(Circulation. 1996;94:467-471.)
© 1996 American Heart Association, Inc.
Articles |
the Divisions of Cardiovascular Diseases and Internal Medicine (R.B.M., R.A.N., A.J.T.) and Thoracic and Cardiovascular Surgery (H.V.S., G.K.D.), Mayo Clinic and Mayo Foundation, Rochester, Minn.
| Abstract |
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Methods and Results The clinical, ECG, echocardiographic, cardiac catheterization, and surgical data were analyzed for 65 patients 20 to 70 years old with hypertrophic obstructive cardiomyopathy who had surgical treatment between 1986 and 1992. Specific symptoms and overall functional status were evaluated before surgery and at the end of the first postoperative year. Subsequent long-term clinical postoperative follow-up was also obtained. The extent of postoperative improvement was measured by the presence and severity of persistent symptoms, overall New York Heart Association (NYHA) functional class, and patients' self-perceptions of overall improvement. Of the patients, 95% were in NYHA functional class III or IV before surgery: 95% had dyspnea, 62% had angina, 63% had near-syncope, and 23% had syncope. The overall early mortality rate was 4.6%; there was no mortality among the 45 patients who underwent isolated septal myectomy. At the 1-year postoperative evaluation, 89% of survivors were in NYHA functional class I or II, and 47% believed that they had 100% improvement. Significant improvement (as defined) was seen in 67% of patients with dyspnea, 90% with angina, 86% with near-syncope, and 100% with syncope. The 5-year survival rate was 92%.
Conclusions The results of the present study reaffirm the efficacy of surgical treatment of hypertrophic obstructive cardiomyopathy in patients who are severely symptomatic despite optimal medical therapy and serve as a useful reference by which the surgical approach can be compared with new and potentially promising treatment alternatives.
Key Words: Key Words cardiomyopathy echocardiography myectomy mortality surgery
| Introduction |
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Recently, dual-chamber pacing was proposed as an appropriate therapeutic alternative for patients with hypertrophic obstructive cardiomyopathy. The lower risk and cost of this procedure and the initial beneficial results have prompted some investigators7 to advocate dual-chamber pacing in all patients with severely symptomatic hypertrophic cardiomyopathy before consideration of septal myectomy. Surgical myectomy is a technically challenging procedure with a steep learning curve. With the massive myocardial hypertrophy, continued improvements in myocardial preservation techniques may alter the risk-benefit ratio of this procedure. To reach a decision about optimal therapy for patients with hypertrophic obstructive cardiomyopathy, it is necessary to know the risks and results of the operation in the current surgical era. The purpose of the present study was to examine the clinical outcome of adult patients who had septal myectomy for hypertrophic obstructive cardiomyopathy between 1986 and 1992, with an emphasis on the presence and severity of specific symptoms.
| Methods |
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Surgical Technique
Transaortic septal myectomy was performed in all patients. Additional procedures were performed in several patients.
Standard cardiopulmonary bypass techniques were used with moderate (25°C to 32°C) systemic hypothermia. Myocardial protection was achieved with cold blood (n=45) or crystalloid (n=20) potassium cardioplegia with topical cooling. The subaortic obstruction was approached by way of an aortotomy, and the septal resection was begun by making two parallel longitudinal incisions, the first beneath the nadir of the right coronary cusp and the second beneath the commissure between the right and left coronary cusps. The incisions were joined superiorly, and a bar of muscle was excised past the bulging septum to the level of the papillary muscles. Additional myocardium was removed between this resection and the lateral attachment of the anterior mitral leaflet. For the patient with midventricular obstruction, further resection was carried out below the level of the papillary muscles. The left ventricular outflow tract was then inspected and palpated for completeness of relief of outflow tract obstruction, and the aortotomy was repaired.
Clinical Outcome
Early mortality was defined as death in the hospital or within 30 days after surgery. Patients were evaluated after a suitable convalescence period (
1 year; mean, 12.1±4.4 months). This evaluation included a detailed description of each patient's perceived improvement (ie, minimal [0%, 25%], 50%, 75%, or 100%), their functional status (overall New York Heart Association [NYHA] functional class), and severity of any persisting symptoms. Significant improvement in symptoms of dyspnea and angina was defined as a change from moderate or severe symptoms before surgery to mild or no symptoms after surgery. Significant improvement in syncope and near-syncope was defined as a change from the presence of these symptoms before surgery to their absence after surgery. Subsequent long-term clinical follow-up (maximum, 73 months) was also obtained. Follow-up was achieved through return clinic visits, mailed questionnaires, correspondence with referring physicians, and telephone interviews with patients.
Statistical Analysis
Survival curves were estimated with the use of the Kaplan-Meier method.
| Results |
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Clinical Presentation
All patients except 1 were symptomatic. The latter had a high resting left ventricular outflow systolic pressure gradient and a very strong family history of hypertrophic cardiomyopathy and sudden cardiac death. As shown in Fig 1
, dyspnea was the most common symptom (95% of patients), and two thirds of the patients with this complaint had severe dyspnea. Other symptoms included angina in 62% of patients, near-syncope in 63%, syncope in 23%, and palpitations in 46%. Arrhythmias and congestive heart failure had been documented in 17% and 28% of the patients, respectively. Of the 65 patients, 95% were in NYHA functional class III or IV. Three patients presented with acute pulmonary edema and cardiogenic shock and required emergency operation for flail mitral leaflet, which caused severe mitral regurgitation.
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Medications
Various regimens of cardiac drugs had been prescribed, some of which were not well tolerated. At the time of preoperative assessment, 59 patients (91%) were taking either a ß-blocker or a calcium channel blocker, and 20 (31%) were taking both drugs. ß-Blockers were being used in 45 patients (69%) (two thirds of whom were taking propranolol [mean daily dose, 230 mg]), and calcium channel blockers were being used in 34 (52%) (four fifths of whom were taking verapamil [mean daily dose, 360 mg]). Seven patients (11%) were taking disopyramide.
ECG
In 7 patients (11%), the preoperative rhythm was atrial fibrillation. One patient had a paced rhythm, and the other 57 patients (88%) were in sinus rhythm. Left atrial enlargement (a negative terminal deflection of the P wave in lead V1 of
40 ms in duration) was present in 74% of the patients in sinus rhythm. The PR interval was prolonged (>200 ms) in 27% of patients and was equal to 200 ms in 27%. The shortest PR interval was 140 ms. Left bundle-branch block was present in 5 of the 65 patients (8%). Of the 60 patients without left bundle-branch block, 55% had left ventricular hypertrophy according to the criteria of Sokolow and Lyon10 : SV1 plus RV5 or RV6 of >35 mV. Two patients had giant negative T waves; these were defined as T-wave inversion of
10 mV. Q waves were considered abnormal if they were
40 ms in duration or 25% of the R wave in depth; 5 patients had pathological Q waves.
Two-dimensional and Doppler Echocardiography
The pattern of hypertrophy of the left ventricle varied; in 11 of the 65 patients (17%), there was concentric or diffuse hypertrophy. One patient had a predominantly midventricular pattern of hypertrophy. The basal two thirds or the entire septum was hypertrophied in all of the other patients (81%). The mean maximal left ventricular wall thickness was 24.6±4.2 mm (range, 18 to 33 mm). The mean peak resting left ventricular outflow pressure gradient was 66±39 mm Hg (range, 0 to 180 mm Hg). Provocation was performed in 33 patients with either amyl nitrite inhalation or the Valsalva maneuver. The mean peak provoked gradient was 89±43 mm Hg (range, 10 to 196 mm Hg). Five patients had provoked gradients of <50 mm Hg; all of these patients had significant gradients provoked at cardiac catheterization. The corrected left ventricular ejection time was prolonged (429±27 ms) and correlated weakly with the peak resting gradient (r=.33). According to the assessment of jet area with color flow imaging, mitral regurgitation was at least moderate in 40 patients (61%), mild in 18 (28%), and trivial or absent in 7 (11%). Analysis of the timing and direction of the regurgitant jet11 was performed; the mitral regurgitation was primarily due to systolic anterior motion of the mitral valve leaflet(s) in 49 patients (85%). Five patients had dense calcification of the mitral valve or annulus (or both), 3 had a flail mitral leaflet, and 1 had prolapse of the posterior leaflet of the mitral valve.
Cardiac Catheterization
Fifty-two patients (80%) underwent coronary arteriography, and 5 (10%) were found to have significant (
50% stenosis) coronary artery disease. The mean peak resting systolic pressure gradient between the left ventricle and aorta in 31 patients who underwent a hemodynamic study was 62.9±42 mm Hg (range, 0 to 150 mm Hg). The mean left ventricular end-diastolic pressure was 24.8±6 mm Hg (range, 12 to 35 mm Hg). Of the 30 patients who had severity of mitral regurgitation evaluated at cardiac catheterization, 6 (20%) were graded as 4/4, 3 (10%) were graded as 3/4, 6 (20%) were graded as 2/4, and 12 (40%) were graded as 1/4. The 3 other patients (10%) had no mitral regurgitation.
Surgical Results
For the 45 patients (69%) who had only septal myectomy, the mean cross-clamp time was 32 minutes. In 16 patients, the resected septal specimen was weighed (mean weight, 2.99±1.6 g). Additional procedures were performed in 20 patients (31%) (Table
). The three emergency procedures were performed to replace (n=1) or repair (n=2) flail mitral valve leaflets due to chordal rupture. A second period of cardiopulmonary bypass was required in 5 patients: 2 had additional septal resection, 1 had additional resection and mitral valve repair, 1 had mitral valve replacement, and 1 had aortic valve repair after a retraction injury was recognized. No patient had a surgically induced ventricular septal defect.
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The left ventricular outflow pressure gradient was measured intraoperatively in 53 patients. The mean peak gradient in 38 patients at rest was 73.0±35 mm Hg before myectomy and 8.7±11 mm Hg after myectomy. In 15 other patients whose rest gradients before myectomy were <25 mm Hg, isoproterenol was infused and a peak provoked gradient was measured; it averaged 83.1±35 mm Hg before myectomy and 13.0±11 mm Hg after myectomy. The mean premyectomy-to-postmyectomy reduction in the intraoperative rest and provoked gradients was 67.8±33.3 and 71.6±37 mm Hg, respectively.
A second operation during the initial hospitalization was required in 4 patients: to control mediastinal bleeding in 1, for permanent pacemaker implantation in 1, for mitral valve replacement in 1, and for aortic valve replacement with placement of a left ventricular assist device in 1.
None of the 45 patients (0%) undergoing isolated septal myectomy died. Three patients who had concomitant procedures died, for an overall early mortality rate of 4.6%. One of these patients, a 66-year-old man, also underwent excision of a left atrial myxoma. He died 7 days after surgery from septicemia, with renal and hepatic failure. A 26-year-old woman with a severe form of biven-tricular hypertrophic cardiomyopathy also underwent right ventricular septal myectomy. In the postoperative period, recurrent ventricular fibrillation developed, and a left ventricular assist device was placed; however, she died after a gradual deterioration in her low cardiac output state. A 39-year-old man who also underwent mitral valve replacement died from severe diastolic heart failure 2 weeks after being discharged home. All 3 patients undergoing emergency surgery survived.
Postoperative ECG
The postoperative predischarge ECG showed atrial fibrillation in 6 patients (10%) and new left bundle-branch block in 24 of 58 patients (41%). Other conduction disturbances (nonspecific intraventricular conduction delay, left anterior hemiblock, and bifascicular block) developed in 3 patients. One patient developed complete heart block, requiring implantation of a permanent pacemaker.
Clinical Outcome
In the early convalescent phase (
3 months), 1 patient had a nonQ-wave myocardial infarction (a 64-year-old man who had multivessel coronary artery bypass graft surgery at the time of septal myectomy), 1 patient had a nondebilitating stroke (a 69-year-old woman who had septal myectomy and was in atrial fibrillation and taking warfarin at the time of hospital discharge), and 1 patient had mitral valve replacement for severe mitral regurgitation (a 67-year-old woman who had had emergency mitral valve repair of a flail leaflet).
Clinical evaluation was performed at the end of the first postoperative year (12.1±4.4 months) in 61 of the 62 early survivors (98%). At this time, 90% of patients perceived an improvement of
50%, 76% considered themselves improved by
75%, and 47% believed that their improvement was 100%. Ten percent perceived no or minimal improvement. At 1 year after surgery, 89% of the patients were in NYHA functional class I or II (Fig 2
), and 49% (30 of 61 patients) were asymptomatic and unlimited in their activities. Overall, persistent symptoms were much less severe (Fig 1
). Significant improvement, defined as a change from moderate or severe symptoms before surgery to mild or no symptoms after surgery, occurred in 37 of 55 patients (67%) with dyspnea and in 27 of 30 patients (90%) with angina. Significant improvement in near-syncope and syncope, defined as a change from the presence of these symptoms before surgery to their absence after surgery, occurred in 32 of 37 patients (86%) with near-syncope and in all 14 patients (100%) with syncope. New syncope developed after surgery in two patients. The extent of clinical improvement was similar in patients who had left bundle-branch block after surgery and in those who did not (P=.71). One year after surgery, 28 patients (46%) were taking ß-blockers (mean daily propranolol dose, 130 mg), and 16 (26%) were taking calcium channel blockers (mean daily verapamil dose, 230 mg).
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Arrhythmias
The arrhythmia documented most often both before and after surgery was atrial fibrillation. Seven patients had persistent atrial fibrillation before surgery; 6 of these 7 survived, and 4 of them were in sinus rhythm at 1 year after surgery. Five of 6 patients with paroxysmal atrial fibrillation before surgery were in sinus rhythm 1 year after surgery. New atrial fibrillation developed in the first postoperative year in 5 patients. Therefore, at 1 year after surgery, 8 of 61 patients (13%) were in atrial fibrillation compared with 13 of 65 patients (20%) with either persistent or paroxysmal atrial fibrillation before surgery. There was a trend toward smaller left atrial size on the predischarge postoperative echocardiogram (left atrial volume, 83±44 versus 88±43 mL before surgery, P=.06). Two patients had nonsustained ventricular tachycardia on 24-hour ambulatory ECG monitoring before surgery.
Outcome After 1 Year
The median length of long-term follow-up was 19.5 months (mean, 28.2±19.9 months; range, 4.5 to 73 months). One of 61 1-year survivors (2%) died (Fig 3
); this patient was undergoing chronic hemodialysis for reasons unrelated to his cardiac disease and died of pulmonary embolism 3 years after septal myectomy. Atrial fibrillation developed late (on average, 2 years after surgery) in 4 of the 53 late survivors (8%) who were in sinus rhythm at the 1-year postoperative evaluation.
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At
2 years after surgery, 2 patients had recurrent and worsening symptoms attributable to their cardiac disease, and they received medical treatment. Further surgical treatment was necessary in 2 other patients: 1 patient underwent mitral valve replacement 6 years after myectomy for severe mitral regurgitation, and 1 patient underwent aortic valve replacement 4 years after myectomy for severe aortic regurgitation. The latter patient had required aortic valve repair after retraction trauma at the time of septal myectomy.
| Discussion |
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By all measures, including patients' self-perception, significant improvement occurred in most of the patients. The patients with angina or syncope, in particular, had nearly complete resolution of their symptoms. Patients who had dyspnea as the predominant presenting symptom also had improvement but not to the same extent, and 16 of the 61 patients (26%) had at least moderate residual dyspnea when evaluated 1 year after surgery. Dyspnea is a consequence of various pathophysiological processes that occur in hypertrophic cardiomyopathy, the most important contributor being abnormal diastolic function. Due to abnormal loads on the left ventricle, nonuniformity, and abnormal calcium metabolism,12 there is impaired left ventricular relaxation. The markedly hypertrophied walls may also be stiff and noncompliant. Although surgical treatment will not benefit patients with abnormal compliance, it may benefit some patients who have dyspnea by decreasing the contraction load at end systole, thus increasing the rate of early relaxation.12 Postoperative reduction in the severity of systolic anterior motioninduced mitral regurgitation as a result of septal myectomy probably also has a role in improving dyspnea.
Although surgical treatment benefits most patients with hypertrophic obstructive cardiomyopathy early after surgery, they continue to require careful long-term surveillance. New atrial fibrillation, often not well tolerated in patients with hypertrophic cardiomyopathy, occurred in 6 patients during the postoperative follow-up period of the present study. Long-term survival, in this and other surgical series,1 2 4 13 14 15 is, nevertheless, good.
Recent reports have demonstrated a modest gradient reduction and symptomatic improvement through implantation of a dual-chamber pacemaker in patients with hypertrophic obstructive cardiomyopathy at both short- and intermediate-term follow-up.7 16 17 The mechanism of benefit is unclear but may be related to both an acute reduction in the left ventricular outflow gradient induced by alteration in septal activation and a long-term ventricular remodeling effect. There may also be a decrease in the severity of mitral regurgitation, but the left atrial size does not change.17 Questions remain regarding the efficacy of dual-chamber pacing in all patients.18 Pacing from the right ventricle acutely has been shown to cause a deterioration in diastolic function due to prolongation of relaxation and alteration of atrioventricular synchrony19 20 ; the chronic effect of long-term pacing on diastolic function is unknown. Long-term follow-up of large numbers of patients undergoing implantation of a permanent pacemaker is required to determine the ultimate role of this therapeutic modality.
Thus, the optimal treatment of the subset of patients with hypertrophic obstructive cardiomyopathy who remain severely symptomatic despite optimal medical therapy is unclear. However, based on the present as well as other recent studies,14 15 surgical treatment should be viewed as a safe, efficacious, and rational therapeutic option. It should be performed at medical centers where cardiologists and cardiac surgeons are intimately familiar with this condition and septal myectomy as well as these patients' subsequent postoperative care.
| Footnotes |
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Received September 19, 1995; revision received January 23, 1996; accepted January 29, 1996.
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R. A. Nishimura and D. R. Holmes Jr. Hypertrophic Obstructive Cardiomyopathy N. Engl. J. Med., March 25, 2004; 350(13): 1320 - 1327. [Full Text] [PDF] |
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W. G. van Dockum, F. J. ten Cate, J. M. ten Berg, A. M. Beek, J. W. R. Twisk, J. Vos, M. B. M. Hofman, C. A. Visser, and A. C. van Rossum Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging J. Am. Coll. Cardiol., January 7, 2004; 43(1): 27 - 34. [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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B. J. Maron, S. A. Casey, R. G. Hauser, and D. M. Aeppli Clinical course of hypertrophiccardiomyopathy with survival to advanced age J. Am. Coll. Cardiol., September 3, 2003; 42(5): 882 - 888. [Abstract] [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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M. S. Maron, I. Olivotto, S. Betocchi, S. A. Casey, J. R. Lesser, M. A. Losi, F. Cecchi, and B. J. Maron Effect of Left Ventricular Outflow Tract Obstruction on Clinical Outcome in Hypertrophic Cardiomyopathy N. Engl. J. Med., January 23, 2003; 348(4): 295 - 303. [Abstract] [Full Text] [PDF] |
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S. Firoozi, P.M. Elliott, S. Sharma, A. Murday, S.J. Brecker, M.S. Hamid, B. Sachdev, R. Thaman, and W.J. McKenna Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathy. A comparison of clinical, haemodynamic and exercise outcomes Eur. Heart J., October 2, 2002; 23(20): 1617 - 1624. [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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B. J. Maron Hypertrophic Cardiomyopathy: A Systematic Review JAMA, March 13, 2002; 287(10): 1308 - 1320. [Abstract] [Full Text] [PDF] |
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W. J McKenna and E. R Behr Hypertrophic cardiomyopathy: management, risk stratification, and prevention of sudden death Heart, February 1, 2002; 87(2): 169 - 176. [Full Text] [PDF] |
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S. F. Nagueh, S. R. Ommen, N. M. Lakkis, D. Killip, W. A. Zoghbi, H. V. Schaff, G. K. Danielson, M. A. Quinones, A. J. Tajik, and W. H. Spencer III Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy J. Am. Coll. Cardiol., November 15, 2001; 38(6): 1701 - 1706. [Abstract] [Full Text] [PDF] |
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W.J. McKenna, S. Sharma, and P.M. Elliott Management strategies in hypertrophic cardiomyopathy: influence of age and morphology Eur. Heart J. Suppl., October 1, 2001; 3(suppl_L): L10 - L14. [Abstract] [PDF] |
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W. Mazur, S. F. Nagueh, N. M. Lakkis, K. J. Middleton, D. Killip, R. Roberts, and W. H. Spencer III Regression of Left Ventricular Hypertrophy After Nonsurgical Septal Reduction Therapy for Hypertrophic Obstructive Cardiomyopathy Circulation, March 20, 2001; 103(11): 1492 - 1496. [Abstract] [Full Text] [PDF] |
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R. Flores-Ramirez, N. M. Lakkis, K. J. Middleton, D. Killip, W. H. Spencer III, and S. F. Nagueh Echocardiographic insights into the mechanisms of relief of left ventricular outflow tract obstruction after nonsurgical septal reduction therapy in patients with hypertrophic obstructive cardiomyopathy J. Am. Coll. Cardiol., January 1, 2001; 37(1): 208 - 214. [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. Spencer III and R. Roberts Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy : The Need for a Registry Circulation, August 8, 2000; 102(6): 600 - 601. [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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L Faber, A Meissner, P Ziemssen, and H Seggewiss Percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy: long term follow up of the first series of 25 patients Heart, March 1, 2000; 83(3): 326 - 331. [Abstract] [Full Text] |
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S. R. Ommen, R. A. Nishimura, R. W. Squires, H. V. Schaff, G. K. Danielson, and A. J. Tajik 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., July 1, 1999; 34(1): 191 - 196. [Abstract] [Full Text] [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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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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