Percutaneous Transluminal Septal Myocardial Ablation in Hypertrophic Obstructive Cardiomyopathy
Results With Respect to Intraprocedural Myocardial Contrast Echocardiography
From the Department of Cardiology, Heart Center NRW, Ruhr-University of Bochum, Bad Oeynhausen, Germany.
Correspondence to PD Dr Hubert Seggewiss, Department of Cardiology, Heart and Diabetes Center NRW, Ruhr-University of Bochum, Georgstr 11, D-32545 Bad Oeynhausen, FRG. E-mail seggewiss.hubert{at}t-online.de
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Percutaneous transluminal septal myocardial ablation (PTSMA) has been introduced as an alternative procedure for reducing the left ventricular outflow tract gradient (LVOTG) in hypertrophic obstructive cardiomyopathy. We report on the acute and mid-term results in 91 symptomatic patients with respect to intraprocedural myocardial contrast echocardiography (MCE).
Methods and Results—PTSMA was intended for 46 women and 45 men (54.1±15.5 years). In 2 patients, the intervention could not be completed. In the first 30 patients the target vessel was determined by probatory balloon occlusion alone and in the remainder by additional intraprocedural MCE. Resting LVOTG was reduced from 73.8±35.4 to 16.6±18.1 and nostextrasystolic LVOTG from 149.3±42.5 to 61.9±43.0 mm Hg (P<0.0001 each). In 10 (11%) patients, permanent DDD pacemaker implantation was necessary. Two (2%) patients died, 1 from ventricular fibrillation associated with treatment for chronic obstructive pulmonary disease after 9 days and 1 from fulminant pulmonary embolism after 2 days. After 3 months, mean New York Heart Association class was reduced from 2.8±0.6 to 1.1±1.0 (P<0.0001). The LVOTG remained reduced to 14.6±25.5 mm Hg at rest and 49.1±48.7 mm Hg (P<0.0001 each). Four patients underwent successful repeat PTSMA. Determination of the target vessel by MCE was associated with a higher rate of acute (92% vs 70%; P<0.01) and mid-term (94% vs 64%; P<0.01) success.
Conclusions—PTSMA is a promising nonsurgical technique for reduction of symptoms and LVOTG in hypertrophic obstructive cardiomyopathy. MCE has been shown to be a useful addition to probatory balloon occlusion for target vessel selection. Prospective, long-term observations of larger populations and a comparison with the established forms of therapy are necessary to determine the definitive significance of PTSMA.
Key Words: hypertrophy • cardiomyopathy • ablation • contrast media • echocardiography
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Nonsurgical catheter treatment of hypertrophic obstructive cardiomyopathy (HOCM) was introduced in 1994.1 In patients considered to be candidates for surgical myectomy, alcohol-induced percutaneous transluminal septal myocardial ablation (PTSMA) reduces symptoms and left ventricular (LV) outflow tract gradients (LVOTG).1 2 3 4 5 6 7 Intraprocedural myocardial contrast echocardiography (MCE) as an imaging technique has been integrated into the procedure by our group.8 We report on acute and mid-term results in the first 91 patients treated with PTSMA with respect to this technical modification.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Population
Between January 1996 and December 1997, 182 patients with HOCM were referred to our center for further evaluation. Interventional treatment was intended in 91 of these who were seen with the following inclusion criteria: New York Heart Association/Canadian Cardiovascular Class (NYHA/CCS) functional class III or IV, LVOTG >50 mm Hg at rest or >100 mm Hg at provocation (Valsalva maneuver, isoproterenol, or postextrasystole) and
1 septal
branch suitable for intervention. Patients with class II symptoms were
accepted for intervention if medical treatment was not tolerated or if
a high LVOTG was combined with the presence of multiple risk factors
for sudden cardiac death.9 10 Patients with
coexistent cardiac abnormalities requiring surgery were
excluded. Myectomy had been performed in 5 (6%) patients 8.5±2.5
years (range 4 to 11) before PTSMA; 5 (6%) patients had not responded
to previous DDD pacemaker implantation. Further detailed baseline data
are displayed in Table 1
.
|
Written informed consent was given before intervention, after intensive discussion of the various treatment options, with special attention to the novelty of PTSMA and the absence of long-term experience.
Preinterventional Studies
The study protocol with preinterventional and postinterventional
workup is shown in Table 2.
Echocardiographic measurements were obtained following
ASE11 guidelines. LVOTG was assessed by
continuous wave Doppler echocardiography (CWDE)
at rest and at Valsalva maneuver. Mitral regurgitation
and systolic anterior movement (SAM) of the mitral valve
apparatus were graded semiquantitatively (ie, from 0=absent
to 3=severe/with complete septal apposition12 ).
Symptom-limited bicycle exercise tests in upright position-starting
with 25 W and increasing by 25 W every 2 minutes-were performed in
patients with functional class <IV and LVOT resting gradients
<100 mm Hg. Pulmonary artery mean pressure was measured
at rest and at supine bicycle exercise with the above-mentioned
protocol.
|
Intervention
Before PTSMA, a diagnostic left heart
catheterization was performed. The first 30 patients
underwent PTSMA as previously described by
Sigwart1 and by our own
group3 6 with measurement of the LV inflow tract
pressure by a Brockenbrough catheter introduced transseptally. From
patient 31 onward, LV inflow tract pressure was measured with a 5F
multipurpose or modified-4 sideholes only at the pigtail segment-5F
pigtail catheter (Cordis) by a retrograde approach and with careful
placement of the catheter tip to exclude entrapment. Aortic pressure
was monitored by the percutaneous transluminal
coronary angioplasty guiding catheter after exclusion of an
aortic valve gradient. The LVOTG was assessed at rest and after a
premature ventricular beat. All patients received a 4F
transfemoral pacemaker lead (Cordis) introduced into the right
ventricular apical region and 10 000 IU IV heparin as
antithrombotic prophylaxis.
The presumed target vessel was then selectively intubated with a
0.014-inch guide wire through a 7F or 8F percutaneous
transluminal coronary angioplasty guiding catheter (Figure 1). A short, slightly oversized
over-the-wire balloon (1.5 to 3.0 mm) was introduced and inflated,
and the distal vessel bed was contrasted. After exclusion of dye reflux
into the left anterior descending coronary artery (LAD), and if
probatory vessel closure by the inflated balloon had resulted in
significant LVOTG reduction, the alcohol was injected in fractions of 1
mL in the first 30 patients.
|
In the remaining patients, additional intraprocedural MCE was performed
to determine the target vessel. After verification of the correct
balloon position and the hemodynamic effect of
probatory balloon occlusion, 1 to 2 mL of the echo contrast agent
(Levovist, concentration 350 mg/mL; Schering) was injected through the
inflated balloon catheter under continuous transthoracic
echocardiographic imaging. Alcohol was given only when
the area of maximum flow acceleration, that is, gradient formation, and
opacified septal myocardium were adjacent to each other
(Figure 2). In case of mismatch, the
diagnostic coronary angiogram was revised and the
procedure repeated with another septal branch.
|
After definitive identification of the target vessel, patients received 0.15 to 0.3 mg IV buprenorphine just before the alcohol injection. The balloon remained inflated for 10 minutes after the alcohol administration to enhance tissue contact and to exclude alcohol reflux into the LAD. Finally, hemodynamic measurements were repeated.
Follow-Up Studies
All patients were monitored on the coronary care unit
(CCU) for 48 hours. The vascular sheaths were removed after
normalization of the coagulation measurements. Cardiac enzymes and ECG
controls were done every 4 hours; echo and CWDE studies were done once
per day. Before discharge, noninvasive follow-up was performed as shown
in Table 2
. If possible, medical treatment was continued with a
cardioselective ß-blocker or, in case of
contraindications, with verapamil. After 3 months, all
patients underwent clinical and noninvasive follow-up; 70 (80%)
patients had additional recatheterization.
Statistics
Patient data were collected in a relational database (Filemaker
3.0, Claris Corp) and analyzed with the Statview 4.5 (Abacus
Concepts) and Winstat 3.1 (Kalmia Co Inc) statistical software
packages. Results of continuous variables are displayed as
mean±SD. Student's t tests for paired and unpaired samples
were used for group comparisons (baseline measurements, in-hospital
follow-up, and 3-month follow-up as well as comparisons between the
patients with and those without MCE for target vessel selection).
Frequency distributions were assessed with the
2 test. ANOVA was performed when comparing
more than 2 groups. Differences were considered significant if the
2-tailed P value was <0.05.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Technical Aspects
PTSMA was completed in 89 patients, with a mean procedural time of 98±33 minutes (46 to 190) and a fluoroscopy time of 14±10 minutes (3 to 45). The amount of contrast dye was 262±127 mL (50 to 680), the amount of alcohol injected 3.4±1.7 mL (1.5 to 11), with 1.1±0.3 target vessels occluded.1 2 3 Since introduction of MCE, only 1 vessel was occluded per session. In 5 (8.5%) out of 59 patients, the target vessel was found originating from a diagonal or intermediate branch of the left coronary artery. Despite MCE introduction, intervention time decreased with growing experience (Table 4
). In 2 patients, alcohol ablation was not performed: The
septal branch could not be reached with a guide wire in 1 patient; in
another patient with repeat PTSMA, a stable balloon position could not
be achieved. These patients underwent surgery later on.
|
Complications
In the Catheterization Laboratory
Chest pain induced by alcohol injection could be managed by
central analgesics in all patients. In 1 patient with significant
pericardial effusion induced by a penetrating pacer lead, emergency
percutaneous pericardiocentesis was performed and PTSMA
successfully continued. Complete heart block developed in a total of 62
(70%) patients. At CCU admission, complete heart block was still
present in 31 patients (35%). All patients left the
catheterization laboratory in stable
hemodynamic condition.
During In-Hospital Course
After failed compression therapy, 1 patient needed surgery for a
false aneurysm at the puncture site. Two patients required
blood transfusions because of groin hematoma. Pericardial effusion
without hemodynamic compromise was seen in 5 patients.
In 3 patients with pulmonary comorbidity, respiratory problems
developed, mechanical ventilation being necessary in 1 of these. In
another patient with severe pulmonary obstructive disease,
exacerbation and intensive (topical and intravenous)
treatment with ß-agonists was associated with the first death of our
series6 caused by intractable
ventricular fibrillation 9 days after a successful
intervention. A femoral vein thrombosis, probably induced by the
indwelling pacemaker lead, leading to fulminant pulmonary
embolism and refractory shock 36 hours after PTSMA, was diagnosed by
postmortem examination only.
Ten (11%) patients required permanent DDD pacemaker implantation:
because of sustained trifascicular block in 4 and intermittent
conduction problems in 6 patients, in 1 of these 11 days after
intervention. Introduction of MCE was associated with a higher rate of
rapid recovery of the atrioventricular (AV) conduction
and a reduction of the pacemaker implantation rate from 17% to 7%
(Table 4).
Until Follow-Up
One patient underwent thrombectomy of a symptomatic
femoral vein thrombosis 3 weeks after discharge and a normal
postoperative course. Clinically relevant rhythm disturbances
or other HOCM complications were not seen in the follow-up period after
PTSMA.
Cardiac Enzyme Changes
The creatine kinase (CK) peak was 676±347 U/L (201 to 1940) after
10.6±4.9 hours (4 to 24) with an MB fraction of 85±49 U/L (18 to
281). The GOT peak was 110±64 U/L (21 to 446). Maximum enzyme rise
correlated with the amount of alcohol injected, not with the
hemodynamic efficacy of PTSMA. The CK-MB peak was
significantly lower in the patients with MCE for target vessel
selection (Table 4).
ECG Changes
In 52 (58%) patients, a new bundle branch block was present
after PTSMA. The right branch was predominantly affected (43%). After
3 months, 9 of these bundle branch blocks had disappeared. Two patients
with DDD pacemaker implantation after PTSMA showed complete LVOTG
elimination and stable recovery of the AV conduction at follow-up.
Symptoms and Exercise Tolerance
A number of patients reported symptomatic improvement
in the catheterization laboratory. After 3 months 82
(94%) out of the returning 87 patients reported significant
improvement of symptoms and exercise tolerance, with a mean NYHA class
reduction from 2.8±0.6 to 1.1±1.0 and a maximum tolerated workload
improvement from 87.5±59.4 to 110.3±9.5 W (P<0.05).
Complete elimination of symptoms was reported by 29 (33%) patients.
Clinical improvement was more frequent and more pronounced in the
patients with an MCE-guided intervention (Table 4).
Hemodynamic Effects: LVOT Obstruction
LVOTG at rest was reduced from 73.8±35.4 to 36.4±29.3
mm Hg (P<0.001) after probatory balloon occlusion and to
16.6±18.1 mm Hg (P<0.0001) after alcohol injection.
Postextrasystolic gradients and the
obstruction-associated phenomena of SAM and mitral
regurgitation were reduced in a parallel way (Table 3). In 75 (84%) patients, a short-term
hemodynamic success as defined by a complete
elimination of LVOTG (Figure 3) or a
reduction of >50% was achieved in 21 (70%) of 30 patients without
and in 54 (92%) of 59 patients with intraprocedural echo monitoring
(P<0.01).
|
|
After 3 months, in 59 (84%) of 70 patients with
recatheterization, sustained LVOTG reduction was seen;
in 30 (43%) of these the LVOTG showed further regression as compared
with the acute results. Hemodynamic mid-term success
rate (>50% LVOTG reduction) again was higher in the MCE group (45 of
48 [94%] vs 14 of 22 [64%]; P<0.01). Further on, the
rate of LVOTG recurrence was lower (1 of 48 [2%] vs 5 of 22
[23%]; P<0.05; Table 4).
The CWDE measurements of the LVOTG as well as the echo data concerning
SAM and mitral regurgitation, available in all 87
patients, paralleled the invasive data (Table 3). In all 4 (5%)
patients who underwent repeat PTSMA after 3 months, this led to
complete LVOTG elimination.
Systolic and Diastolic LV Function and LV
Hypertrophy
Until discharge, all patients developed a circumscript akinesia of
the subaortic septum. In the patients with MCE guiding, this area
matched with the region opacified intraoperatively (Figure 2). Global
LV function remained unchanged. Late diastolic mitral
inflow was accentuated together with a prolonged deceleration time of
the early mitral inflow wave (Table 3). Until follow-up, left atrial
diameter significantly decreased as well as LV
end-diastolic pressure and mean pulmonary artery
pressures. Both septal and LV posterior wall thickness showed
significant regression (Table 3).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Obstruction of LV outflow, diastolic dysfunction, and rhythm disturbances including sudden cardiac death are the main problems in patients with HOCM.9 10 Medical therapy, surgical myectomy, and AV sequential pacing predominantly aim for LVOTG reduction.13 14 15 16 17 18 19 Although the effect of medical treatment and AV sequential pacing on symptoms and LVOT obstruction is often limited,19 the good symptomatic and hemodynamic results of surgery are overshadowed by considerable perioperative morbidity and mortality rates.16 17 18 After successful surgery, however, patients also tend to have improved markers of diastolic LV function and a favorable prognosis.9 10
Forty years after the first descriptions,20 21 interventional cardiology is now developing a new treatment option for HOCM.1 2 3 4 5 6 7 8 22 The induction of a limited "therapeutic" infarction within the hypertrophied septal myocardium1 leads to localized thinning and contractile dysfunction, expands the LV outflow tract, and thus reduces LVOTG and depending symptoms. The first preliminary studies leading to this catheter-based imitation of surgical myectomy date from the 1980s (Reference 11 and Berghoefer G, personal communication, 1989). In 1994, probatory balloon occlusion of septal branches of the left coronary artery, leading to transient ischemia-induced LVOTG reduction, was reported.2
In 1995, Sigwart1 published the first report on definitive alcohol-induced septal reduction in 3 severely symptomatic patients. The first small series showed promising results concerning symptoms and LVOTG reduction,3 4 6 7 with acceptable complication rates.
Our experience with 91 patients is in line with these reports. Baseline data show that the clinical spectrum of HOCM in terms of disease severity and complications is well represented in our patient group.9 10 Notably, patients with prior surgical myectomy and DDD pacemaker implantation could also be treated effectively.6 The previous experience concerning ongoing LVOTG reduction and absence of complications until mid-term follow-up was confirmed3 6 as well as our strategy of awaiting the remodeling process before considering a repeat PTSMA or other nonmedical treatment options.
An important improvement of the new method in our opinion has been gained by the integration of echocardiographic monitoring.8 23 Analysis of the first patients6 8 had shown that probatory balloon occlusion of the presumed target vessel did not reliably predict the definitive treatment result. In some of these patients, up to 3 vessels had to be occluded for satisfactory LVOTG reduction.3 4 In view of the cases of HOCM with spontaneous LV dilatation24 and LVOTG reduction, carrying a particularly bad prognosis, we tried to optimize the amount of ablated myocardium.
With intracoronary injection of the echo contrast agent, opacification of the strategic septal area involved in LVOTG formation and thus a definition of the extent and localization of the induced necrosis was possible in all cases.
By the routine use of MCE, in 5 out of 59 patients the culprit septal branch originated not from the LAD but from intermediate or diagonal branches and would have been missed without intraprocedural echo monitoring. Furthermore, patients with MCE-guided PTSMA showed favorable acute and mid-term results at a lower cost in terms of myocardial loss as assessed by the enzyme peaks. Importantly, the rate of LVOTG recurrence after a short-term success was significantly reduced. In the future, the reduction of sustained AV conduction disturbances may also translate into a reduced rate of pacemaker implantations. Currently, the pacemaker implantation rate after MCE-guided PTSMA (7%) is comparable to that associated with surgical myectomy.16 18
As far as diastolic and global systolic LV function is concerned, our hemodynamic follow-up data demonstrate improvement of LV end-diastolic pressure as well as a reduction of pulmonary artery pressure both at rest and with exercise. The changes of the mitral inflow pattern should therefore not be interpreted as an aggravation of diastolic dysfunction. In contrast, it seems more likely that a preexisting pseudonormalization of the mitral inflow pattern regressed as a consequence of a reduced transmitral driving pressure. The reduction of left atrial dimensions lends further support to this interpretation.25
Surprisingly, not only septal hypertrophy decreased as a consequence of the therapeutic infarction, but also LV posterior wall thickness. This may be due to relief of the pressure overload and may also have influenced diastolic function parameters.
Taking into account the fact that a learning curve is still present in this series, PTSMA seems to be a quite safe procedure. Complications, however, must be considered as previously reported, that is, thoracic discomfort, AV conduction disturbances, ventricular dysrhythmias, and death.1 3 4 6 7 The first death,6 associated with severe chronic obstructive pulmonary disease, led us to include routine preinterventional assessment of lung function in the study protocol and to prolong CCU monitoring in affected patients. The second death from pulmonary thromboembolism underlines the importance of timely sheath removal from the femoral vessels. In the case of sustained AV conduction disturbances, a transjugular pacing lead should be inserted. Ventricular septal defects and cerebral events, also possible from a theoretic point of view, have not been observed to date.
Limitations
Several limitations must be considered in this report. We did not
perform invasive electrophysiological
studies in our patients to assess the risk of ventricular
tachyarrhythmias or AV conduction disturbances.
The echo indexes used are rough markers of diastolic LV
function. Considering the effect of MCE on target vessel selection and
treatment results, learning curve effects cannot be ruled out.
Finally, the patients were not randomly assigned to interventional treatment but by individual indication. A comparison with established forms of nonmedical treatment of HOCM is thus not possible.
Conclusions
PTSMA is a promising interventional treatment modality for
patients with HOCM who do not show satisfactory response to medical
therapy. Without the operative trauma including cardiopulmonary
bypass, in >90% of the patients elimination or a substantial
reduction of the LVOT gradient is possible. Intraprocedural
echocardiographic monitoring has proven to be an
important improvement of the new method. Future work should be directed
at reducing the rate of AV conduction system lesions and definitive
pacemaker implantations on the one hand and at early and reliable
recognition of those patients with irreversible conduction defect on
the other hand. Furthermore, the long-term effect of PTSMA on global
systolic and diastolic function and on prognosis
remains to be assessed. A prospective registry of all interventionally
treated patients with HOCM will be very helpful in clarifying these
issues. The definitive value of PTSMA as compared with other treatment
modalities remains to be studied in a prospective, randomized
trial.
Received May 22, 1998; revision received August 10, 1998; accepted August 11, 1998.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet. 1995;346:211–214.[Medline] [Order article via Infotrieve]
2.
Gietzen F, Leuner C, Gerenkamp T, Kuhn H. Relief of
obstruction in hypertrophic cardiomyopathy by
transient occlusion of the first septal branch of the left
coronary artery. Eur Heart J. 1994;15:125.
Abstract.
3. Gleichmann U, Seggewiss H, Faber L, Fassbender D, Schmidt HK, Strick S. Kathetertherapie der hypertrophen obstruktiven Kardiomyopathie. Dtsch Med Wochenschr. 1996;121:679–685.[Medline] [Order article via Infotrieve]
4.
Knight CJ, Kurbann AS, Seggewiss H, Henlein M, Gunning
M, Harrington D, Fassbender D, Gleichmann U, Sigwart U. Nonsurgical
septal reduction for hypertrophic obstructive
cardiomyopathy: outcome in the first series of
patients. Circulation. 1997;95:2075–2081.
5.
Kuhn H, Gietzen F, Leuner C, Gerenkamp T. Induction of
subaortic septal ischemia to reduce obstruction in hypertrophic
obstructive cardiomyopathy. Eur Heart
J. 1997;18:846–851.
6.
Seggewiss H, Gleichmann U, Faber L, Fassbender D,
Schmidt HK, Strick S. Percutaneous transluminal septal
myocardial ablation in hypertrophic obstructive
cardiomyopathy: acute results and 3-months
follow-up in 25 patients. J Am Coll Cardiol. 1998;31:252–258.
7.
Seggewiss H, Gleichmann U, Faber L. The management of
hypertrophic cardiomyopathy. N Engl
J Med. 1997;337:349–350.
8. Faber L, Seggewiss H, Fassbender D, Bogunovic N, Strick S, Gleichmann U. Catheter treatment in hypertrophic obstructive cardiomyopathy: identification of the perfusion area of septal branches by myocardial contrast echocardiography. Eur Heart J. 1997;18(suppl):368. Abstract.
9.
Spirito P, Seidman CE, McKenna WJ, Maron BJ. The
management of hypertrophic cardiomyopathy.
N Engl J Med. 1997;336:775–785.
10.
Wigle DE, Rakowski H, Kimball BP, Williams WG.
Hypertrophic cardiomyopathy: clinical spectrum and
treatment. Circulation. 1995;92:1680–1692.
11.
Sahn DJ, De Maria AN, Kisslo J, Weyman A. The committee
on M-mode standardization of the American Society of
Echocardiography. Circulation. 1978;58:1072–1083.
12.
Pollick C, Rakowsky H, Wigle ED. Muscular subaortic
stenosis: The quantitative relationship between SAM and the
pressure gradient. Circulation. 1984;69:43–49.
13. Braunwald E, Lambrew CT, Rockoff S, Ross J, Morrow AG. Idiopathic hypertrophic subaortic stenosis: a description of the disease based on analysis of 64 patients. Circulation. 1964;30(suppl IV):3–213.
14.
Fananapazir L, Epstein ND, Curiel RV, Panza JA, Tripodi
D, McAreavey D. Long-term results of dual-chamber (DDD) pacing in
obstructive hypertrophic cardiomyopathy.
Circulation. 1994;90:2731–2742.
15.
Kappenberger L, Linde C, Daubert C, McKenna W, Meisel
E, Sadoul N, Chojnowska L, Guize L, Gras D, Jeanrenaud X, Ryden L, and
the PIC Study Group. Pacing in hypertrophic obstructive
cardiomyopathy. Eur Heart J. 1997;18:1249–1256.
16.
McCully RB, Nishimura RA, Tajik AJ, Schaff HY,
Danielson GK. Extent of clinical improvement after surgical treatment
of hypertrophic obstructive cardiomyopathy.
Circulation. 1996;94:467–471.
17. Morrow AG, Brockenbrough EC. Surgical treatment of idiopathic hypertrophic subaortic stenosis: technique and hemodynamic results of subaortic ventriculotomy. Ann Surg. 1961;154:181–189.[Medline] [Order article via Infotrieve]
18.
Robbins RC, Stinson EB, Daily PO. Long-term results of
left ventricular myotomy and myectomy for obstructive
hypertrophic cardiomyopathy. J Thorac
Cardiovasc Surg. 1996;111:586–596.
19. Nishimura RA, Hayes DL, Ilstrup D, Holmes DR, Tajik AJ. Effect of dual-chamber pacing on systolic and diastolic function in patients with hypertrophic cardiomyopathy: acute Doppler echocardiographic and catheterization hemodynamic study. J Am Coll Cardiol. 1996;27:421–430.[Abstract]
20. Brock R. Functional obstruction of the left ventricle (acquired aortic subvalvular stenosis). Guy's Hosp Rep. 1957;106:221–228.[Medline] [Order article via Infotrieve]
21. Teare D. Asymmetrical hypertrophy of the heart in young adults. Br Heart J. 1957;20:1–8.
22.
Brugada P, De Swart H, Smeets JLRM, Wellens HJJ.
Transcoronary chemical ablation of ventricular
tachycardia. Circulation. 1989;79:475–482.
23. Faber L, Seggewiss H, Fassbender D, Strick S, Gleichmann U. Guiding of PTSMA in obstructive hypertrophic cardiomyopathy by myocardial contrast echocardiography: a case report. J Intervent Cardiol. In press.
24. Hina K, Kusachi S, Iwasaka K, Nogami K, Moritani H, Kita T, Taniguchi G, Tsuji T. Progression of left ventricular enlargement in patients with hypertrophic cardiomyopathy: incidence and prognostic value. Clin Cardiol. 1993;16:403–407.[Medline] [Order article via Infotrieve]
25.
Nishimura RA, Tajik AJ. Evaluation of
diastolic filling of left the ventricle in health and
disease: Doppler echocardiography is the
clinician's Rosetta Stone. J Am Coll Cardiol. 1997;30:8–18.Catheter treatment is a new option for patients with
symptomatic hypertrophic obstructive
cardiomyopathy. We report on the acute and mid-term
results in 91 patients. Peri-interventional mortality was 2%. In
85%, a >50% reduction or elimination of the left
ventricular outflow tract gradient was achieved, leading to
marked symptomatic improvement without relevant
complications until follow-up after 3 months. Treatment results were
improved by intraprocedural use of myocardial contrast
echocardiography.[Abstract]
This article has been cited by other articles:
 |
|
 |
|
  J. Wang, J. M. Buergler, K. Veerasamy, Y. P. Ashton, and S. F. Nagueh Delayed untwisting: the mechanistic link between dynamic obstruction and exercise tolerance in patients with hypertrophic obstructive cardiomyopathy. J. Am. Coll. Cardiol., September 29, 2009; 54(14): 1326 - 1334. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G S Soor, A Luk, E Ahn, J R Abraham, A Woo, A Ralph-Edwards, and J Butany Hypertrophic cardiomyopathy: current understanding and treatment objectives J. Clin. Pathol., March 1, 2009; 62(3): 226 - 235. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S R Ommen, P M Shah, and A J Tajik Left ventricular outflow tract obstruction in hypertrophic cardiomyopathy: past, present and future Heart, October 1, 2008; 94(10): 1276 - 1281. [Full Text] [PDF]
|
|
|
|
 |
|
 T. Butz, H.K. Schmidt, D. Fassbender, H. Esdorn, M. Wiemer, D. Horstkotte, and L. Faber Echo-guided percutaneous coil embolization of a symptomatic massive metastasis of a renal cell carcinoma in the right ventricular outflow tract Eur J Echocardiogr, September 1, 2008; 9(5): 725 - 727. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Butz, D. Horstkotte, C. Langer, H. Esdorn, G. Kleikamp, R. Korfer, and L. Faber Significant obstruction of the right and left ventricular outflow tract in a patient with biventricular hypertrophic cardiomyopathy Eur J Echocardiogr, March 1, 2008; 9(2): 344 - 345. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Fifer and G. J. Vlahakes Management of Symptoms in Hypertrophic Cardiomyopathy Circulation, January 22, 2008; 117(3): 429 - 439. [Full Text] [PDF]
|
|
|
|
 |
|
 W. J. Stewart Imaging the future of transcatheter aortic valve replacement. J. Am. Coll. Cardiol. Img., January 1, 2008; 1(1): 25 - 28. [Full Text] [PDF]
|
|
|
|
 |
|
 M. W. Hansen and N. Merchant MRI of Hypertrophic Cardiomyopathy: Part 2, Differential Diagnosis, Risk Stratification, and Posttreatment MRI Appearances Am. J. Roentgenol., December 1, 2007; 189(6): 1344 - 1352. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Fifer Most Fully Informed Patients Choose Septal Ablation Over Septal Myectomy Circulation, July 10, 2007; 116(2): 207 - 216. [Full Text] [PDF]
|
|
|
|
 |
|
 D. M. Yoerger, C. A. Best, B. M. McQuillan, G. E. Supple, J. L. Guererro, J. E. Cluette-Brown, A. Hasaba, M. H. Picard, J. R. Stone, and M. Laposata Rapid Fatty Acid Ethyl Ester Synthesis by Porcine Myocardium Upon Ethanol Infusion into the Left Anterior Descending Coronary Artery Am. J. Pathol., May 1, 2006; 168(5): 1435 - 1442. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. H. Yacoub Surgical Versus Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy: The Pendulum Swings Circulation, July 26, 2005; 112(4): 450 - 452. [Full Text] [PDF]
|
|
|
|
|
|
R. Roberts and U. Sigwart Current Concepts of the Pathogenesis and Treatment of Hypertrophic Cardiomyopathy Circulation, July 12, 2005; 112(2): 293 - 296. [Full Text] [PDF]
|
|
|
|
|
|
W. G. van Dockum, A. M. Beek, F. J. ten Cate, J. M. ten Berg, O. Bondarenko, M. J.W. Gotte, J. W.R. Twisk, M. B.M. Hofman, C. A. Visser, and A. C. van Rossum Early Onset and Progression of Left Ventricular Remodeling After Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy Circulation, May 17, 2005; 111(19): 2503 - 2508. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Hering, D. Welge, D. Fassbender, D. Horstkotte, and L. Faber Quantitative analysis of intraprocedural myocardial contrast echocardiography during percutaneous septal ablation for hypertrophic obstructive cardiomyopathy Eur J Echocardiogr, December 1, 2004; 5(6): 443 - 448. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Faber, H. Seggewiss, D. Welge, D. Fassbender, H. K. Schmidt, U. Gleichmann, and D. Horstkotte Echo-guided percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: 7 years of experience Eur J Echocardiogr, October 1, 2004; 5(5): 347 - 355. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. O. Cheng, C. D. Kimmelstiel, and B. J. Maron In Percutaneous Transluminal Septal Myocardial Ablation for Hypertrophic Obstructive Cardiomyopathy, It Is Not the Speed of Intracoronary Alcohol Injection But the Amount of Alcohol Injected That Determines the Resultant Infarct Size * Response Circulation, July 20, 2004; 110(3): e23 - e23. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 S. Steinbis Hypertrophic Obstructive Cardiomyopathy and Septal Ablation Crit. Care Nurse, June 1, 2003; 23(3): 47 - 50. [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
T.-H. Park, N. M. Lakkis, K. J. Middleton, J. Franklin, W. A. Zoghbi, M. A. Quinones, W. H. Spencer III, and S. F. Nagueh Acute Effect of Nonsurgical Septal Reduction Therapy on Regional Left Ventricular Asynchrony in Patients With Hypertrophic Obstructive Cardiomyopathy Circulation, July 23, 2002; 106(4): 412 - 415. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
J. X. Qin, T. Shiota, H. M. Lever, D. N. Rubin, F. Bauer, Y. J. Kim, M. Sitges, N. L. Greenberg, J. K. Drinko, M. Martin, et al. Impact of left ventricular outflow tract area on systolic outflow velocity in hypertrophic cardiomyopathy: A real-time three-dimensional echocardiographic study J. Am. Coll. Cardiol., January 16, 2002; 39(2): 308 - 314. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
E. D. Wigle, L. Schwartz, A. Woo, and H. Rakowski To ablate or operate? that is the question! J. Am. Coll. Cardiol., November 15, 2001; 38(6): 1707 - 1710. [Full Text] [PDF]
|
|
|
|
|
|
R. Roberts and U. Sigwart New Concepts in Hypertrophic Cardiomyopathies, Part II Circulation, October 30, 2001; 104(18): 2249 - 2252. [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
L. Faber Acute and long-term results after TASH Eur. Heart J., April 1, 2000; 21(7): 590 - 591. [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
C. J KNIGHT Five years of percutaneous transluminal septal myocardial ablation Heart, March 1, 2000; 83(3): 255 - 256. [Full Text]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||