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J Thorac Cardiovasc Surg 1996;111:586-594
© 1996 Mosby, Inc.
SURGERY FOR ACQUIRED HEART DISEASE |
From the Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif.
Address for reprints: Robert C. Robbins, MD, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247.
Abstract
A retrospective analysis of patients with hypertrophic obstructive cardiomyopathy treated by left ventricular myotomy and myectomy from 1972 to 1994 is reported. There were 158 patients (81 male and 77 female) with a mean age of 50.2 (±17.2) years (range 12 to 80 years). One hundred nine patients (69%) were 60 years of age or younger, and 49 patients (31%) were older than 60 years. The overall mean follow-up period was 6.1 (±4.8) years (range 0.1 to 19.3 years) and was 94% complete with a cumulative total of 956 patient-years. Preoperative exertional dyspnea was present in 84%, chest pain in 70%, presyncope in 54%, syncope in 31%, and cardiac arrest in 5% of patients. Preoperative cardiac catheterization was done in 150 patients, with mitral regurgitation detected in 104 patients (67%). The average maximal provocable left ventricular outflow tract gradient was 118 (±46) mm Hg (range 25 to 250 mm Hg). The average preoperative echocardiographic gradient at rest was 64 mm Hg, 20 mm Hg in the early postoperative period and 10 mm Hg in the late postoperative period. The mean septal thickness was 2.2 (±0.6) cm, 1.9 (±0.7) cm in the early postoperative period (p< 0.05 vs preoperative) and 1.7 (±0.5) cm in the late postoperative period (p< 0.05 vs preoperative). The overall 30-day operative mortality rate was 3.2% (5/158), and 0% for 109 patients 60 years of age or younger. Causes of death included myocardial infarction and left ventricular free wall rupture, myocardial failure from septal perforation, sepsis, cerebrovascular accident caused by thromboembolism, and delayed cardiac tamponade in one patient each. Concomitant coronary artery bypass grafting was performed in 22 patients (19.3% of patients 
40 years of age) and mitral valve replacement in 5 patients (3.2%). One hundred nine patients (69%) are alive, 10 patients (6.3%) were lost to follow-up, and 39 patients died (24.7%, including operative deaths). Actuarial survivals at 1, 5, 10, and 15 years were 92.4% ±2.2%, 85.4% ±3.1%, 71.5% ±4.6%, and 46% ±9%, respectively. The overall linearized death rate for discharged patients was 1.9%/pt-yr, and for cardiac related deaths it was 1.7%/pt-yr. Thirty-nine (36%) of the 109 survivors receivedß-adrenergic blockers, and 30 (28%) received calcium channel blockers. Ninety-four patients had improvement in New York Heart Association functional class, 10 had improvement in symptoms but not in functional class, and 5 had no improvement in functional class or symptoms. Neither preoperative hemodynamic values nor routine echocardiographic measurements significantly correlated with quality of postoperative results. Left ventricular myotomy and myectomy is a safe and reproducibly effective operative treatment for medically refractory hypertrophic obstructive cardiomyopathy, especially for patients 60 years of age or younger. Improvement in functional class and symptoms can be expected in nearly all patients. The results of myotomy and myectomy serve as a standard for comparison with other interventions for medically refractory cardiomyopathy. (J THORACCARDIOVASCSURG1996;111:586-94)
The management of medically refractory hypertrophic obstructive cardiomyopathy (HOCM) has evolved since the introduction more than 30 years ago of transaortic left ventricular myotomy and myectomy (LVMM)
1 to include mitral valve replacement, 2 dual chamber pacing with right ventricular preexcitation, 3,4 and, most recently, induced infarction of the basal interventricular septum. 5 At present, however, the results of LVMM remain the standard by which the efficacy of alternative methods of treatment, particularly in the long term, is judged. In this report, we detail the results of LVMM achieved at a single institution over a 22-year period.
Methods
Patients and preoperative assessment
The records of all patients with medically refractory HOCM treated with LVMM from 1972 to 1994 at Stanford University Medical Center were reviewed. There were 158 patients (84 male and 77 female patients) with a mean age of 50.2 (±17.2) years (range 12 to 80 years). The preoperative New York Heart Association functional classes of the patients are listed in Table I. Exertional dyspnea was present in 83%, chest pain in 70%, presyncope in 54%, syncope in 31%, and a history of cardiac arrest (caused by ventricular fibrillation) in 5% of patients. Preoperative cardiac catheterization was performed in 150 patients, and the hemodynamic values are summarized in Table II. Mitral regurgitation on left ventriculography was detected in 104 patients (67%), and significant coronary artery disease was identified in 22 of 114 patients (19.3%) 40 years old or older.
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6
Indications for surgical therapy
All patients had been treated with ß-adrenergic antagonists or calcium channel blocking agents, or both, before the operation. Operative intervention was recommended for patients who had persistent disabling symptoms and evidence of LVOT obstruction (at rest or on provocation, or both). Patients with angiographically significant coronary artery disease or structural abnormalities of the mitral valve (one with endocarditis and ruptured chordae, three with myxomatous degeneration and ruptured chordae, one with chronic rheumatic valvulitis) underwent concomitant LVMM and coronary artery bypass grafting or mitral valve replacement (two patients required LVMM, bypass grafting, and valve replacement). Three patients with a clinical history of preoperative cardiac arrest received automatic implantable defibrillators (the first in 1987).
Operative technique
The heart is exposed via a median sternotomy with ascending aortic cannulation and bicaval venous cannulation through the right atrium. Cardiopulmonary bypass is commenced with systemic cooling to approximately 30º C. A vent is placed in the main pulmonary artery. A 500 ml dose of cold (4º C) hyperkalemic crystalloid cardioplegic solution is infused once in the aortic root after placement of the aortic crossclamp. Additional myocardial protection is achieved with continuous cold pericardial irrigation with saline solution during the crossclamp interval. An oblique aortotomy is made, and the right coronary cusp of the aortic valve is retracted to expose the IVS.
Inspection and palpation of the IVS are used to assess the site for septal resection. A horizontal mattress stay suture is then placed in the most prominent portion of the septum, and a ribbon retractor is inserted through the aortic valve to the left ventricular apex. Two parallel incisions are then made in the septum, beginning 3 to 5 mm below the aortic anulus and directed toward the left ventricular apex. The first incision is made just to the right of the midpoint of the right coronary cusp and the second incision approximately 1 cm to the left. The length of these incisions is 3 to 4 cm and the maximum depth approximately 1 cm (individualized according to septal thickness). Injury to the mitral valve apparatus is avoided by cutting down onto the ribbon retractor. The intervening bar of muscle is then excised sharply with countertraction applied to the previously placed stay suture. In patients with significant hypertrophy extending into the adjacent anterolateral free wall, a third incision is then made, beginning below the commissure between the left and right coronary leaflets and directed toward the base of the anterolateral papillary muscle. Septal tissue between this incision and the primary trough already created is sharply excised to further increase the cross-sectional area of the LVOT. The resection, as described, is carried out to the maximum extent considered feasible, and for this reason neither intraoperative hemodynamic measurements nor transesophageal echocardiography is used to gauge the adequacy of relief of LVOT obstruction; no patient in this series has required reoperation because of a significant residual gradient.
Postoperative management
Methods for early postoperative management were routine, including administration of inotropic drugs if indicated. If ß-adrenergic blocking drugs had been administered before the operation, these were continued at decreased doses after the operation. Calcium channel inhibitors and disopyramide, if given before the operation, were generally discontinued. From 1972 to 1988, patients were given warfarin for 3 to 4 weeks as prophylaxis against thromboemboli originating from the myectomy site. Since 1988, however, aspirin alone has been used.
Follow-up
Follow-up was obtained by direct patient interview, review of patient records, or information supplied by referring physicians. The overall mean follow-up period was 6.1 (±4.8) years (range 0.1 to 19.26 years) and 6.3 (±5.0) years for the 109 survivors. Follow-up was 94% complete with a cumulative total of 956 patient-years. One hundred nine (69%) patients were living, 10 patients (6.3%) were lost to follow-up, and 39 patients (24.7%) were dead. Operative mortality includes any death within 30 days after the operation.
Statistical analysis
Actuarial survival and specific event-free rates were calculated by the Cutler-Ederer method. Preoperative and postoperative echocardiographic comparisons were done with Student's paired t tests. Multivariant analysis was done by Cox regression analysis.
Results
Early results
The overall 30-day operative mortality rate was 3.2% (5/158); for patients less than 65 years of age it was 0.8% (1/123). The overall mortality rate for patients undergoing LVMM only was 2.3% (3/131). Concomitant coronary artery bypass grafting was performed in 22 patients and mitral valve replacement for organic lesions of the mitral apparatus in five patients (two patients had LVMM, bypass grafting, and valve replacement). The mortality rate in patients undergoing these combined procedures was 7.4% (2/27). Causes of early death included myocardial infarction with left ventricular free wall rupture, myocardial failure after repair of a ventricular septal defect, sepsis with associated multisystem organ failure, stroke resulting from probable thromboembolism, and renal failure resulting from delayed cardiac tamponade associated with excessive anticoagulation. Two ventricular septal perforations (1.3%) were recognized at the time of LVMM and were repaired via a right ventriculotomy. Congestive heart failure developed approximately 2 months after LVMM in one additional patient and a ventricular septal defect was discovered. This was closed with a patch without difficulty, but several weeks after discharge the patient died of a stroke during an episode of atrial fibrillation. Four patients (2.5%) required permanent pacemaker placement for complete heart block; notably, three of these patients had complete right bundle branch block before the operation.
The overall mean cardiopulmonary bypass time was 62.8 (±29.8) minutes (range 33 to 229), and for the LVMM only patients it was 53.1 (±14.3) minutes (range 33 to 125 minutes). The overall mean aortic crossclamp time was 27.1 (±17.3) minutes (range 11 to 131 minutes), and for the LVMM only patients it was 20.9 (±6.8) minutes (range 11 to 54 minutes).
Multivariate analysis identified advanced age, New York Heart Association functional class IV, and elevated mean pulmonary artery pressures as independent predictors of operative death (p = 0.0068).
Late results
Actuarial survival rates at 1, 5, 10, and 15 years were 92.4% (±2.2%), 85.4% (±3.1%), 71.5% (±4.9%), and 46% (±9%), respectively (Fig. 1). Specific event-free rates at 10 and 19 years were 94.6% (±2.41%) and 94.6% (±2.41%) for sudden death, 82.3% (±4%) and 67.5% (±11.3%) for non-cardiac related death, and 86.9% (±3.6%) and 58.4% (±10.7%) for cardiac related death. The overall linearized cardiac related death rate for discharged patients was 1.7%/pt-yr. Causes of late cardiac related death included congestive heart failure (n = 6), sudden unexplained death (n = 3), documented ventricular tachyarrhythmias (n = 2), myocardial infarction (n = 2) (both in patients with preoperatively identified coronary artery disease), stroke (n = 2) (both patients had mitral prostheses and one was in atrial fibrillation), and hemorrhage associated with oral anticoagulation (n = 1). The linearized sudden death rate was 0.5%/pt-yr. None of the sudden deaths occurred in the eight patients with a preoperative history of cardiac arrest.
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Table III.
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Patients with absent or low LVOT gradients
There were 31 patients with LVOT gradients less than 20 mm Hg at rest, as measured by catheterization (before 1984) or by Doppler technique (in the absence of catheterization data). All, however, had provocable LVOT gradients greater than 36 mm Hg. Actuarial survivals and extent of functional benefit for these patients did not differ significantly from those for patients with higher gradients at rest.
Midventricular obstruction
Fourteen patients in this series preoperatively had "midventricular obstruction" as indicated by the appearance of the IVS on two-dimensional study and Doppler localization of the major shift in LVOT flow velocity. At operation, this variant form was confirmed by inspection of the IVS insofar as the most prominent extent of hypertrophic septum was situated below the subaortic location. LVMM was accordingly modified to fully traverse this region. The results, in terms of relief of obstruction and long-term clinical improvement, did not differ significantly from those obtained in patients with more typical subaortic hypertrophy.
Serial echocardiographic studies
The results of preoperative and early and late postoperative two-dimensional transthoracic echocardiographic data are summarized in Table IV. The mean time to late postoperative examination was 36.18 (±45.99) months (range 0.20 to 180.75 months). Postoperative studies showed significant decreases in IVS thickness and LVOT gradient; no patient exhibited a significant residual LVOT gradient persistent over time. The mean value for the IVS/LVPW in these serially studied patients also decreased, and this change was statistically significant at the early and late postoperative studies.
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The symptoms of most patients with HOCM respond favorably to negative inotropic medication. Verapamil continues to be the most effective drug, with sustained improvement in symptoms in over half of treated patients. 7 Symptomatic improvement is related to both a decrease in LVOT gradient and improvement in left ventricular diastolic relaxation with a resulting increase in left ventricular end-diastolic volume without an increase in left ventricular pressure. 8 However, an estimated 15% to 25% of patients with hypertrophic cardiomyopathy have a poor response to medical treatment or become unresponsive to medical therapy and have traditionally been considered candidates for transaortic LVMM. 9,10 The majority of these patients have high LVOT gradients at rest or on provocation. Verapamil should be used cautiously in this subset of patients because of concern regarding exacerbation of LVOT gradient as a result of vasodilatation. 11
Seilar and colleagues 12 suggested that LVMM improved 10-year actuarial survival of patients with HOCM as compared with medical therapy alone; this supports a previous report by Rothlin and coworkers. 13 Survival of patients with the combination of surgical resection and long-term postoperative verapamil was better than operative therapy alone. The authors acknowledged the limitations of the retrospective method of analysis and recognized that the various groups were not really comparable. However, no prospective, randomized study to assess the efficacy of medical versus surgical or combined therapy for HOCM exists or is likely to be conducted. Regardless, the literature generally supports the effectiveness of surgical treatment for medically unresponsive, symptomatic HOCM. 9,11,14
Surgical treatment of HOCM is designed to improve left ventricular systolic function by relief of LVOT obstruction. LVOT narrowing generally occurs in a region of asymmetric septal hypertrophy. It is generally accepted that a Venturi effect causes systolic anterior motion of the anterior mitral valve leaflet and results in LVOT obstruction by a variable degree of abutment of the leaflet against the septum. The goal of operation is to expand the cross-sectional area of the LVOT and thereby diminish or abolish systolic anterior motion of the anterior mitral leaflet; this simultaneously alleviates mitral regurgitation. The most appropriate surgical procedure to accomplish this, however, remains controversial. Cooley, 2,15 Krajer, 16 and their associates have used mitral valve replacement to eliminate obstruction, and MacIntosh and colleagues 17 have proposed selective mitral valve replacement for patients with measured septal thickness less than 18 mm; the rationale for the latter suggestion was the increased risk of septal perforation by LVMM in such patients. In our study, however, we found no correlation between IVS thickness and creation of a ventricular septal defect, and we are aware of no other report in the literature to support mitral valve replacement on the basis of this principle. Further, our data amply confirm the experience of others that LVMM alone dramatically reduces LVOT obstruction and associated mitral regurgitation. 18-20 Replacement of a structurally intact mitral valve is unnecessary, clinically disadvantageous, and conceptually unappealing. The five patients who underwent mitral valve replacement in our series all had intrinsic valve disease that would have continued to impose clinically important valvular dysfunction.
Dual-chamber pacing with ventricular preexcitation has been proposed as an alternative to surgical treatment of patients with medically refractory HOCM. 3,4,21 Pacing results in paradoxical movement of the IVS, thereby increasing the cross-sectional area of the LVOT and abolishing or decreasing the Venturi effect responsible for systolic anterior motion of the mitral valve. The recent report by Fananapazir and associates 21 records impressive intermediate-term results with DDD pacing in 84 patients. Significant improvement in symptoms and LVOT gradients were noted at a mean interval of 2.3 years, with only two sudden deaths during the period of follow-up. Although these data are encouraging, comparison of late results with those obtained by LVMM (e.g., 10 to 20 years) will simply require further follow-up. 22 It is also important to await the reproduction of these data by other centers before DDD pacing can be recommended as the treatment of choice for patients with medically refractory HOCM. In this regard, we would note that a substantial number of patients referred for LVMM at our institution since completion of this review have had implanted DDD pacing systems that failed to provide symptomatic relief. Thus it may be that this form of treatment is best suited for selected patients, such as the elderly. Clearly, criteria that are accurately predictive of outcome with DDD pacing are needed.
Our results confirm that LVMM can be performed with a low operative mortality rate, particularly in younger patients. Indeed, no operative deaths occurred in 109 patients 60 years of age or younger. Only advanced age, severe congestive heart failure, and pulmonary hypertension were identified as independent correlates of operative death. Thus patients in the oldest age quartile (61 to 80 years) sustain an operative mortality rate of 10.2% (5/49 patients). This is comparable to the reports of others who have described operative mortality rates of 5% to 16% for similar subsets of patients. 23-26 Notably, no routine hemodynamic (with the exception of pulmonary artery pressures) or echocardiographic measurements correlated significantly with operative mortality.
The reported annual mortality rate for patients with HOCM ranges from 2% to 4% and generally is dominated by sudden death. 27 In our series, five sudden deaths occurred, yielding an overall linearized rate of 0.5%/pt-yr. None occurred in patients surviving more than 5 years. None of the patients who died suddenly had a preoperative history of cardiac arrest; however, we believe that implantation of an automatic defibrillator at the time of LVMM in such patients is warranted. No other highly specific marker exists because malignant ventricular arrhythmias can be induced by programmed stimulation in the great majority of patients with HOCM. Indeed, 17 of the patients included in the present report had undergone intraoperative electrophysiologic testing before cardiopulmonary bypass, and sustained ventricular tachycardia or ventricular fibrillation was inducible in 14. 28 Inducibility of arrhythmias per se does not constitute an indication for defibrillator implantation.
Most of the remaining late cardiac related deaths were due to congestive heart failure, which may represent the progression of HOCM to a state of depressed contractility and ventricular dilatation or unsustainable deterioration of ventricular compliance or both. A confounding factor is myocardial ischemia resulting from obliterative lesions of small coronary arteries within hypertrophic muscle or from atherosclerotic obstruction of epicardial vessels, or a combination of these features. Often, these pathologic determinants cannot be discriminated.
Altogether, 16 late deaths in our series were classified as cardiac related, resulting in a linearized death rate of 1.7%/pt-yr and, in combination with non-cardiac related deaths, 5-, 10-, and 15-year actuarial survivals of 85%, 72%, and 46%, respectively. These figures are comparable with those described by others, 13, 19, 20, 29, even though the mean age of our patients was somewhat higher than in most previous reports. Age at operation was identified by multivariate analysis as a variable independently associated with late death. Multivariate analysis identified coronary artery disease and preoperative functional class (41 to 60 age quartile) and female gender (61 to 80 age quartile) as independent predictors of late death. In the quartiles of age ranging from birth to 20 and from 21 to 40 years, none of the preoperative variables examined correlated significantly with late mortality. This may be explained by the failure to examine variables that were important, but unavailable, or may simply reflect intrinsic randomness.
LVMM resulted in improvement in functional class and/or symptoms in 95% of our surviving patients. This quality of outcome is similar to the experience of others. 20,30 As with survival, none of the hemodynamic or echocardiographic features analyzed correlated significantly with symptomatic benefit. This is somewhat surprising insofar as the extent of left ventricular hypertrophy was variable, and many patients exhibited substantial thickening of the LVPW before the operation and might have been expected to retain significant disability because of abnormal left ventricular compliance. Whether LVMM that effectively relieves LVOT obstruction also ameliorates left ventricular stiffness remains controversial, partially because of the difficulty of accurately assessing left ventricular diastolic function. In 13 patients included in the present series, measurements of diastolic filling velocities by pulsed Doppler technique suggested improvement in diastolic filling after LVMM. 31 Others have noted similar evidence suggestive of enhanced compliance 14,20; overall, however, definitive information is lacking because of methodologic uncertainty and the difficulty of differentiation between the effects of ischemia and intrinsic myocardial abnormalities. Perhaps newer approaches such as cine magnetic resonance imaging 32 may provide further information that could prove useful in clinical management (e.g., the selection of patients who would benefit from postoperative treatment with a calcium channel blocking agent).
Regardless of these considerations, elimination or reduction of LVOT obstruction by LVMM appears to dominate as the primary determinant of clinical outcome, irrespective of the primary symptom present before the operation. Others have been able to correlate persistence of symptoms with residual obstruction, 20,33 but we were unable to establish a statistically significant association because of the very small number of patients (n = 5) who reported no improvement. Moreover, in these five exceptional patients, residual LVOT gradients as estimated by Doppler interrogation remained below 45 mm Hg (mean 15.6, range 0 to 45 mm Hg), and therefore other elements of the hypertrophic disorder, such as diastolic dysfunction as noted earlier or persistent ischemia resulting from small-vessel disease, must be invoked.
Overall, our experience with transaortic LVMM documents the reproducible efficacy of this procedure. The operative risk is low, particularly in younger patients, and the expectation for sustained relief of symptoms and improved clinical function is high. The long-term results of LVMM serve as an established standard for comparison with other methods of treatment of patients with medically refractory HOCM.
Appendix: Discussion
Dr. Pat O. Daily (San Diego, Calif.)
Your results set the standard for LVMM for HOCM. Your operative mortality overall of 3.2% and 0% in 109 patients less than 60 years of age is quite good. The survival of 85% at 5 years and 72% at 10 years are very good long-term results as well. However, the long-term period that these patients were evaluated, that is, from 1972 to 1995, and then your average follow-up of 6.1 years lead me to ask why with a study period of 23 years was the average follow-up 6.1 years?
Dr. Robbins
That reflects the number of operations that were done most recently. More operations have been done in the past few years.
Dr. Daily
So most of the earlier patients presumably had died and you were not able to obtain follow-up information?
Dr. Robbins
There were 39 deaths totally and only 10 patients were lost to follow-up. I think it just means that more operations were performed most recently.
Dr. Daily
You mentioned that different modalities besides LVMM were used to treat HOCM, one of them being mitral valve replacement; I suppose that is done primarily in Houston. Dual-chamber pacing with ventricular preexcitation is another and induced myocardial infarction of the inferior basal septum is yet another. With those last two methods, do you have any follow-up data or are there any data available in the literature so that one could compare those two methods with LVMM?
Dr. Robbins
The last one we threw in there out of interest. An American Heart Association abstract presented this year, from a cardiology group in Belgium, suggested that if you infarcted the basal septum then that part of the septum would not move and you could get an increase in the size of the LVOT. Interestingly, mitral valve replacement was also brought forward for a subset of patients at the National Institutes of Health, where Dr. Morrow developed these techniques, by his associate Chuck MacIntosh. He suggested that mitral valve replacement was indicated for those patients with septal dimensions less than 18 mm because in his retrospective review of Dr. Morrow's data he found that the incidence of iatrogenic ventricular septal defects was greater. The cardiologists at the National Institutes of Health then embarked on this dual-chamber pacing concept and Lami Fananapazir is the man who has brought this concept forward. Of 84 patients in his most recent report, with a 2-year follow-up, there was a good decrease in the LVOT gradient and symptomatic improvement with only two late sudden deaths. These are very encouraging data. Inasmuch as there is no surgical branch left at the National Institutes of Health, all the patients who flock there are getting dual-chamber pacing. I would point out that Dr. Stinson performed LVMM on several patients who had failure of dual-chamber pacing in the past couple of years.
Dr. Daily
You initially gave your patients warfarin sodium (Coumadin) for anticoagulation, and more recently in the series, aspirin. You had one episode of hemorrhage and one episode of embolization. Do you still use aspirin postoperatively in all patients?
Dr. Robbins
From 1972 until 1988 Dr. Stinson used warfarin and then after a couple of anticoagulation hemorrhage problems occurred he converted to aspirin. He still uses aspirin.
Dr. Daily
With aspirin have you had any more coagulation problems?
Dr. Robbins.
No, he has not seen a problem with bleeding since then, nor any problem with any thromboemboli; probably just luck.
Dr. Daily
You described an interesting subset of 14 patients in whom there was some obstruction of the midportion of the left ventricle. You used an extended incision distally to divide that area. Others have used left ventricular free wall incisions and also a modified Konno procedure to deal with that kind of a problem. Have you used either of those two variations?
Dr. Robbins
No, Dr. Stinson believes that by looking at the preoperative echocardiogram and by digitally examining the LVOT during the operation he is able to customize the incisions for the septal resection. No patients were reoperated on in this series for residual obstruction, which supports his approach to septal resection based on the preoperative echocardiogram and findings at the time of the operation. He also believes, and this is probably controversial in this day and age, that transesophageal echocardiography is not of much benefit to him in doing these operations.
Dr. Daily
Anecdotally, I have used the modified Konno operation in three patients and it does facilitate reaching that more distal area. At the same time, you can get a very good result with respect to opening that part of the obstruction even if you have to patch that part of the interventricular septum.
You described the aortic incision as the typical hockey-stick incision going toward the noncoronary sinus. Do you still use that?
Dr. Robbins.
Yes, sir.
Dr. Daily
For the past 6 years we have been transecting the aorta just above the coronary ostia. It allows us to raise the aortic valve upward on the operating table, better to visualize the subvalvular area that we want to try to resect. We have found that to be a useful technical variation.
On the basis of your results I would certainly suggest that this operation is not just the standard for other modalities of treatment but for others who have performed LVMM and reported their results. It is excellent.
Footnotes
Read at the Twenty-first Annual Meeting of The Western Thoracic Surgical Association, Coeur d'Alene, Idaho, June 21-24, 1995. 
References
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S. R. Ommen, B. J. Maron, I. Olivotto, M. S. Maron, F. Cecchi, S. Betocchi, B. J. Gersh, M. J. Ackerman, R. B. McCully, J. A. Dearani, et al. Long-Term Effects of Surgical Septal Myectomy on Survival in Patients With Obstructive Hypertrophic Cardiomyopathy J. Am. Coll. Cardiol., August 2, 2005; 46(3): 470 - 476. [Abstract] [Full Text] [PDF]
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S. K. Balaram, M. V. Sherrid, J. J. Derose Jr., Z. Hillel, G. Winson, and D. G. Swistel Beyond Extended Myectomy for Hypertrophic Cardiomyopathy: The Resection-Plication-Release (RPR) Repair Ann. Thorac. Surg., July 1, 2005; 80(1): 217 - 223. [Abstract] [Full Text] [PDF]
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B. J. Maron Surgery for Hypertrophic Obstructive Cardiomyopathy: Alive and Quite Well Circulation, April 26, 2005; 111(16): 2016 - 2018. [Full Text] [PDF]
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A. Woo, W. G. Williams, R. Choi, E. D. Wigle, E. Rozenblyum, K. Fedwick, S. Siu, A. Ralph-Edwards, and H. Rakowski Clinical and Echocardiographic Determinants of Long-Term Survival After Surgical Myectomy in Obstructive Hypertrophic Cardiomyopathy Circulation, April 26, 2005; 111(16): 2033 - 2041. [Abstract] [Full Text] [PDF]
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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]
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J.-P. Chang, C.-L. Kao, C.-I Cheng, and Y.-K. Hsieh Septal myectomy with loop electrosurgical electrode for hypertrophic obstructive cardiomyopathy Ann. Thorac. Surg., July 1, 2004; 78(1): 355 - 357. [Abstract] [Full Text] [PDF]
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 F H Gietzen, C J Leuner, L Obergassel, C Strunk-Mueller, and H Kuhn Transcoronary ablation of septal hypertrophy for hypertrophic obstructive cardiomyopathy: feasibility, clinical benefit, and short term results in elderly patients Heart, June 1, 2004; 90(6): 638 - 644. [Abstract] [Full Text] [PDF]
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 K. Minakata, J. A. Dearani, R. A. Nishimura, B. J. Maron, and G. K. Danielson Extended septal myectomy for hypertrophic obstructive cardiomyopathy with anomalous mitral papillary muscles or chordae J. Thorac. Cardiovasc. Surg., February 1, 2004; 127(2): 481 - 489. [Abstract] [Full Text] [PDF]
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 T. Ueno, K. Ikeda, and Y. Koga Modified septal myectomy for small patients with hypertrophic obstructive cardiomyopathy Interactive CardioVascular and Thoracic Surgery, December 1, 2003; 2(4): 650 - 652. [Abstract] [Full Text] [PDF]
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B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, F. J. Ten Cate, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines J. Am. Coll. Cardiol., November 5, 2003; 42(9): 1687 - 1713. [Full Text] [PDF]
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Writing Committee Members, B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines Eur. Heart J., November 1, 2003; 24(21): 1965 - 1991. [Full Text] [PDF]
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M. V. Sherrid, F. A. Chaudhry, and D. G. Swistel Obstructive hypertrophic cardiomyopathy: echocardiography, pathophysiology, and the continuing evolution of surgery for obstruction Ann. Thorac. Surg., February 1, 2003; 75(2): 620 - 632. [Abstract] [Full Text] [PDF]
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K. Minami, D. Boethig, H. Woltersdorf, D. Seifert, and R. Korfer Long term follow-up of surgical treatment of hypertrophic obstructive cardiomyopathy (HOCM): the role of concomitant cardiac procedures Eur. J. Cardiothorac. Surg., August 1, 2002; 22(2): 206 - 210. [Abstract] [Full Text] [PDF]
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F. H. Gietzen, C. J. Leuner, L. Obergassel, C. Strunk-Mueller, and H. Kuhn Role of Transcoronary Ablation of Septal Hypertrophy in Patients With Hypertrophic Cardiomyopathy, New York Heart Association Functional Class III or IV, and Outflow Obstruction Only Under Provocable Conditions Circulation, July 23, 2002; 106(4): 454 - 459. [Abstract] [Full Text] [PDF]
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G Morgan-Hughes and J Motwani Mitral valve endocarditis in hypertrophic cardiomyopathy: case report and literature review Heart, June 1, 2002; 87(6): e8 - 8. [Abstract] [Full Text] [PDF]
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 B. J. Maron Hypertrophic Cardiomyopathy: A Systematic Review JAMA, March 13, 2002; 287(10): 1308 - 1320. [Abstract] [Full Text] [PDF]
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J. Xin, T. Shiota, H. M. Lever, S. R. Kapadia, M. Sitges, D. N. Rubin, F. Bauer, N. L. Greenberg, D. A. Agler, J. K. Drinko, et al. Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1994 - 2000. [Abstract] [Full Text] [PDF]
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 F.A. Schoendube Surgical treatment of hypertrophic obstructive cardiomyopathy Eur. Heart J. Suppl., October 1, 2001; 3(suppl_L): L26 - L31. [Abstract] [PDF]
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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]
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E. H. C. Yu, A. S. Omran, E. D. Wigle, W. G. Williams, S. C. Siu, and H. Rakowski Mitral regurgitation in hypertrophic obstructive cardiomyopathy: relationship to obstruction and relief with myectomy J. Am. Coll. Cardiol., December 1, 2000; 36(7): 2219 - 2225. [Abstract] [Full Text] [PDF]
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N. M. Lakkis, S. F. Nagueh, J. K. Dunn, D. Killip, and W. H. Spencer III Nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy: one-year follow-up J. Am. Coll. Cardiol., September 1, 2000; 36(3): 852 - 855. [Abstract] [Full Text] [PDF]
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W. H. Merrill, G. C. Friesinger, T. P. Graham Jr, B. F. Byrd III, D. C. Drinkwater Jr, K. G. Christian, and H. W. Bender Jr Long-lasting improvement after septal myectomy for hypertrophic obstructive cardiomyopathy Ann. Thorac. Surg., June 1, 2000; 69(6): 1732 - 1735. [Abstract] [Full Text] [PDF]
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F.H. Gietzen, CH.J. Leuner, J. Hegselmann, C. Strunk-Mueller, and H. Khun A reply Eur. Heart J., April 1, 2000; 21(7): 591 - 593. [PDF]
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B. J. Maron, R. A. Nishimura, W. J. McKenna, H. Rakowski, M. E. Josephson, and R. S. Kieval Assessment of Permanent Dual-Chamber Pacing as a Treatment for Drug-Refractory Symptomatic Patients With Obstructive Hypertrophic Cardiomyopathy : A Randomized, Double-Blind, Crossover Study (M-PATHY) Circulation, June 8, 1999; 99(22): 2927 - 2933. [Abstract] [Full Text] [PDF]
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B. J. Maron, R. A. Nishimura, and G. K. Danielson Pitfalls in Clinical Recognition and a Novel Operative Approach for Hypertrophic Cardiomyopathy With Severe Outflow Obstruction Due to Anomalous Papillary Muscle Circulation, December 8, 1998; 98(23): 2505 - 2508. [Abstract] [Full Text] [PDF]
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L. Faber, H. Seggewiss, and U. Gleichmann Percutaneous Transluminal Septal Myocardial Ablation in Hypertrophic Obstructive Cardiomyopathy : Results With Respect to Intraprocedural Myocardial Contrast Echocardiography Circulation, December 1, 1998; 98(22): 2415 - 2421. [Abstract] [Full Text] [PDF]
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N. M. Lakkis, S. F. Nagueh, N. S. Kleiman, D. Killip, Z.-X. He, M. S. Verani, R. Roberts, and W. H. Spencer III Echocardiography-Guided Ethanol Septal Reduction for Hypertrophic Obstructive Cardiomyopathy Circulation, October 27, 1998; 98(17): 1750 - 1755. [Abstract] [Full Text] [PDF]
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M. H. Schonbeck, H. P. Brunner-La Rocca, P. R. Vogt, M. L. Lachat, R. Jenni, O. M. Hess, and M. I. Turina Long-Term Follow-up in Hypertrophic Obstructive Cardiomyopathy After Septal Myectomy Ann. Thorac. Surg., May 1, 1998; 65(5): 1207 - 1214. [Abstract] [Full Text] [PDF]
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 C. Oakley Aetiology, diagnosis, investigation, and management of the cardiomyopathies BMJ, December 6, 1997; 315(7121): 1520 - 1524. [Full Text]
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M. K. Gol, M. Emir, T. Keles, S. A. Kucuker, C. L. Birincioglu, Y. H. Karagoz, T. Kural, O. Tasdemir, S. Goksel, and K. Bayazit Septal Myectomy in Hypertrophic Obstructive Cardiomyopathy: Late Results With Stress Echocardiography Ann. Thorac. Surg., September 1, 1997; 64(3): 739 - 745. [Abstract] [Full Text]
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 P. Spirito, C. E. Seidman, W. J. McKenna, and B. J. Maron The Management of Hypertrophic Cardiomyopathy N. Engl. J. Med., March 13, 1997; 336(11): 775 - 785. [Full Text] [PDF]
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