Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Circulation. 1995;92:122-127

This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schoendube, F. A.
Right arrow Articles by Messmer, B. J.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Schoendube, F. A.
Right arrow Articles by Messmer, B. J.

(Circulation. 1995;92:122-127.)
© 1995 American Heart Association, Inc.

Articles

Long-term Clinical and Echocardiographic Follow-up After Surgical Correction of Hypertrophic Obstructive Cardiomyopathy With Extended Myectomy and Reconstruction of the Subvalvular Mitral Apparatus

Friedrich A. Schoendube, MD, MS; Heinrich G. Klues, MD; Sebastian Reith, MD; Frank A. Flachskampf, MD; Peter Hanrath, MD; Bruno J. Messmer, MD

From the Department of Thoracic Cardiovascular Surgery (F.A.S., S.R., B.J.M.) and Medical Clinic I (H.G.K., F.A.F., P.H.), Klinikum RWTH Aachen, Germany.

Correspondence to PD, Dr Friedrich A. Schoendube, Department of Thoracic Cardiovascular Surgery, Klinikum RWTH Aachen, Pauwelsstr 30, D-52057 Aachen, Germany.


*    Abstract
up arrowTop
 *Abstract
down arrowIntroduction
 down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Background The standard surgical approach to hypertrophic obstructive cardiomyopathy (HOCM) was modified in the present series with a combination of extended myectomy with partial excision and mobilization of the papillary muscles.

Methods and Results Between 1979 and 1992, 58 patients (38 men and 20 women; mean age, 49±24 years) with HOCM were operated on with the use of this different technique. Their intraventricular gradients were 79±33 (±SD) mm Hg at rest and increased to 147±48 mm Hg with provocative maneuvers. Mild-to-moderate mitral regurgitation was present in 60% of the patients, and severe regurgitation was present in 5%. Ten patients required additional aortocoronary bypass graft surgery. Follow-up (mean, 84 months) was complete (100%). Hemodynamic improvement was documented by a significant (P<.01) decrease in left ventricular end-diastolic pressure from 19±9 to 14±6 mm Hg and reduction of basal outflow tract gradients to 5±7 mm Hg at rest and 16±24 mm Hg after provocation. Late mortality was 1.4% per patient-year, and no sudden cardiac deaths occurred during follow-up. Functional status was excellent for 84% of the patients; 8 patients were in New York Heart Association functional class III, and none were in class IV. Echocardiography revealed no outflow tract obstruction.

Conclusions Extended myectomy and reconstruction of the subvalvular mitral apparatus in HOCM result in excellent functional improvement with relief of outflow tract obstruction. The technique can be performed safely despite its more aggressive surgical nature and allows an individualized strategy depending on the patient's extent and distribution of left ventricular hypertrophy.


Key Words: valves • hypertrophy • cardiomyopathy • surgery • echocardiography


*    Introduction
up arrowTop
 up arrowAbstract
 *Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
The standard surgical technique to relieve left ventricular outflow tract obstruction in patients with hypertrophic obstructive cardiomyopathy is transaortic septal myotomy-myectomy.1 2 3 4 5 6 7 8 9 10 11 12 13 14 The rationale for this operation is based exclusively on the assumption that reduced left ventricular outflow tract cross-sectional area is the only, or at least the major, cause of dynamic obstruction.10 15 16 17 Partial resection of the basal ventricular septum obliterates or substantially reduces the basal outflow tract gradient in the vast majority of patients1 2 3 4 5 6 7 8 9 10 11 12 13 14 and thus improves their clinical status. A substantial subset of patients, however, demonstrate persistent obstruction at rest or during provocation or may not be suitable for this approach due to a limited degree of basal septal hypertrophy.8 18 19

A second surgical approach to the pathophysiological mechanisms of the disease concerns the mitral valve itself and consists of mitral valve replacement4 8 20 or, more recently, the combined use of myotomy-myectomy and mitral valve plication.19 These techniques have been applied with respect to the limitations of myotomy-myectomy. Comparable results in reported series indicate that the mitral valve apparatus can be a major component in the development of dynamic outflow tract obstruction. A recent systematic morphological analysis of the mitral valve in hypertrophic cardiomyopathy supported these assumptions and demonstrated significantly enlarged area and length of mitral leaflets in the majority of patients.21 However, long-term morbidity and prosthetic valve–related complications after mitral valve replacement represent a strong obstacle for this strategy.11

A third inroad into the problem that has not received much attention in the past is the contribution of the subvalvular mitral apparatus to the pathogenesis of obstruction with systolic anterior motion (SAM) of the mitral valve and concomitant mitral valve regurgitation. Although malpositioning and hypertrophy of the papillary muscles are well recognized as structural components of hypertrophic obstructive cardiomyopathy and recent studies in animals proved that displacement of papillary muscles can produce significant SAM and left ventricular outflow tract obstruction by itself,22 it is not clear to what extent these malformations of the subvalvular mitral apparatus are involved in patients with the disease. In this report, we describe the long-term results of a surgical approach with extension of myectomy to the left ventricular free wall with the use of a different technique23 24 and with mobilization and partial excision of papillary muscles, thus reconstructing the subvalvular mitral apparatus.


*    Methods
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 *Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Patient Selection and Characteristics
Between January 1979 and December 1992, 58 consecutive patients with obstructive hypertrophic cardiomyopathy underwent surgery for relief of significant left ventricular outflow tract gradients. Patient ages ranged from 15 to 73 years with a mean age of 49 years; 38 (66%) were male. The indication for surgery was based on a combination of the following findings: (1) left ventricular outflow tract peak systolic pressure gradient of >=50 mm Hg under basal conditions or with provocation (Valsalva maneuver, postextrasystolic potentiation, or amylnitrite inhalation); and (2) severe symptoms of exertional dyspnea, fatigue, chest pain, or episodes of impaired consciousness, including syncope, despite adequate and long-term medical treatment with sufficient doses of ß-blockers, verapamil, or both.25 26 27 28

All patients underwent cardiac catheterization before surgery. The majority (75%) had an additional preoperative transthoracic echocardiographic evaluation, including Doppler determination of outflow tract gradients. The most common symptoms were dyspnea (83%) and angina (60%); 44% of the patients reported frequent attacks of dizziness and vertigo, and one third (18 patients) had one or more episodes of syncope. Ninety-one percent of the patients were in New York Heart Association (NYHA) functional class III or IV. Ten patients had significant coronary artery disease and underwent simultaneous bypass surgery. One patient developed significant left ventricular outflow tract obstruction with severe symptoms after successful percutaneous transluminal coronary angioplasty of the circumflex coronary artery and subsequent improvement of left ventricular function. Two patients had chronicled atrial fibrillation before surgery.

Preoperative left ventricular outflow tract gradients under basal conditions were 79±33 mm Hg and increased to 147±48 mm Hg during provocative maneuvers such as amylnitrite inhalation, isoproterenol infusion, Valsalva maneuver, or postextrasystolic potentiation. Two thirds (60%) had mild-to-moderate mitral regurgitation and 5% had severe regurgitation during angiographic studies, believed to be secondary to the mechanisms of outflow obstruction. None of the patients had intrinsic mitral valve disease necessitating primary mitral valve replacement. Two patients received mitral valve reconstruction with modified Kay-Wooler plasty because of residual funnel shape distortion of the anterior leaflet due to high insertion of the papillary muscles. Implantation of a cardioverter-defibrillator was performed simultaneously in one patient due to sustained ventricular tachycardias with repeated episodes of syncope.

Surgical Technique
In patients with significant coronary artery disease, bypass surgery was performed first using standard techniques. All other concomitant surgical interventions were done after relief of the left ventricular obstruction. After institution of cardiopulmonary bypass and cardioplegic arrest at the level of hypothermia (26°C), the basal septum was exposed through an aortotomy. The exact extent of hypertrophy was then assessed by visual inspection and digital palpation. After insertion of a sharp triple-hook retractor to the deepest point of the hypertrophied basal septum, this muscle mass was pulled anterior into the view of the surgeon. A deep myectomy was created by cutting into the direction of the prongs of the retractor. This modified technique enables the surgeon to extend the myectomy deep into the left ventricle and to the left ventricular wall and prevents creation of a ventricular septal defect. In this way, most of the tissue is removed from the deepest point of the basal septum. Also, this myectomy leaves a muscular ring of 2 to 3 mm under the aortic annulus, thus preventing aortic insufficiency. In addition, creation of a large and deep left ventricular outflow tract trough improves access to the deeper structures of the left ventricle. Both papillary muscles are then mobilized down to the apex, and all hypertrophied portions and muscular trabeculae are resected. Excellent overview is mandatory for this part of the operation to ensure safe resection. At the end of the procedure, both papillary muscles should be clearly separated from the wall and from each other in the middle of the ventricle. Right ventricular excisions are performed if necessary from a right ventriculotomy; closure is then done directly or by patch enlargement. More details of the surgical procedures were described recently elsewhere.23 24

Follow-up
Early follow-up was performed in all patients after 6 months for documentation of the initial surgical result and clinical status. Only a subset of the first consecutive 22 patients underwent cardiac catheterization at this time for evaluation of hemodynamic results, including measurements of left ventricular outflow tract gradients at rest and during provocation. Patients operated on after 1983 did not undergo repeated invasive studies, as echocardiography as a noninvasive method had become the routine diagnostic technique to study the morphological and hemodynamic results after extended myectomy. Long-term results were obtained by restudying all patients in 1993 (closing date, November 1993) at our hospital by an experienced cardiologist (Dr Klues) and encompassed a total of 406 patient-years (range, 1 to 174 months; mean, 84 months).

Echocardiography
Transthoracic presurgical two-dimensional echocardiograms were available in 24 of the 58 patients (41%). Postsurgical echocardiographic studies were performed during the latest clinical follow-up in 49 of 50 survivors (98%). Two-dimensional echocardiographic images were obtained in a number of cross-sectional planes by using standard transducer positions as previously described. All studies were recorded on videotape for later off-line analysis. Cardiac dimensions were measured from M-mode echocardiograms according to the recommendations of the American Society of Echocardiography,29 30 including the degree of SAM. In addition, careful continuous-wave and pulsed Doppler tracings were obtained from an apical position so we could study postoperative flow characteristics in the left ventricular outflow tract. Regurgitant jets were visualized by color flow imaging from the appropriate positions. The last five patients in our series were also studied with presurgical and postsurgical transesophageal echocardiography using a multiplane transesophageal probe (Hewlett Packard). In these patients, great care was taken to visualize presurgical and postsurgical anatomic position and morphology of the papillary muscles and mitral valve, usually from a transgastric short-axis (0° rotation) and long-axis (90°) view.

Statistical Analysis
Data are given as mean±1 SD values. Differences between continuous variables were determined with the paired Student's t test where appropriate. Life-table estimates of patient survival were calculated with the Kaplan-Meier method.31 Calculations were performed with STATISTICAL ANALYSIS SYSTEM software (SAS Institute).


*    Results
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
Hemodynamics
Hemodynamic data at initial follow-up (6 months after surgery) showed a significant decrease in left ventricular end-diastolic pressure from 19±9 mm Hg before surgery to 14±6 mm Hg after surgery (P<.01). Simultaneous registration of intraventricular and aortic systolic pressure showed a resting gradient of zero for 70% of these patients and gradients of 5 to 27 mm Hg for the remaining 30%, with a mean postsurgical gradient of 5±7 mm Hg. Provocative gradients were slightly higher, with a mean of 16±24 mm Hg. The individual changes in left ventricular outflow tract gradients at rest and during provocation of this subset of patients are shown in Figs 1Down and 2Down.



View larger version (22K):
[in this window]
[in a new window]
  		Figure 1. Plot showing individual changes in left ventricular outflow tract gradients at rest from 22 patients studied before (PRE-OP) and after (POST-OP) surgery.



View larger version (17K):
[in this window]
[in a new window]
  		Figure 2. Plot showing individual changes in left ventricular outflow tract gradients with provocation from 17 patients studied before (PRE-OP) and after (POST-OP) surgery.

Clinical State
Perioperative mortality (<30 days) was 0%. Two patients died before the initial 6-month follow-up—1 during the initial hospital course 45 days after surgery due to septic multiorgan failure and 1 at 2 months after surgery after hospital discharge due to chronic respiratory failure. Perioperative complications included one transient cerebrovascular accident with full recovery during the hospital stay. Three patients (5%) required permanent pacemaker therapy due to total atrioventricular block after surgery; 2 of them presented with right bundle-branch block before surgery. All perioperative complications were nonfatal and caused no long-term morbidity. Ninety percent of the patients (52 of 58) were in functional class III or IV before surgery. At the initial follow-up, 93% (52 of 56) were in functional class I or II; 31 (53%) improved by two or three functional classes (Fig 3Down). Three of the 4 patients who were in class III 6 months after surgery had severe preoperative symptoms corresponding to functional class IV with dyspnea at rest; only 1 did not improve and remained in functional class III.



View larger version (28K):
[in this window]
[in a new window]
  		Figure 3. Flowchart demonstrating changes in symptomatic state (New York Heart Association functional class) in 58 patients with hypertrophic obstructive cardiomyopathy. Preoperative (PRE-OP) and follow-up data at 6 months after surgery (Initial) and after 84 months (range, 1 to 174) (Long-term) are shown.

Long-term follow-up (closing date, November 1993) comprised 406 patient-years (range, 1 to 174 months; mean, 84 months) and was available for all patients (56 of 56). During this time period, 6 patients died due to congestive heart failure (5) or myocardial infarction (1). Four of these 6 patients were initially in functional class IV. There was no sudden cardiac death during the follow-up period. The linearized annual mortality rate was 1.4% per year (7 of 56); the 10-year survival rate was 86±7%. The actual survival statistics calculated with the Kaplan-Meier method are given in Fig 4Down. The clinical state during late follow-up was still excellent, with 84% (42 of 50) of the survivors in functional class I or II (NYHA). Six patients (12%; 6 of 50) had changed to functional class III; all of them had increasing signs of congestive heart failure. None of the patients were in functional class IV during the latest follow-up. Chronic atrial fibrillation was present in 3 patients (6%).



View larger version (11K):
[in this window]
[in a new window]
  		Figure 4. Actuarial survival proportion (Kaplan-Meier method). Mean follow-up was 84 months.

Echocardiography
Measurements of preoperative ventricular septal thickness were available for 24 patients (41%) and ranged from 15 to 33 mm (25±5 mm). Postoperative septal thickness during the latest clinical follow-up was obtained for 49 of 50 patients (98%) and ranged from 8 to 22 mm (13±4 mm). Direct comparison of those patients in whom both measurements were available showed a significant decrease (P<.001). All patients studied before surgery had severe SAM of the mitral valve with prolonged mitral valve septal contact (3/4+). From the 49 patients studied after surgery, 5 (10%) had trivial SAM (1+); the remaining 90% of the follow-up patients had no SAM. Doppler studies in all of them revealed no flow acceleration at the midcavity level or within the outflow tract; therefore, there was no persistent outflow tract obstruction at rest. By color flow Doppler, 8 (16%) patients had mild aortic regurgitation; the remaining 41 (84%) demonstrated no regurgitation. Mild mitral regurgitation (I°) was present in 18 of 49 patients (37%), but no significant mitral regurgitation occurred. Examples of echocardiographic visualization of the morphological results at long-term follow-up are given in Fig 5Down.



View larger version (130K):
[in this window]
[in a new window]
  		Figure 5. Composition of presurgical and postsurgical transthoracic (AI and AII) and transesophageal (BI and BII and CI and CII) echocardiographic studies from two patients with hypertrophic obstructive cardiomyopathy undergoing extended myectomy and reconstruction of the subvalvular mitral apparatus. AI, Preoperative transthoracic parasternal long-axis view with typical asymmetrical septal hypertrophy. AII, Postoperative study of the same patient; a large, S-shaped myectomy trough was created extending deep into the left ventricle, far beyond the tip of the mitral valve leaflets. Of note, a muscular ring is left under the aortic annulus to prevent aortic regurgitation and ventricular septal perforation. BI, Preoperative transgastric long-axis view (90° rotation) with optimized angulation to visualize the subvalvular apparatus. Both papillary muscles are hypertrophied and almost completely agglutinated onto the left ventricular wall (arrows), especially the anterolateral papillary muscle. The chordae tendinae are short, and there is almost direct continuity with the mitral valve leaflets. BII, Postoperative images from the same view. Both papillary muscles are mobilized from the ventricular wall, allowing a more central position. CI, Preoperative transgastric short-axis view (0° rotation). Both papillary muscles are largely hypertrophied and almost completely incorporated into the global left ventricular musculature. The left ventricular cavity appears small even during end-diastole. CII, Postoperative image; both papillary muscles are mobilized by circumferential incisions (arrows) and clearly separated from each other (large arrows). Global size of the papillary muscles appears smaller, and the left ventricular cavity size appears larger. LV indicates left ventricle; Ao, aorta; LA, left atrium, and MV, mitral valve.


*    Discussion
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
The most prominent morphological feature in hypertrophic obstructive cardiomyopathy is asymmetrical basal ventricular septal hypertrophy.6 14 32 33 Consequently, partial septal myotomy-myectomy appeared to be the surgical strategy of choice to relieve outflow gradients and symptoms in these patients.1 2 3 4 5 6 7 8 9 10 11 12 13 14 Although this technique has been effective in the vast majority of patients, several limitations have been identified over the past 2 decades, including mild hypertrophy (septal thickness <18 mm), unfavorable distribution of hypertrophy, and, recently, abnormalities of the mitral valve leaflets.8 19 As an alternative strategy to circumvent these limitations, mitral valve replacement was successfully used in abolishing outflow obstruction.4 8 20 Long-term complications of prosthetic mitral valve replacement such as thrombosis, thromboembolism, and hemorrhage due to anticoagulation, however, impede general recommendation of this strategy. Recently, a combination of myotomy-myectomy and mitral valve plication was applied to minimize the risk of persistent outflow tract obstruction after simple myectomy, especially when the mitral valve, in the judgment of the surgeon, appeared to be enlarged and hypermobile.19 This technique simultaneously approaches two of the major components of left ventricular outflow tract obstruction: septal hypertrophy and mitral leaflets.16 34 35 36 A third component—the subvalvular apparatus—although earlier described in the disease,17 37 has in large part been ignored, most likely due to the fact that its role in producing SAM of the mitral valve was long undefined. A recent study in animals, however, could prove that anterior displacement of the papillary muscles is capable of producing SAM even in the absence of septal hypertrophy,22 indicating their role as a component of outflow tract obstruction in hypertrophic cardiomyopathy.

In the present report, we describe an alternative surgical technique with modified and extended myectomy combined with reconstruction of the subvalvular mitral valve apparatus by partial excision and mobilization of the papillary muscles. This comprehensive technical approach represents a major deviation from previous techniques in several aspects.

Modified and Extended Myectomy
The success of standard myectomy is obviously limited by the technical difficulty in clearly exposing the entire extent of septal hypertrophy into the view of the surgeon, often leading to insufficient resection or to perforation of the subaortic ventricular septum, creating ventricular septal defect. To improve the surgeon's view and ensure complete longitudinal resection, a sharp triple-hook retractor is inserted to the deepest point of septal hypertrophy and then pulled forward. This technique allows safe resection of the exposed muscle bar, leaving a 2- to 3-mm subaortic ring and thus preventing development of significant aortic regurgitation.

Subvalvular Reconstruction
Careful inspection of the subvalvular mitral apparatus during surgery showed that in hypertrophic cardiomyopathy papillary muscles are not only hypertrophied but also malattached to the lateral ventricular wall, thus pulling actively the anterior mitral valve leaflet against the septum or at least into the high-flow outflow tract jet. Therefore, from the surgical point of view, the malposition of the papillary muscles appears to be a common and relevant component of mitral valve SAM and thus responsible for a certain amount of left ventricular outflow tract obstruction. Consequently, mobilization to the apex of the ventricle and resection of hypertrophied portions including trabeculae led to a more physiological restoration of their anatomic positions within the left ventricle, allowing the mitral valve leaflets to swing away from the high-flow bloodstream in the outflow tract.

The beneficial results of this modified technique could be demonstrated by transthoracic echocardiographic studies during the latest clinical follow-up. None of the patients had persistent SAM of the mitral valve or increased outflow tract flow velocities or developed significant aortic or mitral valvular regurgitation. These results can be attributed to morphological findings, as the shape of the trough, created by our technique, clearly deviates from findings after standard myectomy. The classic Morrow resection results in a rectangular defect starting directly under the aortic annulus and reaching just below the tip of the mitral leaflets, and the thinnest portion of the septum is usually directly below the aortic valve. In contrast, the shape of the trough created by the modified myectomy reaches far below the tip of the mitral valve leaflets down to the midcavity level and results in a more evenly distributed thinning of the ventricular septum (Fig 5Up, AI and AII). A subaortic muscular ring is always preserved at the level where the standard myectomy would usually leave the thinnest portion of septum with the risk of creating an intraoperative ventricular septal defect (Fig 5Up, AII). Changes in left ventricular geometry and papillary muscle function after subvalvular reconstruction are more difficult to detect with standard echocardiography due to its complex three-dimensional appearance. Stop-frame images in Fig 5Up (CI and CII) show the different positions and sizes of the papillary muscles and enlargement of the left ventricular cavity after surgery.

Early series with standard myotomy-myectomy were burdened with a high surgical mortality (10% to 15%), which decreased in most series over the past decades. With our technique, perioperative mortality was 0%. Two patients died during early and six patients died during long-term follow-up, resulting in an annual mortality rate of 1.4%. This result appears to be slightly better than reported annual mortality rates of 2.2% to 4.4%38 ; furthermore, there has been no sudden cardiac death in this series. Concomitant surgical procedures, mainly coronary artery bypass graft surgery, previously described as a significant risk factor for higher surgical mortality (18%),39 did not influence early or late mortality in our series.

Surgical correction of severe hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus was associated with substantial hemodynamic and clinical improvement in the patients during early and late follow-up. Basal left ventricular outflow tract gradient was reduced from 79±33 to 5±7 mm Hg, and provocable gradients were either low or not associated with clinical impairment. The vast majority of the survivors (85%) remained in functional class I or II compared with before surgery, with 90% of patients in functional class III or IV. Similar functional improvements have been reported in other recent series using standard myotomy-myectomy.3 5 7 13 38 The higher incidence of surgical complications with the Morrow procedure, however, indicates a clear advantage of our technique in several aspects. First, none of the patients developed significant incompetence of the aortic valve, which is a common complication of standard myotomy-myectomy40 and is reported to be moderate in 11% to 59% and moderately severe in 3%.1 13 Second, none of the patients had significant postsurgical mitral regurgitation or required primary mitral valve replacement, although three patients had a thin basal left ventricular septum (<18 mm) with severe obstruction, usually considered an indication for primary valve replacement.8 In contrast, the rate of severe mitral regurgitation after standard myotomy-myectomy can be as high as 11%.5 Third, surgical ventricular septal defect occurs in 3% of patients with standard myotomy-myectomy,13 but none of our patients developed defects despite the more aggressive muscular excision.

Only 3 patients (6%) had chronic atrial fibrillation at the latest follow-up, which is in contrast to the rate in the literature of 33% with standard myotomy-myectomy.1 As the new onset of atrial fibrillation in patients with hypertrophic obstructive cardiomyopathy is known to be mainly caused by increased impairment of diastolic ventricular function, this result may also reflect advantages of the presented technique in providing sustained relief of the left ventricle. Permanent pacemaker therapy due to total atrioventricular block was necessary in 3 of 58 patients (5%), which is a slightly higher rate than in other previous series (3%).1 5 13 All occurred among the first 15 patients and could be prevented by placing the medial incision directly underneath the right coronary artery at the nadir of the aortic cusp. Even though total atrioventricular block remains a relevant surgical complication, it should not be considered a major drawback to a surgical approach that has excellent long-term results, especially as double-chamber pacing, including ablation of the atrioventricular node, is reported to be a possible alternative therapeutic strategy in hypertrophic obstructive cardiomyopathy.41

The mechanisms of outflow obstruction in hypertrophic obstructive cardiomyopathy are undoubtedly complex, involving asymmetrical hypertrophy of different left ventricular segments, enlargement of mitral valve leaflets, malposition of hypertrophied papillary muscles, and an increase in outflow tract jets. Surgical approaches to the disease were directed to either basal septal hypertrophy or the mitral valve itself, with the described surgical and long-term risks. The present technique represents a comprehensive surgical approach incorporating several different pathomechanisms of outflow obstruction, namely, septal hypertrophy and malposition of the mitral valve apparatus. In addition, the modified and extended myectomy technique reduces surgical risks of ventricular septal defect and aortic regurgitation despite its more aggressive nature. It is therefore clearly applicable in all patients with severely symptomatic HOCM, and the greatest advantages should occur in patients with mild hypertrophy, in whom standard myotomy-myectomy often leads to insufficient resection with persistent obstruction or ventricular septal defect.


*    References
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
up arrowResults
up arrowDiscussion
*References
 

  1. Beahrs MM, Tajik AJ, Seward JB, Giuliani ER, McGoon DC. Hypertrophic obstructive cardiomyopathy: ten to 21-year follow-up after partial septal myectomy. Am J Cardiol. 1983;51:1160-1166. [Medline] [Order article via Infotrieve]
  2. Bigelow WG, Trimble AS, Wigle ED. The treatment of muscular subaortic stenosis. J Thorac Cardiovasc Surg. 1974;68:384-392. [Medline] [Order article via Infotrieve]
  3. Bircks W, Schulte HD. Surgical treatment of hypertrophic obstructive cardiomyopathy with special reference to complications and to atypical hypertrophic obstructive cardiomyopathy. Eur Heart J. 1983;4(suppl F):187-190.
  4. Cooley DA, Leachman RD, Hallman GL. Idiopathic hypertrophic subaortic stenosis: surgical treatment including mitral valve replacement. Arch Surg. 1971;103:606-612. [Medline] [Order article via Infotrieve]
  5. Krajcer Z, Leachman RD, Cooley DA, Coronado R. Septal myotomy-myectomy versus mitral valve replacement in hypertrophic cardiomyopathy. Circulation. 1989;80(suppl I):I-57-I-64.
  6. Maron BJ, Bonow RO, Cannon RO, Leon MB, Epstein SE. Hypertrophic cardiomyopathy: interrelations of clinical manifestations, pathophysiology, and therapy. N Engl J Med. 1987;316:780-789(pt I), 844-852(pt II). [Medline] [Order article via Infotrieve]
  7. Maron BJ, Epstein SE, Morrow AG. Symptomatic status and prognosis of patients after operation for hypertrophic obstructive cardiomyopathy: efficacy of ventricular septal myotomy and myectomy. Eur Heart J. 1983;4(suppl F):175-185.
  8. McIntosh CL, Maron BJ. Current operative treatment of obstructive hypertrophic cardiomyopathy. Circulation. 1988;78:487-495. [Medline] [Order article via Infotrieve]
  9. Morrow AG, Braunwald E. Functional aortic stenosis: a malformation characterized by resistance to left ventricular outflow without anatomic obstruction. Circulation. 1959;20:181-189. [Medline] [Order article via Infotrieve]
  10. Morrow AG, Reitz BA, Epstein SE. Operative treatment in hypertrophic subaortic stenosis: techniques and the results of pre- and postoperative assessments in 83 patients. Circulation. 1975;52:88-102. [Medline] [Order article via Infotrieve]
  11. Roberts WC. Operative treatment of hypertrophic obstructive cardiomyopathy: the case against mitral valve replacement. Am J Cardiol. 1973;32:377-381. [Medline] [Order article via Infotrieve]
  12. Schulte HD, Lösse B, Bircks W. Surgical technique in subvalvular and midventricular hypertrophic obstructive cardiomyopathy. In: Ghosh P, Unger F, eds. Cardiac Reconstruction. Berlin/Heidelberg, Germany: Springer; 1989:300-307.
  13. TenBerg JM, Maarten JS, Knaepen PJ, Ernst SM, Vermeulen FE, Jaarsma W. Hypertrophic obstructive cardiomyopathy: initial results and long-term follow-up after Morrow septal myectomy. Circulation. 1994;90:1781-1785. [Medline] [Order article via Infotrieve]
  14. Wigle ED, Sasson Z, Henderson MA. Hypertrophic cardiomyopathy: the importance of the site and extent of hypertrophy. Prog Cardiovasc Dis. 1985;28:1-83. [Medline] [Order article via Infotrieve]
  15. Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). Am J Cardiol. 1975;35:337-345. [Medline] [Order article via Infotrieve]
  16. Spirito P, Maron BJ. Pattern of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: assessment by two-dimensional echocardiography. Am J Cardiol. 1984;54:1039-1096. [Medline] [Order article via Infotrieve]
  17. Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. Am Heart J. 1987;113:633-644. [Medline] [Order article via Infotrieve]
  18. Klues HG, Roberts WC, Maron BJ. Anomalous insertion of papillary muscle directly into anterior mitral leaflet in hypertrophic cardiomyopathy. Circulation. 1991;84:1188-1197. [Medline] [Order article via Infotrieve]
  19. McIntosh CL, Maron BJ, Cannon RO, Klues HG. Initial results of combined anterior mitral leaflet plication and ventricular septal myotomy-myectomy for relief of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy. Circulation. 1992;86(suppl II):II-60-II-67.
  20. Cooley DA, Wukasch DC, Leachman RD. Mitral valve replacement for idiopathic hypertrophic subaortic stenosis: results in 27 patients. J Thorac Cardiovasc Surg. 1976;17:380-387.
  21. Klues HG, Maron BJ, Dollar AL, Roberts WC. Diversity of structural mitral valve alterations in hypertrophic cardiomyopathy. Circulation. 1992;85:1651-1660. [Medline] [Order article via Infotrieve]
  22. Levine RA, Vlahakes GJ, Lefebvre X, Guerrero JL, Cape EG, Yoganathan AP, Weyman AE. Papillary muscle displacement causes systolic anterior motion of the mitral valve. Circulation. 1995;91:1189-1195. [Medline] [Order article via Infotrieve]
  23. Messmer BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg. 1994;58:575-577. [Abstract]
  24. Schoendube FA, Klues HG, Reith S, Messmer BJ. Surgical correction of hypertrophic obstructive cardiomyopathy with combined myectomy, mobilisation and partial excision of the papillary muscles. Eur J Cardiol Thorac Surg. 1994;8:603-608. [Abstract]
  25. Adelman AG, Shah PM, Gramiak R, Wigle E. Long-term propranolol therapy in muscular subaortic stenosis. Br Heart J. 1970;32:804-811. [Abstract/Free Full Text]
  26. Flamm MD, Harrison DC, Hancock EW. Muscular subaortic stenosis: prevention of outflow obstruction with propranolol. Circulation. 1968;29:846-858.
  27. Kaltenbach M, Hopf R, Kober G, Bussmann WD, Keller M, Petersen Y. Treatment of hypertrophic obstructive cardiomyopathy with verapamil. Br Heart J. 1979;42:35-42. [Abstract/Free Full Text]
  28. Rosing DR, Idanpaan-Heikkila U, Maron BJ, Bonow RO, Epstein SE. Use of calcium channel blocking drugs in hypertrophic cardiomyopathy. Am J Cardiol. 1985;55:185B-195B. [Medline] [Order article via Infotrieve]
  29. Sahn DJ, De Maria A, Kisslo J, Weyman A. The Committee on M-Mode Standardization of the American Society of Echocardiography recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic methods. Circulation. 1978;58:1072-1083. [Medline] [Order article via Infotrieve]
  30. Tajik AJ, Seward JB, Hagler DJ, Maier DD, Lie JT. Two-dimensional real-time ultrasonic imaging of the heart and great vessels. Mayo Clin Proc. 1978;53:271-303. [Medline] [Order article via Infotrieve]
  31. Kaplan E, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc. 1958;53:475-481.
  32. Brock R. Functional obstruction of the left ventricle (acquired aortic subvalvular stenosis). Guy's Hosp Rep. 1957;106:221-238. [Medline] [Order article via Infotrieve]
  33. Goodwin JF, Hollman A, Cleland WP, Teare D. Obstructive cardiomyopathy simulating aortic stenosis. Br Heart J. 1960;22:403-414.
  34. Maron BJ, Harding AM, Spirito P, Roberts WC, Waller BF. Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy. Circulation. 1983;68:282-293. [Medline] [Order article via Infotrieve]
  35. Moro E, ten Cate FJ, Hugenholtz PG, Roelandt J. Genesis of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an anatomical or dynamic event? Eur Heart J. 1987;8:1312-1321.
  36. Shah PM, Taylor RD, Wong M. Abnormal mitral valve coarction in hypertrophic obstructive cardiomyopathy: proposed role in systolic anterior motion of mitral valve. Am J Cardiol. 1981;48:258-262. [Medline] [Order article via Infotrieve]
  37. Reis RL, Bolton MR, King JF, Pugh DM, Dunn MI, Mason DT. Anterior-superior displacement of papillary muscles producing obstruction and mitral regurgitation in idiopathic hypertrophic subaortic stenosis: operative relief by posterior-superior realignment of papillary muscles following ventricular septal myectomy. Circulation. 1974;49/50(suppl II):II-181-II-188.
  38. Seiler C, Hess OM, Schoenbeck M, Turina J, Jenni R, Turina M, Krayenbühl HP. Long-term follow-up of medical versus surgical therapy for hypertrophic cardiomyopathy: a retrospective study. J Am Coll Cardiol. 1991;17:634-642. [Abstract]
  39. Siegmann IL, Maron BJ, Permut LC, MacIntosh CL, Clark R. Results of operation for coexistent obstructive cardiomyopathy and coronary artery disease. J Am Coll Cardiol. 1989;13:1527-1533. [Abstract]
  40. Sasson Z, Prieur T, Skrobik Y, Folup JC, Williams WG, Henderson MA, Gresser C, Wigle ED, Rakowski H. Aortic regurgitation: a common complication after surgery for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 1989;13:63-67. [Abstract]
  41. Fananapazier L, Epstein ND, Curiel RV, Panza JA, Tripodi D, McAreavey D. Long-term results of dual-chamber (DDD) pacing in obstructive hypertrophic cardiomyopathy. Circulation. 1994;90:2731-2742.[Medline] [Order article via Infotrieve]



This article has been cited by other articles:


Home page
 Eur Heart JHome page
M. Togni, M. Billinger, S. Cook, and O. M. Hess
Septal myectomy: cut, coil, or boil?
Eur. Heart J., February 1, 2008; 29(3): 296 - 298.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
B. J. Maron, J. A. Dearani, S. R. Ommen, M. S. Maron, H. V. Schaff, B. J. Gersh, and R. A. Nishimura
The case for surgery in obstructive hypertrophic cardiomyopathy
J. Am. Coll. Cardiol., November 16, 2004; 44(10): 2044 - 2053.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart J SupplHome page
U. Sigwart
Non-surgical myocardial reduction for patients with hypertrophic obstructive cardiomyopathy
Eur. Heart J. Suppl., October 1, 2001; 3(suppl_L): L38 - L42.
[Abstract] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schoendube, F. A.
Right arrow Articles by Messmer, B. J.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Schoendube, F. A.
Right arrow Articles by Messmer, B. J.

Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 1995 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.