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Ann Thorac Surg 2004;78:2118-2122
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

Septal Myectomy Results in Regression of Left Ventricular Hypertrophy in Patients With Hypertrophic Obstructive Cardiomyopathy

Subrato J. Deb, MDa, Hartzell V. Schaff, MDa,*, Joseph A. Dearani, MDa, Rick A. Nishimura, MDb, Steve R. Ommen, MDb

a Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota, USA
b Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA

Accepted for publication May 20, 2004.

* Address reprint requests to Dr Schaff, Division of Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA
schaff{at}mayo.edu

Presented at the Poster Session of the Fortieth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 26–28, 2004.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterized by ventricular hypertrophy that occurs in the absence of predisposing cardiovascular stimuli; approximately one quarter of patients with HCM will have left ventricular (LV) outflow tract obstruction. Transaortic septal myectomy relieves outflow gradients and improves symptoms, but the effect of operation on ventricular hypertrophy is not well defined.

METHODS: We reviewed 60 patients who underwent septal myectomy for obstructive HCM; all had complete two-dimensional and Doppler studies including calculation of LV mass and LV mass index before operation and after dismissal.

RESULTS: Before myectomy the mean LV outflow gradient was 67 ± 44 mm Hg, and at dismissal the mean LV outflow gradient was 12 ± 13 mm Hg (p < 0.004). We found a significant decrease in the LV mass and LV mass index that occurred early after operation and persisted beyond 2 years follow-up. The early decrease in LV mass was greatest in patients younger than 50 years, but patients of all ages benefited from extended septal myectomy with decrease in LV hypertrophy.

CONCLUSIONS: Transaortic septal myectomy results in significant decreases in LV mass and LV mass index. This favorable remodeling occurs early after operation and persists beyond 2 years. Whether the regression of LV mass continues to decrease or stabilize over time is unclear.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 References
 
Hypertrophic cardiomyopathy (HCM) is a genetic disorder with a wide spectrum of phenotypic expression and a prevalence of 1 in 500 among adults [1, 2]; it is the most common cause of sudden cardiac death in the young [3]. The morphology of HCM is highly variable. Most commonly, the hypertrophy is asymmetric and prominent in the ventricular septum; however, in some patients, the LV hypertrophy extends from the septum to the free walls resulting in concentric hypertrophy [4]. Indeed, most patients show a diffuse distribution of LV hypertrophy with or without septal prominence. Abnormal diastolic function in these patients with normal or reduced ventricular cavity size contributes to the development of heart failure.

In 25% to 50% of patients with HCM, enlargement of the septum coupled with systolic anterior motion (SAM) of the mitral valve will produce LV outflow obstruction [5, 6]. It is possible, then, that the underlying cardiomyopathy is worsened by further hypertrophy in response to LV outflow obstruction. In some patients, symptoms may progress as a result of this cycle of septal hypertrophy causing LV outflow tract obstruction, which then produces further hypertrophy.

The issue of secondary hypertrophy (and its reversibility) in patients with hypertrophic obstructive cardiomyopathy (HOCM) is important because the magnitude of LV hypertrophy is an essential determinant of prognosis [7]. Recent studies have demonstrated that LV hypertrophy can regress after nonsurgical septal reduction therapy [8]. The purpose of our study was to determine if the LV mass regresses after successful extended septal myectomy in patients with HOCM.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Patient Selection
From January 1996 through December 2000, 309 patients underwent extended septal myectomy at the Mayo Clinic. Among this group, we identified 60 patients who had complete two-dimensional and Doppler echocardiographic examinations before surgical intervention and late after hospital dismissal. All 309 patients had follow-up echocardiograms; however, to be included in our study, patients had to have determination of LV mass by echocardiography before operation and during follow-up. For this investigation, we selected only patients who underwent transaortic myectomy for septal hypertrophy localized to the subaortic region. We excluded patients with disproportionate hypertrophy involving the apical or midventricular septum. We further excluded patients who had concomitant aortic valve stenosis or obstructive congenital lesions of the LV outflow tract.

Patient Characteristics
The study group consists of 33 women and 27 men with a median age of 47 years (range 21 to 77 years). Presenting symptoms included dyspnea on exertion in 56 patients (93%), decreased exercise tolerance in 27 (45%), angina in 22 (37%), syncope in 22 (37%), and palpitations in 11 patients (18%). Five patients (8%) had a family history of HCM. Preoperatively, median New York Heart Association functional class was III (range I to IV). Previous cardiac operation had been performed in 3 patients (5%); 2 patients had undergone previous septal myectomy, and 1 had undergone previous pulmonary valvotomy. One patient was 30 weeks pregnant at the time of operation, 1 patient had the diagnosis of LEOPARD syndrome [9], and 3 patients had a history of mitral valve endocarditis.

Almost all patients had medical management before operation; ß-blocker therapy was noted in 48 patients (80%), calcium-channel blockers in 27 (45%), and disopyramide in 5 (8%). Twenty-two patients (37%) were taking both ß-blockers and calcium-channel blockers. Thirty-seven patients (62%) were in sinus rhythm at operation and 7 (11%) in atrial fibrillation. Sixteen patients (27%) had a paced rhythm due to a previously placed dual-chamber pacemaker to control their symptoms [10]. No patients in the study group had prior septal artery ablation.

Baseline Echocardiographic Measurements
Echocardiographic measurements in the 60 patients were made according to the recommendations of the American Society of Echocardiography [11] and as previously described from our Clinic [12]. Left ventricular mass was calculated by the corrected American Society of Echocardiography simplified cubed equation: LV mass (g) = 0.8 {1.05 ([LVID + IVST + PWT]3 – [LVID]3)}, where LVID = LV internal dimension, IVST = interventricular septum thickness, and PWT = posterior wall thickness. Importantly, measurements of septal thickness were made in a region remote from the area of myectomy. Body surface area (BSA) was calculated by the formula BSA = (0.0001) x (71.84) x (weight)0.425 x (height)0.725, where weight is measured in kilograms and height in centimeters. Left ventricular mass was divided by BSA to calculate LV mass index (LVMI). The most recent echocardiogram in relation to the operation was chosen as the baseline study, and median time from baseline echocardiogram to operation was 0.7 months (range 1 day to 8 months). Variables are expressed as mean ± standard deviation unless otherwise specified.

Table 1 summarizes the baseline echocardiographic characteristics of the 60 patients. The peak (maximum instantaneous) and mean gradients were 96 ± 38 mm Hg and 67 ± 44 mm Hg, respectively. Fifty-one patients (85%) had SAM of the mitral valve apparatus documented at the time of preoperative echocardiography, and median mitral regurgitation grade was 2.5 (range 1 to 4). Preoperative LV dimensions are shown in Table 2.


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  		Table 1. Hemodynamic Measurements

 

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  		Table 2. Left Ventricular and Atrial Dimensions

 
Surgical Data
Operations were performed using cardiopulmonary bypass (2.4 L · min–1 · m–2) at normothermia or mild (32°C) hypothermia, and antegrade cold blood cardioplegia was used for myocardial protection. All patients had intraoperative transesophageal echocardiography, and we also directly measured simultaneous LV and aortic pressures before and after myectomy. Before myectomy, the measured peak-to-peak LV outflow gradient was 62 ± 27 mm Hg.

Average length of cardiopulmonary bypass was 59 ± 31 minutes, and average cross-clamp time was 42 ± 21 minutes. Extended transaortic septal myectomy was performed through a low oblique aortotomy. Exposure of the septum and subsequent myectomy was facilitated by insertion of a cardiotomy sucker through the aortic valve in such a way as to depress and protect the mitral valve apparatus. Visualization of the septum was enhanced by external compression and rotation of the heart using sponge forceps.

The myectomy was begun with an upward incision in the septum at the nadir of the right aortic cusp; this incision was carried upward and leftward over to the attachment of the anterior mitral valve leaflet. The incisions were deepened and lengthened toward the apex until the surgeon was certain all obstructive muscle had been removed.

Data Collection and Analysis
Follow-up was complete in all patients, and data were obtained from clinic visits and outpatient echocardiograms. To further analyze echocardiographic data, we categorized follow-up studies into two groups—those obtained between 6 months and 2 years (< 2 years) and those obtained after 2 years (> 2 years). To address the possible influence of age on regression of hypertrophy, we divided our cohort into groups younger than 50 years and 50 years and older. Two group comparisons for continuous data were made using the Student's paired t test. For all statistical calculations, p < 0.05 was accepted as significant.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
Surgical Procedures and Early Outcome
Concomitant operations were performed in 10 patients (17%), and major procedures included mitral valve repair in 4 patients, mitral valve replacement (mechanical prosthesis) in 1 patient, Cox-maze procedure in 1 patient, and pulmonary valve replacement (bioprosthesis) in 1 patient. Minor procedures included closure of a patent foramen ovale in 2 patients and unroofing of an intramyocardial coronary artery in 1 patient. The average amount of septal muscle resected was 4 ± 2 g. Pathologic examination of specimens from all patients revealed the typical findings of myocyte hypertrophy, myocyte disarray, interstitial fibrosis, and endocardial fibrosis without evidence of amyloid protein deposition [2, 13].

On intraoperative transesophageal echocardiography, 19 patients (32%) had some degree of residual SAM at the conclusion of the operation; in most instances, this condition was mild and improved with time and restoration of intravascular volume. In addition, aortic valve regurgitation after myectomy was mild in 7 patients and moderate in 1 patient. Two patients had ventricular septal defects that required closure through the right ventricle.

Two patients (3%) required reexploration for excessive mediastinal hemorrhage. Of these, 1 patient had undergone extended septal myectomy and the Cox-maze III procedure, and the other had undergone extended septal myectomy and mitral valve repair. Median hospital stay was 6 days (range 4 to 24 days). No instances of heart block were noted, and the most common complication was new-onset postoperative atrial fibrillation, which occurred in 13 patients (22%).

Early and Late Postoperative Echocardiographic Data
Follow-up was complete in all 60 patients and extended to a median of 28.4 months (range 2 to 86 months). Overall median New York Heart Association functional class improved and was I (range I to II). One patient underwent reoperation for severe tricuspid valve regurgitation 41 months after myectomy and the Cox-maze III procedure; he remained in sinus rhythm. There were no late deaths.

As depicted in Table 1, LV ejection fraction decreased to 0.67 (p < 0.05) early after operation; ejection fraction remained in a normal range, but less than baseline, during late follow-up. At dismissal, the mean LV outflow gradient was 12 ± 13 mm Hg (p < 0.004 versus baseline) and remained at this level during follow-up. Seventeen patients (29% of those studied) had evidence of SAM at hospital dismissal, but in most, this was chordal SAM and the degree of mitral regurgitation was trivial.

We observed consistent reductions in mean and peak instantaneous gradients at all time points measured after myectomy (Table 1). There was a trend toward continued decline in both the mean and peak gradients beyond 2 years in comparison with less than 2 years, but this difference did not reach statistical significance. Septal wall thickness was significantly reduced (p < 0.05) at dismissal and both early and late follow-up (Table 2). In contrast, the posterior wall thickness remained unchanged at dismissal but decreased within 2 years (p < 0.05).

Left Ventricular Mass Regression
The LV mass and LVMI decreased significantly at all time points after the operation (Fig 1). This reduction in ventricular hypertrophy was observed early after operation; at dismissal, the measured LV mass was reduced by 19%. Patients younger than 50 years experienced a significant early reduction (p < 0.05) in LVMI; in older patients there was a nonsignificant trend toward early regression (Fig 2).



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  		Fig 1. Left ventricular (LV) mass ({square}) and left ventricular mass index ({blacksquare}) before and after transaortic septal myectomy. Mass regression was apparent on the early postoperative study and continued through the first 2 years after the operation. *p < 0.05 versus baseline.

 


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  		Fig 2. Early change in left ventricular (LV) mass among younger and older patients. *p < 0.05 versus baseline. {blacksquare} = younger than 50 years; {square} = older than 50 years.

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
The clinical course of HCM varies widely, and previous estimates of annual mortality rates of 3% to 6% per year likely overestimate true mortality because early studies often originated in tertiary referral centers with a disproportionate number of symptomatic and high-risk patients [4, 6, 17]. Indeed, more recent population-based investigations suggest that the annual mortality is much lower, approximately 1% per year [5]. Nevertheless, risk of cardiac death is clearly increased in certain subgroups of patients with HCM including those with prior cardiac arrest, syncope, ventricular arrhythmias, or a history of sudden death in family members with HCM [1].

The effect of LV outflow tract obstruction on prognosis of patients with HCM has been debated, but recently Maron and colleagues [5] documented a twofold increase in risk of cardiac death in patients with obstruction, and this increased probability of mortality was independent of other risk factors. Further, patients with HOCM had increased risk of progression of symptoms during follow-up. The important negative influence of hypertrophy in HCM is further emphasized by the finding that the magnitude of hypertrophy is an independent predictor of sudden death in patients with HCM [7].

The important finding in this study was that relief of LV outflow obstruction by septal myectomy results in an early and sustained decrease in LV mass and LV mass index. The decrease in ventricular mass is greater than would be expected based simply on the amount of septal muscle resected at operation. Indeed, the calculated reduction in LV mass after myectomy was 15 times greater than the measured amount of muscle removed during operation. Further, it is unlikely that the reduced LV mass is artifactual because measurement of ventricular dimensions and wall thickness were performed at sites remote from the myectomy.

Regression of hypertrophy has been documented in patients undergoing nonsurgical septal reduction by alcohol septal artery ablation. In a study of 26 patients undergoing this procedure, Mazur and colleagues [14] found a 37% decrease in myocardial mass after 2 years of follow-up. Reduction in hypertrophy correlated significantly with early reduction in outflow tract gradient. In a similar study of 64 patients, Shamim and colleagues [8] reported a decrease in LV mass from 410 to 287 g over a mean follow-up of 3 years after alcohol septal artery ablation. In both of these studies, LV mass decreased further during follow-up, whereas in our surgical patients there appeared to be more rapid reduction in hypertrophy with little change beyond 2 years. It is possible that the early reduction in hypertrophy after septal myectomy relates to the immediate reduction in outflow tract gradient. The difference may also relate to the use of permanent pacemakers, which were necessary in 27% of patients after nonsurgical septal reduction; no patients in our surgical series had heart block.

The finding of early reduction in ventricular mass after relief of LV outflow obstruction was unexpected but has been documented after valve replacement for sever aortic valve stenosis. In an investigation of ventricular remodeling after aortic valve replacement with stentless bioprostheses, Gelsomino and colleagues [15] found the LV mass index reduced by 17% at the time of hospital dismissal. Rapid regression of LV mass has also been observed during treatment of systemic hypertension; in one report, LV mass decreased within 1 month of initiation of nifedipine [16].

Our study has limitations that should be recognized. The investigation was retrospective and the patients were not consecutive. The 60 patients were chosen because they had complete calculations of ventricular mass by echocardiography at specific time points. All 309 patients who underwent extended septal myectomy during the study had echocardiographic evaluation, both preoperatively and at dismissal, but many of these patients had follow-up at their local medical centers, and echocardiograms were not sufficiently detailed to permit calculation of ventricular mass. Similarly, some follow-up echocardiograms performed at our center were not complete in this regard. It might be argued that patients in the study had "less" satisfactory surgical outcomes because they were more likely to return to our clinic for follow-up and had more detailed echocardiographic examinations. The alternate hypothesis, that patients selected because of availability of mass calculations represent a more favorable surgical group, seems much less tenable. Overall, it is our impression that the patients in the study were representative of the larger group as judged by relief of outflow gradient and symptomatic improvement. Continued observation over a longer period of time will provide further information on the regression of ventricular mass.

The beneficial effect of septal myectomy on relief of symptoms in patients with HOCM is clearly established [17], but regression of LV mass after operation had not been documented until now. Because of the relatively poor prognosis of patients with severe hypertrophy and LV outflow tract obstruction, these data suggest a mechanism by which septal myectomy may improve both symptoms and survival in patients with HOCM.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Maron BJ. Hypertrophic cardiomyopathy. JAMA. 2002;287:1308–1320[Abstract/Free Full Text]
  2. Marian AJ, Roberts R. The molecular genetic basis for hypertrophic cardiomyopathy. J Mol Cell Cardiol. 2001;33:655–670[Medline]
  3. Maron BJ, Shirani J, Poliac LC, Mathenge R, Roberts WC, Mueller FO. Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles. JAMA. 1996;276:199–204[Abstract/Free Full Text]
  4. Maron BJ. Hypertrophic cardiomyopathy. Lancet. 1997;350:127–133[Medline]
  5. Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med. 2003;348:295–303[Abstract/Free Full Text]
  6. Ommen SR, Nishimura RA. Hypertrophic cardiomyopathy: echocardiographic basis of therapy. ACC Curr J Rev. 2001;10:46–49
  7. Spirito P, Bellone P, Harris KM, Bernabo P, Bruzzi P, Maron BJ. Magnitude of left ventricular hypertrophy predicts the risk of sudden death in hypertrophic cardiomyopathy. N Engl J Med. 2000;342:1778–1785[Abstract/Free Full Text]
  8. Shamim W, Yousufuddin M, Wang D, et al. Nonsurgical reduction of the interventricular septum in patients with hypertrophic cardiomyopathy [retracted in: N Engl J Med 2003;348:951]. N Engl J Med. 2002;347:1326–1333[Abstract/Free Full Text]
  9. Coppin BD, Temple IK. Multiple lentigines syndrome (LEOPARD syndrome or progressive cardiomyopathic lentiginosis). J Med Genet. 1997;34:582–586[Abstract/Free Full Text]
  10. Ommen SR, Nishimura RA, Squires RW, Schaff HV, Danielson GK, Tajik AJ. Comparison of dual-chamber pacing versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy: a comparison of objective hemodynamic and exercise end points. J Am Coll Cardiol. 1999;34:191–196[Abstract/Free Full Text]
  11. Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimension echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989;2:358–367[Medline]
  12. McCully RB, Nishimura RA, Bailey KR, Schaff HV, Danielson GK, Tajik AJ. Hypertrophic obstructive cardiomyopathy: preoperative echocardiographic predictors of outcome after septal myectomy. J Am Coll Cardiol. 1996;27:1491–1496[Abstract]
  13. Lamke GT, Allen RD, Edwards WD, Tazelaar HD, Danielson GK. Surgical pathology of subaortic septal myectomy associated with hypertrophic cardiomyopathy. A study of 204 cases (1996–2000). Cardiovasc Pathol. 2003;12:149–158[Medline]
  14. Mazur W, Nagueh SF, Lakkis NM, et al. Regression of left ventricular hypertrophy after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation. 2001;103:1492–1496[Abstract/Free Full Text]
  15. Gelsomino S, Frassani R, Morocutti G, et al. Left ventricular mass regression after aortic valve replacement with CryoLife-O'Brien stentless aortic bioprosthesis. J Heart Valve Dis. 2001;10:603–610[Medline]
  16. Kurnik PB, Innerfield M, Wachspress JD, Eldredge WJ, Waxman HL. Left ventricular mass regression after aortic valve replacement measured by ultrafast computed tomography. Am Heart J. 1990;120:919–927[Medline]
  17. McCully RB, Nishimura RA, Tajik AJ, Schaff HV, Danielson GK. Extent of clinical improvement after surgical treatment of hypertrophic obstructive cardiomyopathy. Circulation. 1996;94:467–471[Abstract/Free Full Text]



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