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Original Articles: Adult Cardiac

Mitral Valve Abnormalities in Hypertrophic Cardiomyopathy: Echocardiographic Features and Surgical Outcomes

^a Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic, Cleveland, Ohio
^b Department of Cardiovascular Medicine, The Cleveland Clinic, Cleveland, Ohio
^c Department of Quantitative Health Sciences, The Cleveland Clinic, Cleveland, Ohio

Accepted for publication January 15, 2008.

^_* Address correspondence to Dr Smedira, Kaufman Center for Heart Failure, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic, 9500 Euclid Ave/F24, Cleveland, OH 44195 (Email: smedirn{at}ccf.org).

	Abstract

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

 
Background: Functional and intrinsic mitral valve (MV) abnormalities are common in hypertrophic cardiomyopathy (HCM); however, morphologic characteristics constituting indications for surgical intervention are incompletely defined. This study was conducted to define the echocardiographic features of MV pathology in patients with HCM and relate these to repairability of the MV, MV procedures performed, durability of repair, and survival.

Methods: From 1986 to 2003, 851 patients with HCM underwent operation, and 115 had a concomitant MV procedure. Detailed analysis of their 784 transthoracic and transesophageal echocardiograms, performed intraoperatively and postoperatively, was conducted. Outcomes were assessed by cross-sectional follow-up.

Results: Sixty-seven patients (58%) underwent MV repair, and 48 (42%) had MV replacement. The mean left ventricular outflow tract peak gradient was 70 ± 50 mm Hg. Systolic anterior motion was present in 95%. Valve abnormalities were degenerative in 36 (31%), myxomatous in 23 (20%), papillary muscle in 23 (20%), restrictive chordal in 22 (19%), restrictive leaflet in 80 (70%), and long leaflet in 64 (56%). Patients undergoing MV repair had higher prevalence of long leaflets and degenerative MV pathology. The anterior mitral leaflet was 3.0 ± 0.49 cm in the repair group vs 2.5 ± 0.40 cm in the replacement group (p = 0.0001). MV replacement patients were older, more symptomatic, and had more renal dysfunction and lower hematocrits. By 3 years, 91% of patients with a repair were free of reoperation.

Conclusions: Intrinsic MV pathology is frequently observed in HCM patients with symptomatic obstruction who undergo myectomy. Echocardiography can identify MV features predictive of successful valve repair. Repair, although durable, is feasible in only about half of patients.

	Introduction

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

 
Hypertrophic cardiomyopathy (HCM) is a genetic disorder resulting in unexplained hypertrophy of the left ventricle. In up to 60% of patients, altered geometry of the left ventricular outflow tract (LVOT), septal hypertrophy, and systolic anterior motion (SAM) of the mitral valve (MV) lead to an outflow tract gradient and symptomatic hypertrophic obstructive cardiomyopathy (HOCM) [1]. Hypertrophic obstructive cardiomyopathy is also associated with a variety of intrinsic abnormalities of the MV [2], including anomalous mitral papillary muscles or chordae [3], direct papillary insertion into the mitral leaflet [4], chordal rupture [5], and MV prolapse.

One autopsy study suggested that HCM was associated with increased mitral leaflet area in 70% of cases [6]. Several surgical series suggest that concomitant MV surgery is required in 11% to 20% of patients [3, 7]; however, indications for this are incompletely defined, as are echocardiographic predictors of the type of procedure required. This study aimed to define echocardiographic characteristics of intrinsic MV abnormalities leading to surgical intervention in patients with HCM and relate these to valve repairability, durability of repair, and survival.

	Patients and Methods

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

 
Patients
From January 1986 to January 2003, 851 symptomatic patients underwent operation for HCM at The Cleveland Clinic. These 851 were established after personal review (B.W.L., N.G.S.) of all patients undergoing operation for HCM for any reason during this period, using consensus criteria [8]. Of these, 115 (14%) underwent a concomitant MV procedure, with 102 undergoing a concomitant septal myectomy, leaving 13 patients with HOCM who underwent MV replacement alone. Valve repairs were done in 67 patients (58%), and 48 (42%) had valve replacement with a mechanical valve (n = 39) or bioprosthesis (n = 9). The mean age was 59 ± 14 years, and 56% were men. These and other patient characteristics are presented in Table 1. Data were extracted from the Cardiovascular Information Registry (CVIR), a database maintained concurrently with patient care, and were approved for use in research by the Institutional Review Board (IRB), with patient consent waived.

A segmental description of MV morphology and pathology, including anulus, leaflets, and subvalvar apparatus, was made from the echocardiographic review, and the surgeon's gross inspection was recorded in the operative note. Each valve was coded by 2 independent, experienced observers and then organized into 6 nonmutually exclusive groups (Fig 1; Table 2). The length of the anterior and posterior MV leaflets was measured on intraoperative TEE when available.

View larger version (56K): [in this window] [in a new window]   Fig 1. Mitral valve morphology. (A) Degenerative: thin leaflets with excessive mobility. This is a classic example of torn chordae to the P2 segment of the posterior leaflet with resultant anteriorly directed jet and systolic anterior motion of anterior leaflet with a posteriorly directed jet. (B) Myxomatous: similar to degenerative (A), with thickened redundant leaflets. (C) Papillary muscle: most common variant, with large anteromedial muscle inserting directly into A1 segment of mitral leaflet. (D) Restrictive chordae: single or multiple (shown) secondary chordae restricting anterior leaflet mobility and tenting leaflet into left ventricular outflow tract. (E) Restrictive leaflet: thickened leaflet often associated with anular calcification. (F) Long leaflet: defined by anterior leaflet length >2.5 cm and posterior leaflet length >2.0 cm; one or both can be elongated.

Postoperative echocardiograms or echocardiographic reports from The Cleveland Clinic and outside institutions were reviewed. Among 67 patients undergoing repair, 140 echocardiograms were available for review in 63 patients. Fifty percent of echocardiograms were obtained within 2 weeks of operation, and 25% more than a year later (Appendix Fig 1 _^*).

View larger version (11K): [in this window] [in a new window]   Appendix Fig 1. Number of patients (black bars) with echocardiograms available at and beyond various time points and number of echocardiographic measurements (gray bars) available for analysis.

Repairability
Multivariable logistic regression analysis was used to identify factors distinguishing patients undergoing MV replacement rather than repair. Bootstrap bagging was used for variable selection [15, 16], with automated analysis of 1000 resampled data sets. Factors occurring in 50% or more of these analyses were considered reliably identified at p < 0.05.

Durability of mitral repair
Among patients undergoing MV repair, longitudinal ordinal logistic regression for repeated measurements (SAS PROC GENMOD, SAS Inc, Cary, NC) was used to investigate the temporal pattern of the regurgitation grade at follow-up TTE. This method accounted for multiple records per patient. Only 10 electrocardiograms revealed 3+ or 4+ mitral regurgitation and so were collapsed into a single category for analyses. Because of the limited ability of PROC GENMOD to explore multivariable relations, ordinary multivariable logistic regression was initially used to screen variables under the assumption of independence. These variables were then investigated by manual backward elimination, and those with p < 0.05 retained.

Survival
Overall and stratified nonparametric survival estimates were obtained by the Kaplan-Meier method. A parametric method was used to resolve the number of phases of instantaneous risk of death (hazard function) and to estimate shaping parameters [17].

Continuous data are summarized as means ± standard deviations, or as 15th, 50th (median), and 85th percentiles when distributions were skewed. Wilcoxon rank sum tests and t tests were used to investigate group differences. Categoric data are summarized as frequencies and percentages, and group comparisons were made using ² tests (Fisher exact test where appropriate). Proportions are accompanied by asymmetric 68% confidence limits (CL) equivalent to ± 1 standard error.

	Results

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

 
Morphologic Features
Echocardiography documented restrictive leaflet abnormalities in 80 patients and elongated leaflets in 64 (Table 2). Degenerative and myxomatous pathologies were present in 59 (51%). Subvalvar chordal and papillary muscle abnormalities were found in 22 and 23 patients, respectively. Nearly all of the myxomatous valves had severe MR but the lowest LVOT gradients (Table 3); conversely, restricted chordal abnormalities were associated with the least prevalence of severe MR and the highest LVOT gradients. Septal thickening was similar for all morphologic categories. Systolic anterior motion was present at rest in 107 of the 113 patients (95%) in whom it could be accurately assessed (Appendix Table 1 _^*). Of 6 patients who did not have SAM at rest, it developed in 1 patient in provocative testing, did not develop in 3, and was not noted in 2. All patients had mitral regurgitation at rest, with most in grade 3+ (30%) or 4+ (47%). Myxomatous valves had the most variable regurgitant jet directions; jet direction was predominately posterior and central in all other morphologic categories, including those with long leaflet morphology (Appendix Table 2 _^*).

All patients undergoing MV repair also had a septal myectomy. A number of repair techniques were used (Table 5). Only 11 repairs (16%) included an anuloplasty ring.

Durability of Mitral Valve Repair
Postoperative mitral regurgitation
Early after operation, the proportion of patients with perfect mitral competence (grade 0 regurgitation) declined to about 35% at 1 year, and those with severe mitral regurgitation (grade 3+ or 4+) rose to about 10% (Fig 2). The only risk factors for higher grade of mitral regurgitation, in addition to the temporal trend depicted, was older age at repair (p = 0.04).

View larger version (7K): [in this window] [in a new window]   Fig 2. Risk-unadjusted estimate by echocardiography of postoperative mitral regurgitation (MR) after MV repair. The lines depict results of an ordinal longitudinal analysis that accounted for repeated echocardiograms of the same patient. Symbols represent grouped data that do not account for repeated measures, graphed to lend credibility to the solid lines. Squares, no MR; open circles, 1+ MR; filled circles, 2+ MR; triangles, 3+ or 4+ MR. Based on patient age of 50 years.

View larger version (6K): [in this window] [in a new window]   Fig 3. Freedom from mitral valve replacement (MVR) after repair or attempted repair. Each circle represents a replacement, the vertical bars are 68% confidence limits (CL) equivalent to ± 1 standard error, and the numbers in parentheses represent patients at risk. The solid line is the parametric estimate enclosed within dashed 68% CLs.

View larger version (7K): [in this window] [in a new window]   Appendix Fig 2. Instantaneous risk of death (hazard function) after mitral valve repair or replacement in patients with hypertrophic cardiomyopathy. Solid line is parametric estimate enclosed within 68% confidence limits.

View larger version (7K): [in this window] [in a new window]   Fig 4. Survival after mitral valve repair or replacement in patients with hypertrophic cardiomyopathy. Each circle represents a replacement, vertical bars are 68% confidence limits (CL) equivalent to ± 1 standard error, and numbers in parentheses represent patients at risk. The solid line is the parametric estimate enclosed within dashed 68% CLs.

View larger version (8K): [in this window] [in a new window]   Fig 5. Survival in patients undergoing operation for hypertrophic cardiomyopathy with accompanying valve repair (filled circles) or replacement (open circles) for mitral valve abnormalities. Vertical bars are 68% confidence limits (CL) equivalent to ± 1 standard error, and numbers in parentheses represent patients at risk. The solid line is the parametric estimate enclosed within dashed 68% CLs.

	Comment

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

Principal Findings
A wide range of intrinsic MV abnormalities frequently coexist in patients with septal hypertrophy and dynamic LVOT obstruction. Although MV morphology appeared to affect the severity of mitral regurgitation and magnitude of LVOT gradient, it was independent of the degree of septal hypertrophy. Patient and valve characteristics influenced the likelihood of valve replacement, and with the exception of the Alfieri stitch, valve repairs were reproducible and durable in the intermediate term.

Echocardiography and Valve Morphology
Almost all patients in this series had resting SAM with severe mitral regurgitation. The presence of severe regurgitation without SAM suggests intrinsic MV disease, and detailed evaluation of regurgitant jet direction and MV morphology may define the valve pathology. Anterior regurgitant jet direction suggests underlying degenerative or myxomatous posterior leaflet pathology. Anomalous papillary muscle insertions, tethering chordae, and long leaflets can be readily determined by echocardiography. Differentiating intrinsic MV regurgitation from dynamic obstruction can be particularly difficult in patients with restricted, calcified, and thickening leaflets with resting SAM. Intrinsic MV disease is often obscured by the uniform presence of dynamic mitral regurgitation, but presence of mitral regurgitation without SAM or presence of an anteriorly directed jet is strong evidence for intrinsic MV disease.

Many small case series describe specific MV abnormalities in patients with HCM, but only one sizeable report has been published that examined the pathology of 94 excised MVs [6, 18, 19]. These valves tended to have a larger area, were longer, and frequently had direct insertion of the papillary muscle onto the anterior leaflet. Echocardiography provides substantially more detailed assessment of in vivo MV function and morphology, and our challenge was to synthesize this information for clinical decision making.

Leaflet Morphology and Surgical Results
Restrictive leaflets with valve calcification and thickening were the most common form of intrinsic MV disease identified, and calcification was a risk factor for valve replacement. The mechanism of valve thickening and calcification is unknown, but the trauma of repetitive septal contact could result in fibrosis, retraction, and regurgitation. Both biologic and mechanical prostheses were used to treat restrictive leaflet pathology. Fear of posterior or lateral ventricular wall perforation from a tall valve strut protruding into a small ventricular cavity has been reduced by development of biologic MVs with substantially reduced strut height. These new valves offer older patients an alternative to mechanical valve replacement but do not eliminate need for careful orientation of valve struts to avoid mechanical LVOT obstruction. A concomitant myectomy will still be necessary in most cases [7]. We have no experience treating restricted leaflets with leaflet area extension using glutaraldehyde-treated autologous pericardium[20].

A wealth of experience has been accumulated assessing and treating patients with prolapse or flail leaflets from degenerative and myxomatous valve disease [21, 22]. Time-tested surgical techniques of leaflet segment resection and leaflet height reduction with sliding valvuloplasties were used in this series. Annuloplasties were infrequently used to avoid inducing SAM of the anterior leaflet, and this approach did not affect repair durability during the relatively short follow-up period. If an annuloplasty were used, an "oversized" incomplete band would appear to be safest.

Leaflet elongation was common and could involve one or both leaflets. Whether leaflet elongation is an early form or variant manifestation of myxomatous MV disease, where excessively tall anterior or posterior leaflets have been long described, is unknown. Many elongated leaflets were thickened, as seen in myxomatous disease and as reported in the pathology series. Our impression was that many patients with elongated anterior leaflets had less septal hypertrophy; however, measured leaflet length correlated with degree of septal hypertrophy, refuting this hypothesis. Multiple repair techniques to reduce leaflet height have been described. Plicating the anterior leaflet along its long axis (tip of leaflet to base), whether in its central portion or leaflet edge, makes the most sense, is easily accomplished through the aortic valve, and is our preferred method of repair. Plicating perpendicular to the long axis has been used successfully [23].

Reports of subvalvar abnormalities of the MV have focused on insertion of the papillary muscle, most commonly the anterolateral, which Kanani and Anderson [24] note is more correctly described as superoposterior, directly onto the mitral leaflet [18]. In addition to papillary muscle anomalies, we also found chordal abnormalities resulting in tethering of the anterior mitral leaflet toward the LVOT. Wide mid-to-apical resection of the septum, papillary muscle mobilization off the lateral wall, and excision of a portion of the excessively hypertrophied papillary muscle have been described to manage this anomaly [25]. Tethering secondary chordae have been excised, and a very anteriorly displaced anterior papillary muscle chordae complex has been excised and function established by attaching polytetrafluoroethylene neochordae to the most posterior papillary muscle head of the anterolateral complex.

This variability of subvalvar anatomy and papillary muscle alignment is most likely related to abnormal valve morphogenesis [26]. After 5 to 6 weeks of gestation, the LV septum undergoes involution, with both chordae and papillary muscles originating from septal muscle tissue. Failure of chordae to develop would explain the direct insertion of papillary muscle onto the leaflet. Whether abnormal blood flow, sarcomeric protein gene mutations found in HCM, or both, result in a malpositioned anterior papillary muscle and subvalvar abnormalities is unknown. Septal hypertrophy and abnormal MV morphogenesis may be conceptually similar to abnormal bicuspid valvulogenesis and its associated deficiencies in fibrillin, endothelium-derived nitric oxide synthase, and the ubiquitin fusion degradation 1 gene [27].

The repair techniques used in this series are evolving. We thought the simplicity of the Alfieri stitch and that it could be placed through the aortic valve at myectomy would render it useful for treating patients with hypertrophy and intrinsic MV disease; however, frequent recurrence of mitral regurgitation has led us to abandon this technique. If standard valve repair techniques are insufficient, then replacement is preferred. A competent repair is durable, with excellent short-term freedom from recurrent mitral regurgitation and SAM.

Strengths and Limitations
This is a single institution's consecutive experience with surgical management of MV pathology accompanying HCM. However, HCM and its treatment has been a particular focus of our institution for many years, and our experience is extensive. We did not analyze MV morphology in HCM patients in whom no operation for mitral disease was deemed necessary; thus, we do not know characteristics of more minor valve morphology. Echocardiographic follow-up was limited to that available from treating cardiologists rather than from a systematic protocol; thus, it is limited to short-term results. The frequency of MV abnormalities requiring surgical intervention is much higher than has been reported. Careful review of operative reports suggests that this reflects a referral bias rather than overtreatment.

Clinical Implications
Assessing patients with symptomatic left ventricular hypertrophy requires detailed echocardiographic evaluation. In addition to provocative maneuvers in patients without resting obstruction, a detailed assessment of MV anatomy and function must be completed before embarking on therapies. Many valves can be repaired with the expectation of lasting durability. Valve replacement with a low-profile biologic prosthesis is now possible when indicated, without concerns for ventricular perforation.

Our experience suggests that the clinical and research focus of hypertrophic obstructive cardiomyopathy should expand beyond septal hypertrophy and myocyte abnormalities and begin to examine the complex and little understood relationship of the septum, sarcomere proteins, and morphogenesis of MV leaflets and subvalvar apparatus [9, 10].

	Appendix

 

	Acknowledgments

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

 
This study was supported in part by the Kenneth Gee and Paula Shaw, PhD, Chair in Heart Research, held by Dr Blackstone. We thank Michelle Miluk, RN, BSN, for data adjudication and checking; Diana Dolney, RN, MSN, for data collection and patient follow-up; Angela York for database management; and Jocelyn Piskach, Karen Mrazeck, Wanda Weaver, Patricia White, and Sherry El Sakr for completion of patient follow-up.

	Footnotes

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

 
^_* The Appendix Figures 1, 2 and Tables 1, 2 are available only online. To access them, please visit: http://ats.ctsnetjournals.org and search for the article by Kaple, Vol. 85, pages 1527–1536.e1–2.

	References

Top Abstract Introduction Patients and Methods Results Comment Footnotes Acknowledgments References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Bruce W. Lytle Eugene H. Blackstone Nicholas G. Smedira Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kaple, R. K. Articles by Smedira, N. G. Search for Related Content PubMed PubMed Citation Articles by Kaple, R. K. Articles by Smedira, N. G. Related Collections Valve disease Related Article