Skip Navigation

European Journal of Echocardiography 2004 5(5):347-355; doi:10.1016/j.euje.2004.01.001
© 2004 by European Society of Cardiology
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Faber, L.
Right arrow Articles by Horstkotte, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Faber, L.
Right arrow Articles by Horstkotte, D.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2004, The European Society of Cardiology

Echo-guided percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: 7 years of experience

Lothar Fabera,*, Hubert Seggewissb, Dirk Welgea, Dieter Fassbendera, Henning K. Schmidta, Ulrich Gleichmanna and Dieter Horstkottea

aDepartment of Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr-University Bochum, Georgstr. 11, D-32545 Bad Oeynhausen, Germany
bMedical Clinic, Leopoldina-Hospital, Schweinfurt, Germany

Received 21 July 2003; received in revised form 22 December 2003; accepted after revision 5 January 2004.

* Corresponding author. Tel.: +49-5731-97-2070; fax: +49-5731-97-1874. lfaber{at}hdz-nrw.de


    Abstract
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Aims: To analyze the impact of intra-procedural echocardiographic imaging on the interventional strategy in ethanol-induced septal ablation (PTSMA) for symptomatic hypertrophic obstructive cardiomyopathy (HOCM), based on a single-center experience of 7 years.

Methods and results: PTSMA was intended for refractory symptoms in 337 patients (pts.) with HOCM (mean age: 54±15 years), with 312 procedures completed by injection of 2.8±1.2 ml ethanol. In 25 pts. (8%) the intervention was aborted without ethanol injection, mostly because of echocardiographic findings (n = 18/6%). An echocardiography-driven target vessel change was necessary in 33 pts. (11%). In the 312 pts. who received ethanol, permanent pacing was necessary in 22 cases (7%). In-hospital mortality was 1.3% (4 pts.). After 3 months, mean NYHA functional class was reduced from 2.9±0.5 to 1.5±0.6 (p<0.0001) along with a gradient reduction from 60±33 to 13±18 mmHg at rest, and from 120±43 to 38±35 mmHg with provocation (p<0.0001 each). Exercise capacity improved from 94±51 to 115±43 W, peak oxygen consumption from 18±4 to 21±6 ml/kg/min (p<0.01 each). There was no significant difference regarding residual gradients in pts. with different levels of immediate gradient reduction during probatory balloon occlusion.

Conclusions: Catheter-based septal ablation is an effective non-surgical technique for reducing symptoms and outflow gradients in HOCM. Intra-procedural echocardiographic guidance has a cumulative impact on the interventional strategy in about 15–20%, and clearly identifies pts. who should not receive ethanol but undergo a surgical myectomy.

Keywords: Hypertrophic obstructive cardiomyopathy; Percutaneous septal ablation; Left ventricular outflow tract gradient; Myocardial contrast echocardiography


    Introduction
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Catheter-based septal ablation for symptomatic obstructive hypertrophic cardiomyopathy (HOCM) refractory to medical treatment was introduced in 1994.1 Comparable to surgical myectomy as the standard therapy for this group of patients (pts.), ethanol septal ablation reduces symptoms and left ventricular outflow tract (LVOT) obstruction together with obstruction-associated abnormalities such as mitral regurgitation due to systolic anterior movement (SAM) of the mitral valve.1–5 Intra-procedural myocardial contrast echocardiography has been shown to be helpful for target vessel selection. Furthermore, improvement of clinical and hemodynamic results, and prevention of misplacement of the ethanol-induced necrosis as a source of potentially fatal complications6–10 were observed with this approach. We now report on our experience with septal ablation accompanied by routinely performed echocardiographic monitoring, labeled as PTSMA (percutaneous transluminal septal myocardial ablation), accumulated over a period of nearly 7 years in a series of 337 consecutive patients.


    Methods
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Patient selection for septal ablation
Criteria for patient selection have been described previously,5,9,11 and follow largely those established for septal myectomy. Patients with symptoms limiting daily activities (NYHA or CCS functional class > II, or exercise-induced syncope) together with a substantial degree of outflow obstruction (pressure drop > 50 mmHg at rest and/or >100 mmHg with provocation) were considered candidates for the intervention. Prior to PTSMA, a routine workup included exercise testing (spiroergometry and pulmonary artery catheterization/pressure measurement with exercise) and a thorough risk assessment to identify candidates with the need for implantation of an automatic defibrillator.12 Furthermore, a diagnostic left heart catheterization and a coronary angiogram were performed. A summary of the baseline variables in our pts. is shown in Table 1.


View this table:
[in this window]
[in a new window]

 
Table 1 Baseline data in 337 pts. with HOCM

 
Technique of echo-guided percutaneous septal ablation
All patients received a transfemoral pacemaker lead introduced into the RV apical region, usually via the left groin. A PTCA guiding catheter (6–7 F) was introduced via the right femoral artery and advanced into the left coronary artery. Pre-obstructive left ventricular pressure was measured with a modified 5 F pigtail catheter (side holes at the pigtail segment only) advanced via the left femoral artery, aortic pressure and the pressure drop across the outflow tract were monitored using the guiding catheter. The outflow tract gradient was assessed at rest, with a Valsalva maneuver, and with post-extrasystolic augmentation. After completion of the baseline hemodynamic measurements, an analgesic (usually 5–10 mg of morphine i.v.) and 7500–10,000 IU of Heparin were administered.

The presumed target vessel, i.e. one of the proximal septal perforator arteries, was then intubated selectively with a 0.014 inch PTCA guidewire (Fig. 1A–C). A short, slightly oversized over-the-wire balloon (1.5–3.0 mm) was introduced and inflated, and the distal vessel bed contrasted. At this time point, the LVOT gradient with probatory balloon occlusion was measured. After exclusion of dye reflux into the LAD, intra-procedural transthoracic contrast echocardiography was routinely performed. From the apical transducer position, the morphology of the left ventricular outflow tract and the mitral valve with its SAM was studied together with the obstructive outflow jet. Special attention was required to exactly define site and intensity of septal–mitral contact (Fig. 1D).


Figure 1
View larger version (101K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Figure 1 Interventional and echocardiographic sequence of a (super-selective) septal ablation procedure for symptomatic HOCM. Angio sequence: first major septal perforator artery with two sub-branches (black arrows) as the presumed target vessel (A, white arrow: lead of the temporary pacemaker, white arrowhead: pigtail catheter in the left ventricle), balloon within the proximal part of the septal perforator, (B) distal vessel bed with 2 sub-branches contrasted angiographically, (C) balloon advanced super-selectively into the left/basal sub-branch. Corresponding echo sequence: subaortic septum as target region in typical SAM-associated, subaortic obstruction (D, dotted line), (E) test injection of the echo contrast agent in balloon position of (B) highlighting the basal half of the septum plus a right ventricular papillary muscle (white arrows), (F) after super-selective balloon position of (C), correct opacification of the target region is achieved. RA: right atrium, RV: right ventricle, LA: left atrium.

 
The echo contrast agent (1.0–1.5 ml of a suspension of capillary-crossing, air-containing microspheres with a galactose-based shell stabilized by palmitine acid, mean diameter 7–8 µm, available as "Levovist®" [Schering]; concentration: 350 mg/ml) was then injected slowly into the vessel through the central lumen of the inflated balloon catheter. The opacification of the perfusion area was assessed from the apical (Fig. 1E) as well as from parasternal or subcostal transducer positions in order to verify its spatial extension in the subaortic–apical as well as in the anterior–posterior direction.

If the echo-enhanced area spatially matched with the obstructive jet and included the coaptation region between septum and SAM, and after exclusion of any opacification distant from the septal target area, the procedure was completed by a slow (ca. 1 ml/min) and, if necessary, repeated ethanol injection (Fig. 1F). Insulin syringes of 1 ml are very useful for this purpose. In case of a mismatch or an otherwise inaccurate contrast depot (Figs. 1E and 2C, BGo), ethanol was not given but another target vessel intubated, and the testing procedure repeated. In case that no vessel could be identified that exclusively highlighted the target region, a safe ethanol administration was considered impossible, and the procedure was stopped.


Figure 2
View larger version (57K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Figure 2 Variety of structures at risk for alcohol-induced necrosis as detected by intra-procedural echocardiography: (A) Baseline 4-chamber view in a patient who had myectomy 5 years ago and underwent septal ablation because of class III symptoms and significant SAM-associated (arrow) recurrent obstruction. Target region marked by arrowheads. Test injection into the first presumed target vessel produces opacification of a right papillary muscle (B, arrows), test injection into a second septal perforator leads to LV cavity contrast (C) without any opacification within the target region, injection into the third target vessel correctly highlights the target region (D, arrowheads).

 
The maximum ethanol dose was also guided by echocardiography: once complete opacification of the septal target region by the ethanol "depot" was documented, no further ethanol was given regardless of the acute gradient reduction. As a rule of thumb, the predicted ethanol dose in our institution was 1.0–1.25 ml for every 10 mm of septum thickness as measured by the pre-interventional echo.

If the target dose of ethanol was injected, the balloon remained inflated for an additional period of 10 min to enhance tissue contact and to exclude any spillover into the vessel from which the septal perforator originated. After that period, the balloon was retracted and the hemodynamic measurement repeated. The intervention was terminated with an angiogram to visualize occlusion of the target vessel and to exclude damage to the left coronary artery tree.


    Results
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Acute results and complications of percutaneous septal ablation
Between January 1996 and December 2002, in 337 out of 760 cases evaluated in our institution (44% of the total cohort of HCM patients), a PTSMA was attempted. The baseline characteristics of our patient cohort are displayed in Table 1. Out of these 337 pts., 312 (92%) received an average dose of 2.8±1.2 ml ethanol. Doses of >5 ml were no longer used from 1997 onward, when the importance of a local remodeling phenomenon became obvious.10 In 25 patients the intervention was aborted without ethanol injection (see section "Impact of intra-procedural echo monitoring on the interventional strategy"). The resting gradient acutely dropped from 60±33 to 19±22 mmHg, the maximum provocable gradient was reduced from 120±44 to 64±47 mmHg. However, at the end of the intervention, in 119 pts., a significant provocable outflow obstruction (>100 mmHg) was still present.

Mean CK peak was 542±264 U/l with an MB fraction of 63±35 U/l (normal values: <80 and <15 U/l, resp.). Transient AV conduction problems occurred in 168 pts. (54%); permanent AV sequential pacing was required in 22 pts (7%). Peri-interventional mortality was 1.3% (4 deaths); the reasons for these are shown in Table 2. During the 3 months of follow-up there was one additional death in a pt. with coexistent coronary artery disease who developed an acute posterior infarction 4 weeks after intervention. Postmortem examination revealed plaque rupture in a mildly sclerotic right coronary artery. There were no further cardiac complications.


View this table:
[in this window]
[in a new window]

 
Table 2 Reasons for peri-interventional death after septal ablation

 
Clinical and hemodynamic short-term results of percutaneous septal ablation
Follow-up after 3 months is now 97% complete (n = 302). Self-reported exercise capacity had improved in 279 pts. (91%); 164 pts. (54%) reported to be free of symptoms. Average NYHA functional class improved from 2.9±0.5 to 1.5±0.6 along with a mean increase in exercise capacity from 94±51 to 115±43 W and an increase in peak oxygen consumption from 18±4 to 21±6 ml/kg/min (p<0.01 each). A summary of the follow-up results is shown in Table 3.


View this table:
[in this window]
[in a new window]

 
Table 3 Follow-up results of septal ablation in 302 patients

 
The outflow gradient was reduced from 60±33 to 13±18 mmHg at rest and 120±43 to 38±35 mmHg with maximum provocation (by a Valsalva maneuver or with post-extrasystolic augmentation; p<0.0001 each). In 252 pts. (83%), gradient reduction was >50% relative to baseline values, 121 pts. (40%) were free from outflow obstruction both at rest and with provocation. There was no significant difference regarding residual gradients in pts. with different levels of immediate LVOT gradient reduction during probatory balloon occlusion (<30%: n = 58, >30%: n = 148; or >50%: n = 96).

Septal thickness was reduced from 20±4 to 17±4 mm, left atrial diameter from 49±7 to 46±7 mm (Fig. 3). There was a slight increase in end-diastolic LV diameter (Table 3), however, LV dilatation exceeding the individual normal value or a global deterioration of systolic LV function was not observed.


Figure 3
View larger version (59K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Figure 3 Optimal morphologic and hemodynamic result of PTSMA. In a patient with classical subaortic, SAM-dependent (A, arrow) LVOT obstruction at rest, augmented after PVC (C), follow-up echo (B) shows the myectomy-like ablation lesion that eliminates SAM and LVOT gradient (D) both at rest and after a PVC. LA: left atrium, Ao: aortic root.

 
In 23 pts. (8%) presenting with persistent class III symptoms, 3 had significant (>100 mmHg with provocation) residual outflow gradients, and were scheduled for myectomy in 2 and a re-PTSMA in 1 case according to septal morphology on follow-up echocardiography and/or individual preference by the patient. In the remaining 20 pts., severely symptomatic despite significant gradient reduction or gradient elimination, an advanced disease stage with severe diastolic dysfunction was considered causative in 8 pts., obesity (BMI >30) in 7, and significant pulmonary comorbidity in 5 cases.

Impact of intra-procedural echo monitoring on the interventional strategy
In 33 pts. (11%) of the 312 cases who received ethanol it was necessary to change the target vessel because of contrast-induced echo enhancement at a site remote from the septal target region, including an atypical (i.e., non-LAD) origin of the target septal perforator in 8 pts. (3%). In two pts., up to four vessels had to be tested before ethanol application was considered safe.

Contrast injection into the vessels tested led to opacification of a wide range of LV and RV structures suggesting threatening necrosis of these areas, and included all sites of the left ventricle, left and right papillary muscles, and the right ventricular free wall (Figs. 1E and 2B, CGo). Two patients with extensive right ventricular wall opacification experienced hypotension, correctable by volume expansion. Rapid deflation of the balloon and retrieval of the catheter system led to normalization of the myocardial texture in all these cases within minutes. No persisting hemodynamic deterioration due to ischemia and/or contrast injection was observed, even in those pts. with extensive areas of myocardial opacification.

Furthermore, in the 25 pts. (8%) of the initial cohort who did not receive ethanol, echocardiographic findings (see Figs. 1E and 2Go) not correctable by a target vessel change were the main reason (n = 18/322; 6%). In the remaining 7 pts. (2%), technical problems (inability to reach any target vessel, unstable balloon position) led to abortion of the procedure.


    Discussion
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
The localized "therapeutic infarction"3 induced by the ablation procedure as a result of ethanol injection into a septal perforator artery leads to thinning of the involved area and widening of the left ventricular outflow tract. These effects eliminate or reduce systolic anterior movement of the mitral valve, and ultimately the outflow gradient.7–14 After a local remodeling process that may need several months, and that usually is completed after a year, the morphologic result resembles that of a surgical myectomy10 with a channel-like subaortic ablation lesion in place of the protruding muscle bulge. A significant gradient reduction is associated with an increase in exercise capacity corresponding to 1 or 2 NYHA classes, improvement of left ventricular diastolic function, reduction of SAM-associated mitral regurgitation, and reduction of left atrial size.9,13

From a technical viewpoint, the key issue of septal ablation is the identification of the correct target vessel supplying exactly and exclusively the septal area involved in LVOT gradient formation. Originally, probatory balloon occlusion of that vessel was used for this purpose.2,4 The effect of transient ischemia on the left ventricular outflow gradient was thought to be a reliable predictor of the final result. However, the range of spontaneous gradient variability may be as high as 50%; and the intervention itself (analgesic and sedative agents, volume expansion by radiographic contrast agents and/or repeated catheter flushing, ischemia-induced thoracal discomfort and pain) may have a profound influence on gradient severity. In the first published report on this ablation technique, it was obvious that only 50% of the patients demonstrated a significant reduction of the outflow gradient following probatory occlusion of a septal perforator.16 In the first published septal ablation series,2 also based on hemodynamic testing by probatory balloon occlusion, the rate of non-responders was 17% (3/18). In our own experience, after treatment of 30 patients it was obvious that a more sophisticated method had to be introduced for target vessel selection.6,9 The first echo-guided PTSMA was performed in our institution in late 1996. Since then, echo monitoring of septal ablation is our routine approach, and our and others' experiences with this technique has repeatedly been reported.6–10,13,15 Echocardiographic monitoring enables visualization of the "strategic" septal area involved in the formation of the outflow gradient, thereby defining the area and extent of future necrosis. Our current data demonstrate that approximately 90% of patients with symptomatic HOCM can be treated effectively by an echocardiography-targeted ablation, and with very low rates of fatal events and sustained pacemaker dependency.

On the other hand, intra-procedural echocardiographic guidance of target vessel selection identified some patients who did not seem to have any septal perforator artery that exclusively supplied the obstructive myocardial region, and thus would have allowed a safe ethanol injection. These pts. should not be treated by ethanol septal ablation but offered a surgical intervention. The phenomenon of opacification distant from the target septal region, very likely indicating to threatening necrosis of these areas and structures if ethanol were injected, cannot be anticipated by hemodynamic testing. Recent pathologic research showing an unexpected extension of the perfusion area in 20% of septal perforator arteries in explanted hearts,17 and a current case report comparing a failed and a successful procedure,18 both support this hypothesis. Thus, the main reason to not give ethanol in our cohort was the intra-procedural echocardiographic finding of contrast away from the septal target region not correctable by a target vessel change.

If the ethanol injection can be safely given, the second importance of echo monitoring is to define the end of the intervention. The strategy to eliminate the outflow gradient during one interventional session, sometimes requiring ethanol doses as high as 10 ml, has been completely abandoned in our and others' practice years ago.5,15 In our current practice, once an appropriate impregnation of the target region has been documented by echocardiography, the procedure is stopped irrespective of the hemodynamic acute effect, taking into account the remodeling process which will bring the outflow gradient further down during the weeks following intervention.10 This impregnation usually is seen with a dose of 2.0–2.5 ml of ethanol. However, based on the observation of the local remodeling process, other groups have also reduced the ethanol dose.19

Transthoracic imaging in the supine position on the catheterization table may be challenging. It was, however, possible to monitor the procedure in all pts. treated using modern ultrasound equipment and the tissue harmonic imaging mode, including one pt. who underwent PTSMA under mechanical ventilation. In this critically ill pt. monitoring via the transesophageal approach was unable to exactly define the area highlighted by the contrast agent due to distal overshadowing covering the septum. With routine transthoracic imaging from the apex, shadows fall over the atrial region, which is not of vital importance for the ablation procedure.


    Limitations
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Limitations of this report mainly arise from the fact that it is a single-center observational study. A review of the literature shows that other groups using different, partly non-echo-guided septal ablation techniques have achieved comparable clinical and hemodynamic results. However, the patient cohort reported here more than doubles that of the second largest cohort in the literature.19 Since we routinely use echo-guided ablation since 1996, from our own data a comparison to other septal ablation methods cannot be made, and a randomized multi-center study with respect to this issue does not exist. However, the focus of this report is the safety aspect of septal ablation rather than its well-known hemodynamic efficacy. Furthermore, to our knowledge other groups have not yet reported on their ablation results on an "intention to treat" basis; it is thus unknown in how many cases, and why, a planned intervention was aborted. Finally it may be mentioned that a recent ACC/ESC consensus document on HCM has stated that "myocardial contrast echocardiography guidance ... is important in selecting the appropriate septal perforator branch"20 without neglecting that "some groups prefer a pressure-angiographic and fluoroscopy guided technique".


    Conclusions
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Echo-guided septal ablation is an effective treatment option for patients with HOCM who do not show a satisfactory response to medical therapy. Clinical and hemodynamic results seem to be comparable to surgical myectomy. An interventional strategy that closely relies on the findings of intra-procedural contrast echocardiography, as does surgical myectomy on transesophageal echocardiographic monitoring, leads to elimination or substantial reduction of the outflow gradient and to symptomatic improvement in more than 90% of patients. Echocardiographic monitoring of septal ablation also prevents complications following induction of a necrosis remote from the septal target area, and thus substantially adds to the safety of the procedure.


    Acknowledgements
 
We are indebted to the staff of the Bad Oeynhausen echo lab, Mrs. Y. Kim, Mrs. C. Schaksmeier, and Dipl. Ing. N. Bogunovic, for their excellent echocardiographic imaging.


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 

  1. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet (1995) 346:211–214.[CrossRef][Web of Science][Medline]
  2. Knight C.J., Kurbaan A.S., Seggewiss H., Henein M., Gunning M., Harrington D., et al. Non-surgical septal reduction for hypertrophic obstructive cardiomyopathy: outcome in the first series of patients. Circulation (1997) 95:2075–2081.[Abstract/Free Full Text]
  3. Braunwald E. Induced septal infarction: a new strategy for hypertrophic obstructive cardiomyopathy. Circulation (1997) 95:1981.[Free Full Text]
  4. 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.[Abstract/Free Full Text]
  5. Seggewiss H., Gleichmann U., Faber L., Fassbender D., Schmidt H.K., 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.[Abstract/Free Full Text]
  6. Faber L, Seggewiss H, Fassbender D, Strick S, Bogunovic N, Gleichmann U. Guiding of interventional myocardial ablation in obstructive hypertrophic cardiomyopathy by myocardial contrast echocardiography: first experiences. Eighth Essen-Mayo-Mainz Symposium, Essen, October 1996.
  7. 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 Interv Cardiol (1998) 11:443–448.[CrossRef][Web of Science]
  8. Lakkis N.M., Nagueh S.F., Kleiman N.S., Killip D.M., He Z.X., Verani M., et al. Echocardiography-guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation (1998) 98:1750–1755.[Abstract/Free Full Text]
  9. Faber L., Seggewiss H., Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intra-procedural myocardial contrast echocardiography. Circulation (1998) 98:2415–2421.[Abstract/Free Full Text]
  10. Faber L., Seggewiss H., Ziemssen P. Targeting percutaneous transluminal septal ablation for HOCM by intra-procedural echocardiographic monitoring. J Am Soc Echocardiogr (2000) 13:1074–1079.[CrossRef][Web of Science][Medline]
  11. Wigle D.E., Rakowski H., Kimball B.P., Williams W.G. Hypertrophic cardiomyopathy: clinical spectrum and treatment. Circulation (1995) 92:1680–1692.[Free Full Text]
  12. Elliott P.M., Poloniecki J., Dickie S., Sharma S., Monserrat M., Varnava A., et al. Sudden death in HCM: identification of high risk patients. J Am Coll Cardiol (2000) 36:2212–2218.[Abstract/Free Full Text]
  13. Seggewiss H. Current status of alcohol septal ablation for patients with hypertrophic obstructive cardiomyopathy. Curr Cardiol Rep (2001) 3:160–166.[Medline]
  14. Gietzen F.H., Leuner C.J., Raute-Kreinsen U., Dellmann A., Hegselmann J., Strunk-Mueller C., et al. Acute and long-term results after transcoronary ablation of septal hypertrophy (TASH). Eur Heart J (1999) 20:1342–1354.[Abstract/Free Full Text]
  15. Faber L., Meissner A., Ziemssen P., Seggewiss H. Percutaneous transluminal septal myocardial ablation for HOCM: long-term follow-up in the first series of 25 patients. Heart (2000) 83:326–331.[Abstract/Free Full Text]
  16. Kizilbash A.M., Heinle S.K., Grayburn P.A. Spontaneous variability of left ventricular outflow tract gradients in hypertrophic obstructive cardiomyopathy. Circulation (1998) 97:461–466.[Abstract/Free Full Text]
  17. Singh M., Edwards W.D., Holmes D.R., Tajik A.J., Nishimura R.A. Anatomy of the first septal perforating artery: a study with implications for ablation therapy for HCM. Mayo Clin Proc (2001) 76:799–802.[Abstract]
  18. Mayer S.A., Anwar A., Grayburn P.A. Comparison of successful and failed alcohol septal ablations for obstructive hypertrophic cardiomyopathy. Am J Cardiol (2003) 92(2):241–242.[CrossRef][Web of Science][Medline]
  19. Gietzen F.H., Leuner C.J., Obergassel L., Strunk-Mueller C., Kuhn H. 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 (2002) 106:454–459.[Abstract/Free Full Text]
  20. ACC/ESC consensus group on hypertrophic cardiomyopathy. Eur Heart J (2003) 24:1965–1991.[Free Full Text]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Eur Heart JHome page
M. Alam, H. Dokainish, and N. M. Lakkis
Hypertrophic obstructive cardiomyopathy-alcohol septal ablation vs. myectomy: a meta-analysis
Eur. Heart J., May 1, 2009; 30(9): 1080 - 1087.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll Cardiol IntvHome page
P. Sorajja, R. A. Nishimura, S. R. Ommen, C. S. Rihal, B. J. Gersh, and D. R. Holmes Jr
Effect of Septal Ablation on Myocardial Relaxation and Left Atrial Pressure in Hypertrophic Cardiomyopathy: An Invasive Hemodynamic Study
J. Am. Coll. Cardiol. Intv., October 1, 2008; 1(5): 552 - 560.
[Abstract] [Full Text] [PDF]


Home page
Eur J EchocardiogrHome page
M. S. Kim, A. J. Klein, B. M. Groves, R. A. Quaife, and E. E. Salcedo
Left ventricular outflow tract obstruction in the presence of asymmetric septal hypertrophy and accessory mitral valve tissue treated with alcohol septal ablation
Eur J Echocardiogr, September 1, 2008; 9(5): 720 - 724.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll Cardiol IntvHome page
D. H. Kwon, S. R. Kapadia, E. M. Tuzcu, C. M. Halley, E. Z. Gorodeski, R. J. Curtin, M. Thamilarasan, N. G. Smedira, B. W. Lytle, H. M. Lever, et al.
Long-Term Outcomes in High-Risk Symptomatic Patients With Hypertrophic Cardiomyopathy Undergoing Alcohol Septal Ablation
J. Am. Coll. Cardiol. Intv., August 1, 2008; 1(4): 432 - 438.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
P. Sorajja, U. Valeti, R. A. Nishimura, S. R. Ommen, C. S. Rihal, B. J. Gersh, D. O. Hodge, H. V. Schaff, and D. R. Holmes Jr
Outcome of Alcohol Septal Ablation for Obstructive Hypertrophic Cardiomyopathy
Circulation, July 8, 2008; 118(2): 131 - 139.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
S. F. Nagueh, J. M. Buergler, M. A. Quinones, W. H. Spencer III, and G. M. Lawrie
Outcome of Surgical Myectomy After Unsuccessful Alcohol Septal Ablation for the Treatment of Patients With Hypertrophic Obstructive Cardiomyopathy
J. Am. Coll. Cardiol., August 21, 2007; 50(8): 795 - 798.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
M. A. Fifer
Most Fully Informed Patients Choose Septal Ablation Over Septal Myectomy
Circulation, July 10, 2007; 116(2): 207 - 216.
[Full Text] [PDF]


Home page
J Am Coll CardiolHome page
A. W. Heldman, K. C. Wu, T. P. Abraham, and D. E. Cameron
Myectomy or Alcohol Septal Ablation: Surgery and Percutaneous Intervention Go Another Round
J. Am. Coll. Cardiol., January 23, 2007; 49(3): 358 - 360.
[Full Text] [PDF]


Home page
HeartHome page
C. J Knight
Alcohol septal ablation for obstructive hypertrophic cardiomyopathy.
Heart, September 1, 2006; 92(9): 1339 - 1344.
[Full Text] [PDF]


Home page
Journal of Diagnostic Medical SonographyHome page
K. Chadwell
Interventional Echocardiography
Journal of Diagnostic Medical Sonography, July 1, 2006; 22(4): 231 - 240.
[Abstract] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Faber, L.
Right arrow Articles by Horstkotte, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Faber, L.
Right arrow Articles by Horstkotte, D.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?