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(Circulation. 1997;95:2075-2081.)
© 1997 American Heart Association, Inc.
Articles |
Nonsurgical Septal Reduction for Hypertrophic Obstructive Cardiomyopathy
Outcome in the First Series of Patients
From the Royal Brompton Hospital (C.K., A.S.K., M.H., M.G., D.H., U.S.), London, England, and the Heart and Diabetes Centre (H.S., D.F., U.G.), Nordrhein-Westfalen, Universitatsklinik der Ruhr-Universitat Bochum, Bad Oeynhausen, Germany.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background Some patients with hypertrophic obstructive cardiomyopathy may gain symptomatic relief from a reduction in the extent of obstruction to left ventricular outflow. We present the outcome of the first series of patients treated with an alternative method of gradient reduction using catheter techniques.
Methods and Results Eighteen patients were treated with selective intracoronary alcohol injection to induce localized septal infarction. Patients underwent echocardiographic measurement of left ventricular dimensions and Doppler echocardiographic evaluation of left ventricular outflow tract gradients before the procedure, on the first postoperative day, and at a median follow-up of 3 months after the procedure. In addition, patients underwent exercise testing and symptom evaluation before and 3 months after nonsurgical septal reduction. There was a significant reduction in left ventricular outflow tract obstruction after the procedure (preprocedure, 67 mm Hg [95% CI, 48 to 87 mm Hg]; postprocedure, 25 mm Hg [95% CI, 16 to 34 mm Hg]; P=.0006), which persisted at 3-month follow-up (22 mm Hg [95% CI, 12 to 32 mm Hg]; P=.001). This was associated with a significant improvement in symptoms. There was a small but not significant increase in exercise capacity (n=10; preprocedure, 418 seconds [95% CI, 273 to 563 seconds]; postprocedure, 452 seconds [95% CI, 283 to 621 seconds). Left ventricular dimensions were not significantly altered by nonsurgical septal reduction.
Conclusions Nonsurgical septal reduction significantly reduces left ventricular outflow tract obstruction and improves symptoms in some patients with hypertrophic obstructive cardiomyopathy. The technique may provide an alternative to surgical myomectomy in selected patients.
Key Words: cardiomyopathy • stenosis • infarction • catheter ablation • catheterization
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Asignificant number of patients with hypertrophic cardiomyopathy have evidence of left ventricular outflow tract obstruction1 and may suffer symptoms of angina, dyspnea, and syncope as a consequence. In patients who remain symptomatic despite medical treatment, surgical relief of obstruction has been shown to improve quality of life,2 3 even if its prognostic effects remain uncertain in the absence of prospective, randomized, controlled trials. There are several techniques for the surgical removal of the offending portion of the interventricular septum,4 5 6 but all require extracorporeal circulation and are associated with a moderate surgical risk of at least 5%.4 7
A nonsurgical technique to achieve a reduction in septal mass by producing septal infarction using catheter techniques has been proposed by Sigwart.8 The first septal branches of the anterior descending coronary artery supply the myocardium of the proximal interventricular septum, the area of myocardium whose abnormal structure and function are responsible for the production of the left ventricular outflow tract obstruction in hypertrophic obstructive cardiomyopathy. After preliminary observations that temporary occlusion of the first major septal artery decreased the degree of outflow tract obstruction, the creation of permanent septal necrosis rather than temporary septal ischemia by intracoronary alcohol injection was shown to be effective in permanently reducing gradients in three patients with severe hypertrophic obstructive cardiomyopathy.8
We have now treated 18 patients by this novel technique and present
the results of the procedure in this first series of patients in terms
of the immediate hemodynamic effects and the results of
echocardiographic evaluation, exercise testing, and
symptomatic follow-up at a median of 
3 months.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients
Eighteen patients with hypertrophic obstructive cardiomyopathy have been treated with nonsurgical septal reduction. Twelve patients underwent the procedure at the Royal Brompton Hospital, London, UK, and six at the Herz-und Diabeteszentrum Nordrhein-Westfalen, Bad Oeynhausen, Germany, between June 1994 and February 1996, using identical protocols.
All patients had echocardiographic evidence of significant outflow tract obstruction and symptoms of angina or dyspnea despite medical treatment. Five patients had previously undergone permanent pacemaker implantation in an attempt to modify outflow tract obstruction by altering the sequence of left ventricular activation; one had an unsuccessful trial of temporary dual-chamber pacing. In all cases, consent for the new procedure was obtained after careful explanation of the proposed technique of ablation and discussion of the surgical alternatives.
Nine of the patients were male and nine were female. The mean age of
the patients was 49 years (range, 14 to 81 years). Patient
characteristics, symptoms, and baseline therapy are shown in Table 1
. Investigations were performed before and after
nonsurgical septal reduction on identical medical therapy.
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Ethics approval from the Royal Brompton Hospital was first given in August 1992 for five pilot patients and subsequently increased after the initial promising results.
Noninvasive Investigations
Echocardiography
Before the procedure, all patients underwent
transthoracic echocardiography. Resting
left ventricular outflow tract gradients were measured, as
were septal thickness and left ventricular
end-systolic and end-diastolic dimensions.
Echocardiography was repeated on the first
postoperative day and at 3-month follow-up.
Echocardiographic examination was performed using a
Hewlett-Packard Sonos 1500 echocardiograph with a 2.5-MHz
transducer interfaced to it. Left ventricular dimensions
were measured from the minor axis M-mode of the left ventricle,
obtained from the two-dimensional, guided, standard left parasternal
view. Septal thickness was measured from the same trace with the use of
leading-edge methodology. End diastole was taken at the
onset of the Q wave of the superimposed ECG.
Left ventricular outflow tract gradient was measured by use of a nonimaging, continuous-wave Doppler probe positioned at the cardiac apex as identified in the apical four-chamber view by the imaging probe and using the same echogram used at rest, or by use of the Doptek ultrasound system. The pressure gradient was measured in millimeters of mercury (the equivalent of meters per second of outflow tract velocity when the Hewlett-Packard machine was used, or the equivalent of kilohertz when the Doptek system was used).
Exercise Testing
Ten patients performed symptom-limited treadmill exercise tests
before and 3 months after the procedure. A standard Bruce protocol with
the addition of a "stage 0" (3 minutes, 1 mph, 5% gradient) was
used. Five patients underwent measurement of
O2max during the exercise
test: during exercise, subjects breathed through a mouthpiece and a
one-way valve attached to a mass spectrometer (Amis 2000 system,
Innovision). Using a standard inert gas dilution technique, this
allowed on-line measurement of metabolic gas exchange and
minute ventilation every 10 seconds. Patients were instructed to
exercise to their maximum capacity.
Ambulatory Monitoring
Patients underwent 24 hours of ambulatory monitoring before the
procedure and at follow-up. Monitoring was performed with the use of
pregelled electrodes to record two bipolar leads, an anterior
CM5, and an inferior lead. Two-channel
recordings were obtained on magnetic tape by an
amplitude-modulated dual-channel recorder (Reynolds Tracker).
Ventricular tachycardia was defined as six
consecutive beats at a rate of 120 bpm.
Procedure
Retrograde and transseptal cardiac
catheterization was performed as previously
described.8 Resting measurements of the left
ventricular gradient were recorded, and then the
patients underwent provocation with Valsalva maneuver and
dobutamine infusion when measurement of the gradient was
repeated. Gradients were also recorded after
extrasystoles.
The first major septal branch of the anterior descending
coronary artery was then identified and catheterized with a
2- to 2.5-mm coaxial PTCA balloon catheter (Fig 1A and 1B). The hemodynamic effect of temporary
balloon inflation of this vessel was established, and to delineate the
extent of myocardial perfusion of the vessel, the guidewire was
withdrawn and contrast injected through the lumen. If the cannulated
vessel supplied the correct area of the myocardium and its
occlusion resulted in a reduction in the left ventricular
outflow gradient, we proceeded to permanent ablation. After the
administration of diamorphine (5 mg IV), 2 to 5 mL of absolute alcohol
was slowly injected into the septal artery through the central lumen of
the angioplasty catheter and left in situ for 5 minutes, with the
balloon remaining inflated at the origin of the septal artery. After
deflation of the balloon, angiography was repeated to confirm blockage
of the target artery (Fig 1C). Measurements of the left
ventricular outflow gradient were then repeated at rest and
on provocation, as described above. If no single, large, first septal
branch was found and the gradient reduction was small after alcohol
injection, a second or third septal artery was catheterized and the
procedure repeated.
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Statistical Analysis
Data were analyzed by use of paired Student's
t tests. A level of P<.05 was considered
significant. Data are presented as mean (95% CI).
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Immediate Hemodynamic Effects
Resting left ventricular gradient. The left ventricular outflow gradient was reduced or abolished immediately, seconds after the alcohol injection, in most patients. Fig 2
shows pressure tracings before
and after alcohol injection in a typical case (patient 2). Fig 3 illustrates that the gradient after an extrasystole
has also been abolished (patient 1). The mean resting gradient after
the procedure was 8 mm Hg (3 to 13 mm Hg) compared with
51 mm Hg (40 to 63 mm Hg) before the procedure.
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Maximal left ventricular gradient. After alcohol injection, patients were restressed with dobutamine, pacing, and the production of premature ventricular contractions. In most cases, gradients on stress persisted after the procedure, albeit reduced. The mean maximal gradient after the procedure was 29 mm Hg (14 to 43 mm Hg) compared with 119 mm Hg (85 to 153 mm Hg) before the procedure.
Echocardiography
Individual patient Doppler echocardiographic
data, obtained before the procedure and on the first postoperative day,
are shown in Fig 4. In two patients, there was no
reduction in gradient despite a fall in gradient during the procedure.
The mean gradient measured in this way was 25 mm Hg (16 to
34 mm Hg) after the procedure compared with 67 mm Hg (48 to
87 mm Hg) before the procedure.
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ECG Changes
Five patients had permanent pacemakers implanted at the
time of the procedure. In the remaining 13 patients, the most common
ECG change was the development of right bundle-branch block, which
occurred in 11 patients. In 6 patients, this was the only ECG change.
In 3 patients, right bundle-branch block was accompanied by anterior
ST-segment elevation, and in another 2, by the development of anterior
Q waves. The 2 patients who did not develop right bundle-branch block
both developed isolated anterior ST-segment elevation after alcohol
injection.
Size of Infarction
The mean peak rise in creatinine kinase (CK) was 2295
IU (345 to 14 960). These data are skewed by one patient with a very
large enzyme rise (see "Complications"). The median CK rise was
1222 IU.
Complications
Chest pain. At the time of alcohol injection, all
patients experienced chest discomfort of moderate severity lasting for
1 to 2 minutes.
Heart block. Four patients experienced transient complete heart block after the alcohol was administered. The longest duration of complete heart block was 5 minutes.
Ventricular arrhythmias. Two patients developed ventricular arrhythmias after nonsurgical septal reduction. Patient 9, a 14-year-old girl, developed profound bradycardia and then ventricular fibrillation during femoral sheath removal 2 hours after the procedure. The arrhythmia responded to a single 200-J DC cardioversion, and there were no adverse sequelae.
Patient 12 developed several episodes of ventricular tachycardia, requiring DC cardioversion and administration of intravenous amiodarone, in the first 6 hours after the procedure. This patient also had transient occlusion of the left anterior descending coronary artery (LAD) immediately after a second alcohol injection into the first septal artery (because the first injection had been thought to be too distal), presumably as a result of a small amount of alcohol leaking down the main lumen of the LAD. This was associated with marked anterior ST elevation and a rise in CK to 14 960 IU. Angiography was repeated on the first postoperative day and showed restoration of flow down the LAD. The patient made an otherwise uneventful recovery, and follow-up echocardiography has shown left ventricular function to be well preserved, even in the myocardium in the territory of the LAD.
Length of stay. Mean length of stay was 5 days (range, 2 to 11 days).
Three-Month Follow-up Data
Symptoms. Table 2 shows the functional
status of patients and length of follow-up. The majority of patients
experienced considerable improvement in symptoms and quality of
life.
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Holter monitoring. Ambulatory monitoring at 3 months revealed neither ventricular tachycardia nor heart block in any patient.
Exercise testing. Symptom-limited exercise testing was
performed before and after the procedure in 10 patients. Mean exercise
time was 418 seconds (273 to 563 seconds) before nonsurgical septal
reduction, increasing to 452 seconds (283 to 621 seconds) after
(P=NS). Heart rate at maximum exercise was unchanged
(preprocedure, 131 bpm [122 to 139 bpm]; postprocedure, 135 bpm [117
to 152 bpm]). Measurement of
O2max was performed before
and after nonsurgical septal reduction in 5 patients. There was a small
but not significant rise in
O2max (preprocedure, 24.2
mL·kg-1·min-1
[18.4 to 30
mL·kg-1·min-1];
postprocedure, 26.8
mL·kg-1 ·min-1
[19.1 to 34.5
mL·kg-1·min-1]).
Echocardiography. Repeat Doppler
echocardiography at 3 months (n=17) showed that the
reduction in gradient was maintained, with a mean gradient of 22
mm Hg (12 to 32 mm Hg) at follow-up compared with 68 mm Hg
(49 to 87 mm Hg) before the procedure. Individual patient data
are shown in Fig 4
. The majority of patients showed little change in
gradient between evaluation on the first postoperative day and 3-month
follow-up. One patient had an increase in gradient of 20 mm Hg,
and 3 had a fall of 20 mm Hg. In 1 of these latter cases,
magnetic resonance imaging showed further septal thinning and fibrosis.
(See Fig 5.)
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Echocardiographic estimation of left ventricular size showed little variation during the follow-up period. Septal thickness was 2.1 cm (1.8 to 2.4 cm) before the procedure compared with 1.8 cm (1.5 to 2.1 cm) 3 months afterward. There was a small rise in end-systolic dimension (preprocedure, 2.6 cm [2.3 to 3.0 cm]; 3 months after the procedure, 3.0 cm [2.3 to 3.7 cm]) and end-diastolic dimension (preprocedure, 4.5 cm [4.1 to 4.9 cm]; 3 months after the procedure, 4.9 cm [4.3 to 5.5 cm]) during the follow-up period. None of these changes were significant.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The results of nonsurgical septal reduction in this first series of patients with hypertrophic obstructive cardiomyopathy suggest that the procedure produces significant hemodynamic benefit. Follow-up data show that the reduction in left ventricular outflow tract obstruction persists in the medium term and is associated with improved symptoms. The procedure appears to be acceptable in terms of safety and does not predispose to left ventricular dilatation or ventricular arrhythmias.
Established treatments for relief of symptoms in hypertrophic cardiomyopathy are negative inotropic drugs, dual-chamber pacing, and surgical resection. ß-Blockers and other negatively inotropic drugs, such as verapamil and disopyramide, can reduce left ventricular outflow tract obstruction and diminish symptoms.1 9 10 11 However, many patients remain symptomatic despite taking these drugs. Dual-chamber pacing can also reduce left ventricular outflow tract obstruction in hypertrophic cardiomyopathy,12 13 both by altering left ventricular excitation and by optimizing the timing of atrial contraction,14 and has therefore been recommended to patients unresponsive to medical therapy before consideration of surgery. Some patients do not respond to pacing and require surgical intervention.
There are several techniques for the surgical removal of the offending portion of the interventricular septum.4 5 6 Surgical resection is undoubtedly successful palliation for symptomatic patients with severe outflow tract obstruction and compares favorably with conservative treatment.3 The majority of patients derive long-term symptomatic benefit without significant impairment of left ventricular function.15 However, surgery requires extracorporeal circulation and is associated with a moderate surgical risk of at least 5%.4 7
The concept of developing an alternative, nonsurgical method of septal reduction using catheter techniques, thereby avoiding the risks of open heart surgery, was therefore attractive to us and was first conceived after observations were made on the effect of balloon occlusion on the function of focal areas of the myocardium.16 17 Furthermore, the functional significance of reduced septal function subsequent to balloon-induced ischemia was shown in 1983 to be favorable in patients with hypertrophic cardiomyopathy, with marked reduction in intracavity gradients on occlusion of the first major septal artery. These findings have been confirmed by others.18
The reduction in gradient subsequent to induction of permanent septal damage with intra-arterial alcohol injection produces a marked and immediate reduction in left ventricular obstruction. This immediate effect is greater than the echocardiographic findings on the first postoperative day, and in three patients, echocardiography failed to demonstrate a significant effect despite gradient reduction at the time of catheterization. This suggests that there may be a degree of recovery of myocardial function in the early postoperative period. This should be borne in mind during the procedure; in a minority of patients, the proximal interventricular septum is fed by a number of small septal branches rather than one larger first septal artery. In such patients, alcohol injection may be required in more than one branch, and the operator should not be deterred from this by the observation of some degree of gradient reduction after injection down a single, small, branch artery, because the degree of myocardial necrosis will inevitably be small and the gradient may recur over the next few hours. This was certainly the case in the three early procedures that failed to produce lasting benefit.
In contrast, there does not seem to be significant recovery of localized myocardial function and hence outflow tract obstruction after the immediate postoperative period, the results of 3-month Doppler echocardiographic estimation of outflow tract gradients being very similar to those made on the first postoperative day. Indeed, in some cases, there is further gradient reduction and septal thinning, presumably as a consequence of scarring and fibrosis after the infarct.
Global left ventricular performance does not seem to be adversely affected by nonsurgical septal reduction, at least in the medium term, with follow-up echocardiography failing to show significant left ventricular dilatation. This suggests that the reductions in outflow gradients that we observed are not the consequence of depression of overall left ventricular contraction. Furthermore, the extent of infarction produced by the technique may be overestimated by measurement of cardiac enzyme rise, because the pattern and extent of intracellular enzyme leakage after a chemical insult may differ from that seen after ischemic injury.
Although symptomatic improvement has been reported by the
majority of patients, we have not documented any objective evidence of
increased exercise performance, such as enhanced exercise time
or O2max. However, the number
of patients undergoing serial exercise testing was small, and studies
in larger numbers of patients are required to allow a proper evaluation
of the effect of the procedure on the patient's ability to
exercise.
A number of complications have occurred in these first 18 cases. At the time of alcohol injection, all patients experienced a degree of chest discomfort that was surprisingly short in duration, typically lasting for only 1 to 2 minutes. We routinely administered diamorphine a few minutes before alcohol injection. Four patients experienced transient complete heart block after the alcohol was administered, and although in none of these cases was the heart block permanent, it is clearly mandatory, in patients who do not have a permanent pacemaker, to insert a temporary ventricular pacing wire to cover the perioperative period.
Two patients have suffered from ventricular arrhythmias after nonsurgical septal reduction. In the first case, that of a young girl, this was secondary to bradycardia on sheath removal. In the other, several episodes of ventricular tachycardia were the consequence of alcohol leakage down the main lumen of the LAD. This caused transient impaired flow to that artery and was associated with marked anterior ST elevation and a large cardiac enzyme rise. However, arterial patency was restored by the following day, and the patient suffered no longer-term adverse events, left ventricular function being well preserved. To avoid this complication, it is clearly essential that the balloon should be firmly inflated just distal to the origin of the first septal artery. If the balloon is positioned too proximally or if it is of inadequate size, alcohol may leak down the LAD. The chances of leakage are also increased if alcohol is injected for a second time down the same septal branch, because the first injection will inevitably cause partial occlusion of the branch and increase impedance to forward flow. A new type of a compliant, spherically shaped balloon has recently been tested, with good results.
We have shown that nonsurgical septal reduction is a safe method of reducing left ventricular outflow tract obstruction in patients with hypertrophic obstructive cardiomyopathy. The procedure produces significant hemodynamic improvement during medium-term follow-up and is associated with symptomatic improvement. To evaluate its future role in the treatment of symptomatic patients with hypertrophic obstructive cardiomyopathy, however, prospective randomized trials are now required to compare catheter ablation with other forms of therapy, such as pacing and surgery.
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Acknowledgments |
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Dr Knight is a British Heart Foundation Junior Research Fellow.
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Footnotes |
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Reprint requests to Ulrich Sigwart, MD, Department of Invasive Cardiology, Royal Brompton Hospital, Sydney Street, London SW3 6NP UK.
Received August 20, 1996; revision received November 4, 1996; accepted November 23, 1996.
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S. M. Chang, N. M. Lakkis, J. Franklin, W. H. Spencer III, and S. F. Nagueh Predictors of Outcome After Alcohol Septal Ablation Therapy in Patients With Hypertrophic Obstructive Cardiomyopathy Circulation, February 24, 2004; 109(7): 824 - 827. [Abstract] [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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 M. Hamada, Y. Shigematsu, K. Ohshima, J. Suzuki, A. Ogimoto, T. Ohtsuka, and Y. Hara Diagnostic Usefulness of Carotid Pulse Tracing in Patients With Hypertrophic Obstructive Cardiomyopathy Due to Midventricular Obstruction: A Comparison With Idiopathic Hypertrophic Subaortic Stenosis Chest, October 1, 2003; 124(4): 1275 - 1283. [Abstract] [Full Text] [PDF]
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S. M. Chang, S. F. Nagueh, W. H. Spencer III, and N. M. Lakkis Complete heart block: determinants and clinical impact in patients with hypertrophic obstructive cardiomyopathy undergoing nonsurgical septal reduction therapy J. Am. Coll. Cardiol., July 16, 2003; 42(2): 296 - 300. [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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 W. Shamim, M. Yousufuddin, D. Wang, M. Henein, H. Seggewiss, M. Flather, A. J.S. Coats, and U. Sigwart Nonsurgical Reduction of the Interventricular Septum in Patients with Hypertrophic Cardiomyopathy N. Engl. J. Med., October 24, 2002; 347(17): 1326 - 1333. [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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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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 B. J. Maron Hypertrophic Cardiomyopathy: A Systematic Review JAMA, March 13, 2002; 287(10): 1308 - 1320. [Abstract] [Full Text] [PDF]
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 G. Li, M. A. Borger, W. G. Williams, R. D. Weisel, D. A. G. Mickle, E. D. Wigle, and R.-K. Li Regional overexpression of insulin-like growth factor-I and transforming growth factor-{beta}1 in the myocardium of patients with hypertrophic obstructive cardiomyopathy J. Thorac. Cardiovasc. Surg., January 1, 2002; 123(1): 89 - 95. [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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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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 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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P. Boekstegers, P. Steinbigler, A. Molnar, M. Schwaiblmair, A. Becker, A. Knez, R. Haberl, and G. Steinbeck Pressure-guided nonsurgical myocardial reduction induced by small septal infarctions in hypertrophic obstructive cardiomyopathy J. Am. Coll. Cardiol., September 1, 2001; 38(3): 846 - 853. [Abstract] [Full Text] [PDF]
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S. F. Nagueh, S. J. Stetson, N. M. Lakkis, D. Killip, A. Perez-Verdia, M. L. Entman, W. H. Spencer III, and G. Torre-Amione Decreased Expression of Tumor Necrosis Factor-{{alpha}} and Regression of Hypertrophy After Nonsurgical Septal Reduction Therapy for Patients With Hypertrophic Obstructive Cardiomyopathy Circulation, April 10, 2001; 103(14): 1844 - 1850. [Abstract] [Full Text] [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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P.P. Dimitrow, D. Dudek, and J.S. Dubeil The risk of alcohol leakage into the left anterior descending coronary artery during non-surgical myocardial reduction in patients with obstructive hypertrophic cardiomyopathy. Eur. Heart J., March 1, 2001; 22(5): 437 - 437. [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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M. V. Sherrid, D. Z. Gunsburg, S. Moldenhauer, and G. Pearle Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1344 - 1354. [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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P. Spirito, P. Bellone, K. M. Harris, P. Bernabo, P. Bruzzi, and B. J. Maron Magnitude of Left Ventricular Hypertrophy and Risk of Sudden Death in Hypertrophic Cardiomyopathy N. Engl. J. Med., June 15, 2000; 342(24): 1778 - 1785. [Abstract] [Full Text] [PDF]
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H. Seggewiss Percutaneous transluminal septal myocardial ablation: A new treatment for hypertrophic obstructive cardiomyopathy Eur. Heart J., May 1, 2000; 21(9): 704 - 707. [PDF]
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W Ruzyllo, L Chojnowska, M Demkow, A Witkowski, B Kusmierczyk-Droszcz, W Piotrowski, L Rausinska, M Karcz, L Malecka, and W Rydlewska-Sadowska Left ventricular outflow tract gradient decrease with non-surgical myocardial reduction improves exercise capacity in patients with hypertrophic obstructive cardiomyopathy Eur. Heart J., May 1, 2000; 21(9): 770 - 777. [Abstract] [PDF]
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P M Elliott, S J Brecker, and W J McKenna Left ventricular opacification during selective intracoronary injection of echocardiographic contrast in patients with hypertrophic cardiomyopathy Heart, April 1, 2000; 83(4): 7e - 7. [Abstract] [Full Text]
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C. J KNIGHT Five years of percutaneous transluminal septal myocardial ablation Heart, March 1, 2000; 83(3): 255 - 256. [Full Text]
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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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B. Bhargava and R. Agarwal Can We Predict Complete Heart Block After Alcohol Ablation For Hypertrophic Cardiomyopathy? Circulation, December 21, 1999; 100 (25): e144 - e144. [Full Text] [PDF]
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H. Kuhn, F.H. Gietzen, M. Schafers, M. Freick, B. Gockel, C. Strunk-Muller, E. Jachmann, and O. Schober Changes in the left ventricular outflow tract after transcoronary ablation of septal hypertrophy (TASH) for hypertrophic obstructive cardiomyopathy as assessed by transoesophageal echocardiography and by measuring myocardial glucose utilization and perfusion Eur. Heart J., December 2, 1999; 20(24): 1808 - 1817. [Abstract] [PDF]
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U. Sigwart, 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 • Response Circulation, November 9, 1999; 100 (19): e99 - e99. [Full Text] [PDF]
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M. Y. Henein, C. A. O'Sullivan, I. S. Ramzy, U. Sigwart, and D. G. Gibson Electromechanical left ventricular behavior after nonsurgical septal reduction in patients with hypertrophic obstructive cardiomyopathy J. Am. Coll. Cardiol., October 1, 1999; 34(4): 1117 - 1122. [Abstract] [Full Text] [PDF]
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S. F. Nagueh, N. M. Lakkis, K. J. Middleton, D. Killip, W. A. Zoghbi, M. A. Quinones, and W. H. Spencer III Changes in left ventricular filling and left atrial function six months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy J. Am. Coll. Cardiol., October 1, 1999; 34(4): 1123 - 1128. [Abstract] [Full Text] [PDF]
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B.J. Maron New interventions for obstructive hypertrophic cardiomyopathy: promise and prudence Eur. Heart J., September 2, 1999; 20(18): 1292 - 1294. [PDF]
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F.H. Gietzen, Ch.J. Leuner, U. Raute-Kreinsen, A. Dellmann, J. Hegselmann, C. Strunk-Mueller, and H.J. Kuhn Acute and long-term results after transcoronary ablation of septal hypertrophy (TASH). Catheter interventional treatment for hypertrophic obstructive cardiomyopathy Eur. Heart J., September 2, 1999; 20(18): 1342 - 1354. [Abstract] [PDF]
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B. J. Maron, S. A. Casey, L. C. Poliac, T. E. Gohman, A. K. Almquist, and D. M. Aeppli Clinical Course of Hypertrophic Cardiomyopathy in a Regional United States Cohort JAMA, February 17, 1999; 281(7): 650 - 655. [Abstract] [Full Text] [PDF]
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S. F. Nagueh, N. M. Lakkis, K. J. Middleton, D. Killip, W. A. Zoghbi, M. A. Quinones, and W. H. Spencer Changes in Left Ventricular Diastolic Function 6 Months After Nonsurgical Septal Reduction Therapy for Hypertrophic Obstructive Cardiomyopathy Circulation, January 26, 1999; 99(3): 344 - 347. [Abstract] [Full Text] [PDF]
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 L.J. Kappenberger, C. Linde, X. Jeanrenaud, C. Daubert, W. McKenna, E. Meisel, N. Sadoul, L. Chojnowska, L. Guize, D. Gras, et al. Clinical progress after randomized on/off pacemaker treatment for hypertrophic obstructive cardiomyopathy Europace, January 1, 1999; 1(2): 77 - 84. [Abstract] [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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J Kazmierczak, Z Kornacewicz-Jach, M Kisly, R Gil, and A Wojtarowicz Electrocardiographic changes after alcohol septal ablation in hypertrophic obstructive cardiomyopathy Heart, September 1, 1998; 80(3): 257 - 262. [Abstract] [Full Text]
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M. Hamada, K. Kodama, K. Hiwada, U. Sigwart, D. Gibson, M. Henein, and R. Anderson Clinical Significance of Obstruction of the First Major Septal Branch • Response Circulation, July 28, 1998; 98 (4): 377 - 378. [Full Text]
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P. H. Pak, W. L. Maughan, K. L. Baughman, R. S. Kieval, and D. A. Kass Mechanism of Acute Mechanical Benefit From VDD Pacing in Hypertrophied Heart : Similarity of Responses in Hypertrophic Cardiomyopathy and Hypertensive Heart Disease Circulation, July 21, 1998; 98(3): 242 - 248. [Abstract] [Full Text] [PDF]
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S. F. Nagueh, N. M. Lakkis, Z.-X. He, K. J. Middleton, D. Killip, W. A. Zoghbi, M. A. Quinones, R. Roberts, M. S. Verani, N. S. Kleiman, et al. Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy J. Am. Coll. Cardiol., July 1, 1998; 32(1): 225 - 229. [Abstract] [Full Text] [PDF]
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B. Bhargava, R. Agarwal, V. K. Behl, K. S. Reddy, U. Kaul, S. C. Manchanda, and U. Sigwart Alcohol Therapy for Hypertrophic Cardiomyopathy: Is It Time to Toast? • Response Circulation, May 26, 1998; 97(20): 2096 - 2097. [Full Text]
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H. Seggewiss, U. Gleichmann, L. Faber, B. J. Maron, P. Spirito, W. J. McKenna, and C. E. Seidman The Management of Hypertrophic Cardiomyopathy N. Engl. J. Med., July 31, 1997; 337(5): 349 - 350. [Full Text]
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