting studies were performed using two valvuloplasty techniques—conventional double balloon and Inoue balloon—and none of the studies analyzed the data for each of the structural subvalvular components separately; however, several reports42
43
44
using the Inoue technique emphasize that significant subvalvular deformity, as assessed by noninvasive parameters, cannot be used as a single predictive factor of immediate and long-term results for PBMV in both young and adult patients. In another study, 45
patients with severe SVA deformity were more hemodynamically deranged before PBMV and achieved more hemodynamic benefit, compared to patients with mild or moderate SVA involvement; the authors conclude that severe SVA deformity does not have any adverse effect either on immediate results or on intermediate term follow-up. However, severe SVA deformity may impose technical difficulties that may affect procedural immediate results. This is noted with crossing and propagation difficulties such as the balloon impasse, and selection of balloon diameter for the initial inflation.37
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Clinical Implications and Conclusions
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In patients with rheumatic heart disease, the advantages of palliation, preservation, and repair of the native mitral valve over valve replacement are well established.46
47
48
However, prior to deciding on the preferable therapeutic modality, comprehensive clinical, morphologic, and functional assessment of the diseased valve should be performed with all the parameters taken into consideration.
The SVA is an important constituent of the mitral valve structural complex. Models for ex vivo investigations of the mitral valve and chordae tendineae are currently being developed, and may allow better understanding of the SVA in the near future.49
Currently, assessment of SVA morphology and functional anatomy in relation to other valvular components remains a clinical challenge. Decisions should only be undertaken by an integration of noninvasive and invasive parameters prior to and also during an interventional therapeutic procedure—either PBMV or surgery.
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Footnotes
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Abbreviations: MS = mitral stenosis; PBMV = percutaneous balloon mitral valvuloplasty; SVA = subvalvular apparatus; TEE = transesophageal echocardiography; TTE = transthoracic echocardiography
Received for publication August 22, 2002.
Accepted for publication February 26, 2003.
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Abstract
Introduction
