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Ann Thorac Surg 2005;80:217-223
© 2005 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Beyond Extended Myectomy for Hypertrophic Cardiomyopathy: The Resection-Plication-Release (RPR) Repair

^a Division of Cardiothoracic Surgery, St. Luke’s-Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, New York
^b Hypertrophic Cardiomyopathy Program, Division of Cardiology, St. Luke’s-Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, New York
^c Department of Anesthesia, St. Luke’s-Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, New York

Accepted for publication January 10, 2005.

^_* Address reprint requests to Dr Swistel, Cardiothoracic Surgery, St. Luke’s-Roosevelt Medical Center, Columbia University, College of Physicians and Surgeons, 1111 Amsterdam Ave, New York, NY10025 (Email: sbalaram{at}chpnet.org).

	Abstract

Top Abstract Introduction Patients and Methods Results Comment References

 
BACKGROUND: Extended myectomy for left ventricular outflow tract obstruction (LVOTO) due to hypertrophic cardiomyopathy (HCM) has good long-term results. In addition to the midseptal resection (R) for HCM, our group has introduced a novel variation in anterior leaflet plication (P) and release (R) of papillary muscle attachments. We sought to investigate the medium-term success of this three-step repair that addresses all aspects of complex HCM pathology.

METHODS: Nineteen patients underwent resection-plication-release repair for complex HCM pathology. Transesophageal echocardiography was performed on all patients preoperatively and postoperatively to assess adequacy of resection, left ventricular outflow tract gradients, and mitral valve function. All patients underwent transthoracic outpatient echocardiography at a mean follow-up of 2.4 ± 2.1 years (range, 0.5 to 6).

RESULTS: The average age of the patients was 57 ± 14 years. The preoperative peak LVOTO was 137 ± 45 mm Hg. The average degree of mitral regurgitation was 3.1. The average length of stay was 7.5 ± 3.3 days. There were no readmissions or deaths in the group. Initial postoperative transesophageal echocardiography demonstrated marked reduction in LVOTO to 10 ± 17 mm Hg (p < 0.0001) and significant improvement in mitral regurgitation to 0.2 (p < 0.0001). In follow-up, the LVOT gradient remained low at 6 ± 14 (p > 0.0001) and mitral regurgitation remained insignificant at 0.4 (p < 0.0001).

CONCLUSIONS: Anterior leaflet plication and papillary muscle release are logical adjuncts to septal resection in the treatment of the complicated pathophysiology of obstructive HCM. Durable long-term results can be achieved with an aggressive approach to mitral valve pathology in conjunction with extended myectomy.

	Introduction

Top Abstract Introduction Patients and Methods Results Comment References

 
The treatment of hypertrophic cardiomyopathy (HCM) has classically involved septal myectomy as described by Morrow [1]. This decrease in transaortic septal cross-section reduces the outflow tract gradient and improves clinical symptoms [1]. However, difficulty of repair in terms of exposure, imprecision in the amount of septum to remove, and abnormalities of the mitral valve leaflets have resulted in the use of alternative operative techniques with variable results. These have included mitral valve replacement, mitral valve repair, or a combination of myectomy with these other procedures [2–6]. The addition of these techniques emphasizes the historic importance of the mitral valve in outflow tract obstruction.

Over the years, knowledge of the true pathophysiology of left ventricular outflow tract obstruction (LVOTO) has expanded. We now understand that LVOTO is a dynamic process, with the mitral valve playing an important role in outflow tract obstruction [7–13]. Pathology specimen and echocardiographic data demonstrate that the mitral leaflets in HCM are enlarged and positioned anteriorly within the left ventricular cavity [7, 8]. This anterior positioning, in addition to septal hypertrophy, causes a crucial overlap of the inflow and outflow portions of the left ventricle, resulting in systolic anterior motion of the mitral valve with mitral-septal contact [8–14]. The enlarged mitral leaflets, chordal slack, and anterior position of the mitral valve interact with an LV ejection stream that is altered by the septal bulge, resulting in the mitral valve being pushed into the septum [8–14]. It is for this specific morphology that plication of the anterior leaflet has been utilized to decrease redundancy [14, 15].

In addition, we now know there are abnormal connections in the subvalvular mitral apparatus that bind the papillary muscles to the anterior left ventricular wall [16, 17]. Release of these connections and reduction of the papillary muscle diameter allows the mitral leaflets to resume a more normal posterior position [16, 17]. This addresses another element of LVOTO. Based on flow drag pathophysiology as the dominant hydrodynamic force on the leaflet [14], our group has devised a three-step repair (resection-plication-release [RPR]) for HCM that corrects all aspects of the complex dynamics of obstruction.

	Patients and Methods

Top Abstract Introduction Patients and Methods Results Comment References

 
Study Group/Patient Selection
Between 1997 and 2003, 19 patients underwent RPR repair for obstructive HCM at St. Luke’s-Roosevelt Hospital Center. This group was selected from an HCM population of approximately 250 patients, the vast majority of whom are treated only medically to reduce their gradient and alleviate symptoms. According to our protocol, those patients with symptomatic obstruction are given an aggressive trial of pharmacologic therapy initially. Patients are first begun on ß-blockers with gradual increase in dose titrated to a heart rate of 55 to 60 beats per minute. If symptoms and the gradient persist, we usually add disopyramide as a second agent in the controlled release form at 250 or 300 mg two times a day [17]. Patients who cannot tolerate ß-blockers or disopyramide are given a trial of verapamil. Patients who fail this combination are referred for surgical therapy unless they have significant comorbidity that increases their risk of surgery: age more than 70 years, chronic obstructive pulmonary disease, diabetes mellitus, or neurologic, renal, or hepatic dysfunction. Such patients are offered alcohol ablation or dual-chamber pacing. We restrict surgery to patients with high gradients at rest who fail medical therapy.

Echocardiography
Transthoracic echocardiography (TTE) was performed before admission for assessment of gradient, septal and anterior wall thickness to plan the extent of resection, exclude anomalies of the papillary muscles, and to exclude calcification and immobility of the mitral leaflets that might require mitral valve replacement [13]. Echocardiographic gradients were not redone in any systematic fashion. The distance between the aortic annulus and the area of mitral-septal contact was carefully measured in diastole. The distance from the aortic annulus to the far side of the septal bulge was measured to mark the furthest extent of the myectomy into the left ventricle. Mitral valve structure and function were also assessed preoperatively in an outpatient setting. Heavy leaflet calcification, immobility, prolapse, and a central or anteriorly directed mitral regurgitation (MR) jet were used as criteria for valve replacement.

Transesophageal echocardiography (TEE) was performed on all patients preoperatively to remap the location and extent of septal hypertrophy, assess mitral valve function, measure LVOT gradients, and evaluate MR. The degree of MR was scored based on the following: trivial = 1, mild = 2, moderate = 3, severe = 4. The decision to proceed with an RPR repair was made preoperatively based on TTE characteristics but was subject to change based on intraoperative TEE and operative findings. This involved an integrated assessment of the extent of systolic anterior motion, the size of the mitral valve, the slack and redundancy of the mitral valve as assessed by direct visualization, and the presence of abnormal papillary muscle attachments.

Operative Technique
A standard median sternotomy was performed and patients were placed on cardiopulmonary bypass using moderate hypothermia. The aorta was cross-clamped, and anterograde and retrograde cold crystalloid cardioplegia was delivered. After transverse aortotomy and retraction of the aortic valve leaflets, the extent of septal hypertrophy was directly evaluated.

Extended septal myectomy was performed as previously described by Messmer [16]. This procedure involves a more aggressive resection than that done by Morrow [1]. A trefoil hook was utilized to define the anterior/posterior direction and stabilize the muscle. The extent of resection was defined by preoperative TEE when detailed measurements were made in order to ensure adequate length of resection into the LV cavity. Two parallel incisions were made into the bulge and connected to remove the muscle mass. Further resection was performed after careful palpation of the septum and estimating residual ventricular mass. The largest segment of septum typically was best removed on the initial excision (Fig 1, Resection).

View larger version (77K): [in this window] [in a new window]   Fig 1. Resection: A trefoil retractor is used to grasp the septal bulge to allow stabilization and a more complete resection of the septum. Resection of the ventricular septum has evolved to include extended resection deep into the ventricular cavity. It is important to plan the length of septal myectomy preoperatively with detailed measurement by transthoracic echocardiography and transesophageal echocardiography. Resection of the area just proximal to the aortic annulus is avoided; rather, resection is focused on the anterior septum beginning 1 cm below the aortic annulus. The midseptal bulge often extends as much as 4 cm toward the base of the papillary muscles based on preoperative echocardiograms. The goal of the resection should be not only to increase the size of the outflow tract but also to redirect flow anterior and medially, away from the mitral valve. Indeed, the three components of the RPR (resection-plication-release) operation are designed to separate the inflow and outflow portions of the left ventricle that pathologically overlap in obstructive hypertrophic cardiomyopathy.

View larger version (74K): [in this window] [in a new window]   Fig 2. Plication: To decrease redundancy, horizontal plication of the anterior leaflet is performed using interrupted prolene sutures. Transaortic anterior mitral leaflet plication, as described here, has several advantages as a concomitant procedure. It specifically addresses underlying mechanisms of systolic anterior motion: redundancy of the mitral leaflet and chordal slack. Based on preoperative echocardiography, the presence of an enlarged, floppy anterior leaflet may be diagnosed and treated with this horizontal plication.

View larger version (72K): [in this window] [in a new window]   Fig 3. Release: Careful examination of the papillary muscles is performed. The hypertrophic cardiomyopathy disease process can result in abnormal connections between the anterior papillary muscles and the anterior free wall. This abnormal connection displaces the mitral leaflets into the outflow tract. Sharp and blunt dissection of these connections releases the anterior papillary muscle (inset), allowing the valve to fall back into the left ventricular cavity explicitly out of the flow stream.

View larger version (73K): [in this window] [in a new window]   Fig 4. Preoperative and postoperative transesophageal long-axis echocardiograms of a 46-year-old hypertrophic cardiomyopathy patient with severe left ventricle outflow tract obstruction and a preoperative gradient greater than 100 mm Hg. (Top) Preoperatively, significant left ventricular outflow tract obstruction is shown with an elongated floppy anterior mitral leaflet. (AV= aortic valve; LA= left atrium; LV= left ventricle; MV= mitral valve; PRE CPB= before cardiopulmonary bypass.) (Bottom) Postoperative view after extended myectomy, plication of the anterior leaflet, and release of papillary muscles. (POSTCPB= after cardiopulmonary bypass.)

Statistical Analysis
All data were collected in a retrospective manner. Data are presented as mean ± standard deviation. The range of data is also presented. Continuous variables were compared using paired Student’s t test with significance accepted for p values of less than 0.05.

	Results

Top Abstract Introduction Patients and Methods Results Comment References

 
The patient group included 9 women (47%) and 10 men (53%) with a mean age of 56.9 ± 14 years. Common preoperative characteristics included coronary artery disease with history of myocardial infarction (37%), hypertension (42%), diabetes mellitus (21%), and nonsustained ventricular tachycardia (21%). Resting peak LVOTO as measured by echocardiography was 137 ± 44 mm Hg (range, 30 to 230 mm Hg). The mean degree of MR in this group was 3.1 (range, 1 to 4). All patients (100%) had systolic anterior motion present on preoperative TEE. The average ejection fraction was 59% ± 12% (range, 46% to 75%) with a preoperative New York Heart Association symptom class of 3.0 ± 0.9 (range, 2 to 4; Table 1).

All 19 patients underwent RPR repair as described above. Concomitant cardiac surgical procedures included coronary artery bypass grafting (n = 7), aortic valve replacement (n = 2), mitral ring annuloplasty (n = 1), and radiofrequency atrial ablation (n = 1). Average aortic cross-clamp time of all patients was 109 ± 31.8 minutes with a cardiopulmonary bypass time of 157 ± 48.1 minutes (Table 2). One patient was placed back on cardiopulmonary bypass after postoperative TEE demonstrated a persistent gradient. Additional resection of the septum and release of papillary muscles resulted in no detectable gradient or evidence of MR.

There were no deaths during the follow-up period. The average NYHA class at follow-up decreased significantly from 3.0 ± 0.9 to 1.56 ± 0.6 (range, 1 to 3; p < 0.0001). Most patients (18 of 19) remained on a regimen of ß-blockers postoperatively. None required disopyramide. Amiodarone was used in 2 patients (10%) postoperatively. No patient was rehospitalized for heart failure or required reoperation. One patient required placement of a permanent pacemaker for complete heart block. There were no other perioperative morbidities.

Average length of stay was 7.5 ± 3.3 days. The overall hospital stay was lengthened in 4 cases by the need for implantation of an internal defibrillator. The indication for insertion in 3 patients was syncope and preoperative ventricular arrhythmias, and for 1 patient it was ventricular fibrillation arrest with successful resuscitation. Devices were placed, according to our policy, 5 days after the operative procedure.

Initial postoperative TEE in the operating room demonstrated marked reduction in LVOTO gradient to 10 ± 18 mm Hg (range, 0 to 40; p < 0.0001). Significant improvement in mitral valve regurgitation to 0.2 (range, 0 to 1; p < 0.0001) was also demonstrated.

Follow-up (closing date June 2004) was available for all 19 patients (100%). A mean follow-up of 2.4 ± 2.1 years (range, 0.5 to 6) was obtained. There were no deaths during this period. Examination of the most recent echocardiographic data in 2004 for each patient (n = 19) demonstrates that LVOT gradients remained low at 6 ± 15 mm Hg (range, 0 to 51 mm Hg; p < 0.0001). The degree of mitral valve regurgitation remained stable as well, measuring 0.4 (range, 0 to 1; p < 0.0001).

	Comment

Top Abstract Introduction Patients and Methods Results Comment References

 
Hypertrophic cardiomyopathy occurs in 1 in 500 patients in the general population [18]. Left ventricle outflow tract obstruction occurs in approximately 25% of these patients to increase symptoms and worsen prognosis [19]. The pathophysiology of HCM was initially thought to result only from a thickened septum narrowing the LV outflow tract [14]. It is now understood that anterior motion of the mitral valve is a critical component of this complex disease process. It is flow drag, the pushing force of flow, that is the dominant hydrodynamic force resulting in obstruction [8–14]. systolic anterior motion of the anterior leaflet of the mitral valve causes both subaortic obstruction and loss of coaptation with the posterior leaflet, resulting in mitral valve insufficiency. Specific non-HCM leaflet pathology such as myxomatous changes and localized fibrosis may also occur and complicate the picture [14]. As our understanding of this pathology has evolved, we now know that deformity of the mitral valve apparatus and MR are not uncommon in HCM patients. Specifically, Klues and associates [7] determined that although 50% of mitral valves in HCM patients were normal, 44% demonstrated enlarged and elongated mitral valves leaflets in situ. In fact, mitral valve replacement to treat the problem of HCM has been used in the past, demonstrating marked improvement in both clinical symptoms and left ventricular functional parameters [5, 6]. However, the requirement of life-long anticoagulation and the possibility of prosthesis failure have made this an unattractive option. Others have suggested mitral valve repair with ring annuloplasty [20, 21]. Transatrial ring annuloplasty is easy to perform, but the results are inconsistent, as annular dilation is rarely the primarily cause of MR in HCM.

Reticence to increase the complexity of HCM surgery given the historical results of the Morrow procedure has led many authors to advocate septal resection alone as the sole treatment for HCM. A number of large studies over the past 30 years have described long-term follow-up of the surgical management of HCM with myectomy [22–25]. Many of these studies do not address the presence of MR and systolic anterior motion preoperatively and postoperatively, making it difficult to draw conclusions regarding the presence of associated mitral valve abnormalities [22–25]. These reports maintain that mitral valve repair or replacement was unnecessary unless significant structural valve disease was present.

The exact incidence of MR and systolic anterior motion after myectomy alone is thus difficult to determine. Kracjer and colleagues [6] reported a 30% incidence of postoperative MR after myectomy alone with a majority being moderate to severe. Williams and coworkers [26] in 1987 reported a 9% incidence of moderate to severe MR postoperatively with a number of patients (54%) found to have residual systolic anterior motion. The study by Heric and colleagues [22] of 178 HCM patients describes 60 patients with preoperative 3 to 4+ MR. The majority of these patients had myectomy alone with good results, but the report does describe 6 patients who required mitral valve replacement after myectomy owing to a significant gradient or severe MR in the presence of structurally normal mitral valves. However, more recently, Yu and colleagues [27] specifically examined MR and HCM to find that after myectomy alone, fewer than 20% of patients had mild MR, and none required additional mitral valve surgery. However, long-term follow-up was not reported in this patient population.

The addition of extended myectomy and full release of abnormal papillary muscle connections is supported through much of the recent literature [16, 17, 28]. We believe that since the mitral valve apparatus is a critical component of the HCM complex, its repair should be addressed during most HCM surgery. Mitral valve plication is not a new operation used to relieve systolic anterior motion and MR; it has been reported by separate groups besides ours [5, 15, 20, 21]. A recent review of surgical treatment of HCM acknowledged plication as a useful adjunct to myectomy in selected patients with elongated flexible mitral leaflets [28]. We believe, from our practice, that postoperative failures with residual MR and systolic anterior motion may occur more commonly outside of select institutions, but do not necessarily appear in the literature.

For obstructive HCM, the RPR operation-resect, plicate, release-individually addresses each component of the pathologic obstructive process of systolic anterior motion of the mitral valve. Necessary conditions for systolic anterior motion include anterior position of the mitral valve within the left ventricle, a positive angle of attack between LV ejection flow and the mitral valve (the flow stream hits the mitral valve from behind), and chordal slack [8–14].

It should be cautioned that HCM patients may occasionally demonstrate additional mitral valvular pathology apart from leaflet redundancy. This pathology includes calcification, fibrosis, prolapse, or anomalous insertion of the papillary muscle directly into the base or middle of the anterior leaflet without intervening chordae [7, 14]. Formal mitral valve evaluation by preoperative and intraoperative echocardiographic examination detects such mitral pathology and determines those patients who may be better treated with mitral repair or replacement.

Limitations of this study include its small size. Patient selection was based on the presence of HCM with a significant gradient in the presence of MR and systolic anterior motion. Not all of the patients who underwent septal myectomy for HCM at our institution underwent RPR repair; decision to perform the RPR repair was based on the presence of specific morphology as assessed by echocardiography and operative findings. The follow-up for these specific patients has been consistent and ranges over a period of 6 years.

Our study shows that patients may undergo a more complete repair of their HCM pathophysiology with low operative risk and durable results. Because of the small numbers involved, and a referral pattern based on specific morphology, this study was not randomized into groups with and without anterior leaflet plication. We believe that the pathophysiology of obstruction and the potential for residual MR and systolic anterior motion after the standard HCM operation in these select patients justifies these steps in a novel, safe procedure.

In conclusion, because the mitral apparatus is a critical component of the obstructive HCM complex, consideration of this repair should be addressed during HCM surgery. This three-step RPR repair may be a preferred method to comprehensively correct the complex pathophysiology that results in HCM.

View larger version (43K): [in this window] [in a new window]   Fig 5. Preoperative and postoperative parasternal diastolic long-axis transthoracic echocardiograms in a 44-year-old man with symptomatic drug-refractory obstructive hypertrophic cardiomyopathy. (Left) The preoperative images show septal hypertrophy and a large mitral valve anterior leaflet. (Right) The postoperative image shows a very small myectomy resection (arrow) predominantly localized in the area just below the aortic valve. The large anterior mitral leaflet remains.

	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): Sandhya K. Balaram Daniel G. Swistel Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Balaram, S. K. Articles by Swistel, D. G. Search for Related Content PubMed PubMed Citation Articles by Balaram, S. K. Articles by Swistel, D. G. Related Collections Valve disease