A Decade of Percutaneous Septal Ablation in Hypertrophic Cardiomyopathy

Circulation JournalOfficial Journal of the Japanese Circulation Societyhttp://www.j-circ.or.jp

ypertrophic cardiomyopathy (HCM) is clinically de-fined by the presence of left ventricular hypertrophy not attributed to abnormal loading conditions.1 It

is recognized as the most common genetic cardiac disease, occurring in 1 per 500 adults. Compatible with the largely heterogeneous genetic background, involving more than 400 different mutations in at least 10 different contractile proteins, and the influence of multiple modifying factors, the cardiac morphology, pathophysiological characteristics and clinical manifestations vary greatly, even in members of the same family.1 A significant proportion of patients remain asymp-tomatic, but others develop debilitating symptoms of dyspnea on exertion, angina, which may also be atypical, reduced exercise capacity and syncope or may present serious life threatening ventricular arrhythmias leading to sudden death. Most patients have dynamic left ventricular outflow tract (LVOT) obstruction (hypertrophic obstructive cardiomyopa-thy, HOCM), which is accepted as an important cause of significant symptoms in some patients.2,3 In general, treatment of patients with HCM aims at relieving symptoms, reducing the risk of sudden death and offering genetic counselling.1 For patients with significant obstruction the primary focus of treatment is the reduction of the pressure gradient.4 The first line of therapy is medical treatment with β-blockers, or diso-pyramide as first choice and verapamil as second choice.1,4 Cibenzoline, another antiarrhythmic drug, has also been used in some countries with reportedly good results.5,6 However, medical treatment fails to relieve symptoms in a considerable number of patients with LVOT obstruction7 and surgical treat-ment with septal myectomy/myotomy has been the traditional

gold standard treatment for such patients, with excellent results in highly experienced centers.8

Percutaneous transluminal septal myocardial ablation (PTSMA: the injection of alcohol in a septal perforator branch perfusing the basal septum) has emerged as an efficacious alternative treatment option in the past 15 years.9,10 This technique aims to reduce the hypertrophied septum through the production of a small myocardial infarction confined to the part of the septum that is involved in the pathophysiol-ogy of the gradient.11 During the past decade, the existence of a less invasive and widely available therapeutic modality has invigorated interest in the determinants and implications of LVOT obstruction in HCM.

Pathophysiology and Effect of ObstructionEver since the first modern descriptions of HCM 50 years ago, the pathophysiology of LVOT obstruction, together with its clinical implications, has been an issue of controversy in the cardiovascular community.12 Imaging studies over the past 20 years have proven that dynamic LVOT obstruction is produced by contact between the anterior, and less commonly the posterior mitral valve leaflet, and the interventricular septum (IVS) during systole.12 The key event in this process is the systolic anterior motion (SAM) of the mitral valve leaf-let towards the IVS, which is determined by the forceful left ventricular ejection and the morphological characteristics in HOCM: narrow LVOT due to the basal septal hypertrophy, anteriorly displaced mitral valve with elongated leaflets.12,13 The LVOT obstruction represents an increase in left ventricu-

Received October 3, 2010; accepted October 4, 2010; released online November 23, 20102nd Department of Cardiology, University of Athens Medical School, Athens (A.G.R.), Greece; Medizinische Klinik 1, Leopoldina

Krankenhaus, Schweinfurt (H.S.), GermanyMailing address: Professor Dr Med. Hubert Seggewiss, MD, Medizinische Klinik 1, Leopoldina-Krankenhaus, Gustav-Adolf-Str. 8, 97422

Schweinfurt, Germany. E-mail: [email protected] doi: 10.1253/circj.CJ-10-0962All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: [email protected]

A Decade of Percutaneous Septal Ablation in Hypertrophic Cardiomyopathy

Angelos G. Rigopoulos, MD; Hubert Seggewiss, MD

Percutaneous septal ablation has emerged as a less invasive treatment of symptomatic patients with hypertro-phic obstructive cardiomyopathy (HOCM). In the past decade, the availability of this sophisticated technique has revived the interest of cardiologists in left ventricular outflow tract obstruction, which led to the recognition that most patients with HCM have the obstructive type. Follow-up studies have already shown the safety and efficacy of the procedure, which offers symptomatic relief in most patients. Long-term survival is comparable to historical reports after surgical myectomy. Complications are rare and can be further reduced with increased experience of the operators, and the theoretical concern for possible ventricular arrhythmogenicity of the myocardial scar has not been documented by the existing data. Although there are still no randomized trials, percutaneous septal ablation is undeniably a viable alternative for patients with HOCM.

Key Words: Cardiomyopathy; Left ventricular hypertrophy; Septal ablation

H

Advance Publication by J-STAGE

RIGOPOULOS AG et al.

lar afterload, because approximately half of the stroke vol-ume remains to be ejected after the gradient appears. Apart from the stroke volume reduction, SAM is associated with mitral regurgitation and load-dependent diastolic dysfunc-tion, and obstruction causes an increase in left ventricular pressure and coronary flow abnormalities. In the absence of SAM, midventricular obstruction can occur in some patients, because of either muscular apposition causing midventricular obstruction or anomalous insertion of the papillary muscle into the anterior mitral leaflet.14

The basal part of the IVS and the septal artery (arteries) that supply it comprise the recently described “first septal unit”15 and this part of the IVS is involved in the SAM – septal con-tact, which has to be abolished by the interventional treatment. The anterior two-thirds of the IVS are supplied by septal per-forators originating from the left anterior descending (LAD) artery and the posterior one-third is supplied by septal perfo-rators from the posterior descending artery; however, there is a high degree of collateralization between those branches. The target of PTSMA is usually the first larger septal branch, but there is significant variety in its size, angiographic mor-phology, supplying territory and collateralization with other septal branches that needs to be always kept in mind.16,17

Virtually from the initial observations of patients with HCM, it has been resolved that the level of the intraven-tricular pressure gradient measured at rest has only poor cor-relation with the severity of the patient’s symptoms.18 The existence and severity of the obstruction depend on the load-ing conditions of the left ventricle, may vary greatly with physiological or pharmacological provocations that alter left ventricular preload, afterload or contractility, and may change dramatically after meals or alcohol intake.1 Spontaneous vari-ation of the measured gradients from day to day or during the same day has also been observed in some patients.18,19 Despite the recognized dynamic nature of the obstruction, conven-tional measurement of the gradient only in the resting state has created the perception that only one-quarter of patients have LVOT obstruction.2 Nevertheless, most patients with-out an obstruction at rest can generate a significant pressure gradient with provocation (eg, exercise).20 Those observa-tions have shifted our understanding of LVOT obstruction in HCM, because it has been resolved that 25% of patients with HCM have LVOT obstruction at rest, and a total of 75% of patients have obstruction either at rest or with provocation.21 Furthermore, because many patients have symptoms only on exertion, it is obvious that identifying a latent obstruction by measuring the LVOT gradient after provocation is crucial.

The Valsalva maneuver in the catheterization laboratory or during the echocardiographic study is the simplest method of provocation, although exercise echocardiography imitates normal physiology and is more sensitive than the Valsalva.21 Gradient measurement after a fortuitous extrasystolic beat during the Doppler study or a deliberately produced one dur-ing cardiac catheterization can also expose latent obstruc-tion.22 Afterload reduction with amylnitrate or nitroglycerin can also be used, but positive inotropes (eg, dobutamine) are not recommended, however, as they may also yield false-positive results in healthy young people without HCM or in young athletes.2

The mere existence of obstruction measured only at rest has been correlated with clinical deterioration and increased mortality.3,23 Symptomatic patients have a worse prognosis compared with asymptomatic subjects, as have older patients compared with younger ones.3 Patients with obstruction at rest develop atrial fibrillation, a major determinant of clini-

cal deterioration in HCM,24 in a higher proportion than patients without obstruction.25 Severe obstruction has also been correlated with sudden death risk and might be included in the list of clinical risk factors for sudden death (ventricu-lar tachycardia, abnormal exercise blood pressure response, family history of premature death, unexplained syncope, severe left ventricular hypertrophy).26 In conclusion, it has become evident that obstruction in HCM not only influences symptomatic status but may also have prognostic significance.

History of Alcohol Septal AblationThe idea of a nonsurgical interventional treatment for HOCM grew with the advances of interventional cardiology in the 1980s. Early in that decade, it was observed that temporary balloon occlusion of the LAD artery caused left ventricu-lar wall motion abnormalities.27 In particular, patients with HOCM developed nonobstructive physiology after myocar-dial infarction.28 On the other hand, electrophysiologists were trying a chemical septal branch ablation procedure for the treatment of ventricular arrhythmias in patients with coro-nary artery disease.29 Those observations inspired the origi-nal description of the technique of alcohol septal ablation in 1989 (G. Berghoefer, personal communication). In the early 1990s, it was reported that temporary balloon occlusion of the first septal branch led to a gradient reduction in some patients.9,30 The first procedure of alcohol-induced septal branch occlusion in humans was performed by Dr Sigwart in 1994.9 Several years later, echocardiographic guidance with echo-contrast-mediated identification of the target septal branch was introduced, which was clearly the most signifi-cant improvement of the original technique.31

Alcohol septal ablation has gained remarkable popularity and it is estimated that more patients have been treated with the interventional technique in the past decade than with surgical myectomy in the past 45 years.8 A benefit of this growing volume of data is that medium-term results were published in the early 2000s and long-term results have already appeared in the literature.32–38

Description of the Ablation TechniqueThe femoral approach is most convenient for PTSMA. In patients without a permanent pacemaker or implantable car-dioverter defibrillator (ICD), a temporary pacemaker should be placed transvenously in the right ventricular apex through a femoral venous sheath and kept in situ for 24–48 h. If temporary pacing is required for a longer time or ambulatory monitoring is not available post procedure, the jugular or subclavian venous route is preferred. In patients with an implanted pacing device, septal pacing is less reliable than right ventricular pacing and an increased pacing amplitude might be required. Constant recording of the LVOT gradient can be achieved by simultaneous measurement of the left ventricular and aortic pressures with 2 arterial catheters. A specially designed pigtail catheter, with holes only in its distal part and not on the shaft (Cordis, Miami, FL, USA), is inserted through a left femoral artery sheath and remains positioned in the apex of the left ventricle, and a coronary angioplasty guide catheter is positioned at the ostium of the left coronary artery, through a right femoral artery sheath. With this approach, transseptal puncture (and its related risk) can be avoided. Furthermore, the LVOT gradient can be recorded both at rest and during provocative maneuvers, such as Valsalva, and after an extrasystolic beat. Weight-adjusted


Septal Ablation in HCM

heparin is used to prevent thromboembolic complications. In addition, early analgesic medication (preferably with opiates) is essential to suppress pain during the alcohol injection.

Typically, the first large septal branch is angiographically identified as the target branch and an angioplasty guidewire is advanced into it. Although occasionally a stiffer wire offer-ing increased support may be needed, the use of softer wires has been shown to reduce the risk of coronary damage.35 With the guidewire in the septal branch, a short (≤10 mm long) over-the-wire balloon is advanced into the septal branch and inflated at the nominal pressure. It is essential that the balloon catheter should be compatible with the injection of absolute alcohol. In general, a slightly oversized balloon in com-parison with the septal branch diameter is preferred, and overexpansion of a smaller balloon with inflation above the nominal pressure should be avoided. Before inflation, the balloon should be positioned clearly inside the septal branch without impinging on the LAD artery, in order to avoid the possibility of LAD dissection. The guidewire is removed and angiographic contrast dye (1–2 ml) is injected through the lumen of the central guidewire balloon catheter to depict the supply area of the septal branch and exclude the possi-bility of reflux of contrast dye (and consequently of alcohol) into the LAD artery and to identify any existing collateral vessels.17

The first septal branch has been shown to have a surpris-ingly variable anatomy and perfusion bed.16 As well, multi-ple or atypically originating septal branches may further per-plex the choice of the correct branch (Figure 1). In order to ensure accurate identification of the target septal area and to avoid any inappropriate alcohol injection (eg, into the papil-lary muscle or the right ventricular free wall), myocardial con-trast echocardiography is indispensable to the procedure.31,39 Before any alcohol injection, an echocardiographic contrast agent is administered through the central lumen of the bal-loon catheter under real-time transthoracic 2-dimensional echocardiographic and color Doppler monitoring. Injection into the optimal septal branch will cause an obvious opacifica-tion of the septal area next to maximal flow acceleration that involves the point of contact between the mitral valve and the septum during systole. It is evident that myocardial con-trast echocardiography can change the interventional strategy by dictating the need for a change in the target branch or even cessation of the procedure if the proper septal branch can not be identified (Figure 2). Once the correct target has been proven, however, 1–3 ml of absolute alcohol is then injected slowly in 1-ml increments through the central lumen of the balloon under constant fluoroscopy. The total amount of alcohol injected depends on the acute hemodynamic effect and the echocardiographically estimated size of the con-trasted septal area. In fact, it is considered that the use of less alcohol is associated with less complications, and small or ultra low doses of alcohol can have equally effective hemo-dynamic results as larger doses.40

Balloon catheter dislodgement, kinking or severe difficulty in alcohol injection should prompt the termination of the pro-cedure. In order to prevent complications, the balloon should not be deflated or removed earlier than 10 min after the last alcohol injection.11,41 A final coronary angiographic image is taken to show the occluded septal branch and exclude any damage to the coronary arteries.

The patient is subsequently transferred to the coronary care unit for hemodynamic and rhythm monitoring for at least 48 h.

Alcohol septal ablation is referred in the literature under

different acronyms, which reflect substantial technical differ-ences (Table 1). PTSMA, as described, is the most commonly performed technique, but in recent years, various efforts have been made to substitute alcohol with the use of coils, polyvinyl alcohol particles, used angioplasty wires, cyano-acrylate glue, gelatin particles, radiofrequency ablation, and cryoablation. None of these methods has prevailed, however, because the myocardial necrosis caused by alcohol plays a key role in the pathophysiology of septal reduction therapy.

Indications and Patient SelectionIt has been emphasized that the patients who gain the most benefit from PTSMA are the ideal candidates for this inter-ventional treatment.42 Such as patients with drug-refractory symptoms limiting daily activities (NYHA/CCS III or IV) and/or recurrent syncope on exertion, who also have signifi-cant obstruction >30 mmHg at rest and/or >60 mmHg with provocation.2,11 The typical morphology of the “first septal unit” comprises significant thickness of the asymmetrically hypertrophied septum (>15 mm) at the level of the LVOT obstruction, which is related to SAM of the mitral valve. In contrast, other types of left ventricular hypertrophy asso-ciated with HCM, but not involving the septum (eg, apical hypertrophy, hypertrophy limited to the free wall), are defi-nite contraindications for interventional treatment.

Mitral valve regurgitation associated with SAM of the mitral valve is expected to diminish after successful treat-ment. Echocardiographically manifested reduction of mitral insufficiency after acute gradient reduction following intra-venous administration of disopyramide can confirm this con-sideration. In contrast, patients with abnormal mitral valve morphology/structure (eg, extremely long or flail leaflets, anomalous papillary muscle insertion) should be referred for

Figure 1. Left coronary angiography shows 3 septal branches that could potentially be the target branch for alcohol septal ablation. The first (no. 1) originates very proxi-mally from the left anterior descending artery, which makes inserting a wire very difficult. The second (no. 2) bifurcates proximally, thus precluding ablation of the whole branch. The third (no. 3) is the dominant septal branch, which could be the target septal branch for alcohol septal ablation.



extended myectomy and additional mitral valve repair.43

Patients with concomitant coronary artery disease requir-ing revascularization should be individually managed. If percutaneous treatment of the coronary lesion(s) is feasible, it can be primarily performed and PTSMA should follow after confirmation of persistent symptoms at follow up. A com-bined all-in-one approach is warranted only if the target septal

branch originates at the site of a coronary lesion in the LAD artery.44 In that case, 2 angioplasty guidewires are used and a coronary stent is placed in the coronary lesion after alcohol septal ablation is completed.

To date, alcohol septal ablation is not acceptable for pa-tients without significant symptoms who have satisfactory exercise capacity, even if they might have signs of com-

Figure 2. Alcohol septal ablation in the patient shown in Figure 1. (a) An over-the-wire short balloon is inflated in the dominant 3rd septal branch (no. 3 in Figure 1). Transthoracic echocardiography (apical (b) and long-axis (c) views) after injection of contrast agent Levovist® (Schering, Berlin, Germany) shows opacification of the basal part of the IVS with, however, incomplete demarcation of the subaortic section in the vicinity of the area of contact between the septum and the systolic anterior motion (SAM) of the mitral valve leaflet (orange circle). A change of strategy was required and an over-the-wire balloon was finally placed and inflated in the 1st septal branch (no. 1 in Figure 1), which originates very proximally, is smaller and more difficult to access with the angioplasty guidewire (d). Myocardial contrast echocardiography this time shows complete opacification of the basal septum that reaches the endocardial border leaving no uncovered spots (e,f). The dotted lines shows the endocardial border of the septum. IVS, interventricular septum; LA, left atrium; LV, left ventricle; RV, right ventricle.

Table 1. Acronyms of Alcohol Septal Ablation

Acronym Definition Identification of target septal branch Criterion of completion

PTSMA47,48 Percutaneous transluminal septal myocardial ablation

Transthoracic myocardial contrast echocardiography

Alcohol depot in echocardiography

TASH93 Transcoronary ablation of septal hypertrophy

Haemodynamic effect of temporary branch occlusion

Until gradient is abolished

NSRT49 Nonsurgical septal reduction Echocardiographic study with the use of angiographic contrast dye

Until gradient is abolished

NSMR94 Nonsurgical myocardial reduction Hemodynamic effect of temporary branch occlusion

Occlusion of several septal branches until gradient is abolished



pensated hemodynamic overload (eg, dilated left atrium).2,4 It is reasonable, however, that such patients should be kept under close and watchful follow-up evaluation, with regular objective assessment of their exercise capacity in addition to clinical risk stratification for sudden cardiac death. On the other hand, patients who fail to show left ventricular outflow obstruction, even after provocation, are not candidates for interventional treatment.

Pathophysiology of Alcohol Septal AblationEarly after injection, alcohol causes a coagulation necrosis of the myocardium and the septal perforator arteries. The arteries are filled with necrotic debris and “fixed” blood, with neutrophilic infiltration at the margin of the necrotic tissue. Tissue edema appears early in the process, whereas muscle replacement by scar formation develops only after several days.45

The progression of the histological changes affects the hemodynamic response after PTSMA, which shows 3 sepa-rate phases: perioperative, early postoperative and late post-operative.15 The first phase is characterized by akinesia of the ablated septum, caused by stunning, with significant LVOT gradient decrease. In the second phase, the probable edema-tous expansion of the necrotic area of the septum causes an increase in the LVOT gradient in approximately half of the patients, which is evident for approximately 7–10 days with-out any clinical worsening, however.46 In the following few months, thinning of the ablated septum because of scar for-mation will cause a further decrease of the obstruction and the concomitant mitral regurgitation.32,47–50 Studies with SPECT and magnetic resonance imaging (MRI) have shown that the necrotic area produced by PTSMA is ≤10% of the left ven-tricular myocardium.51,52 Furthermore, it has been clearly resolved by nuclear MRI that the scar created by the trans-mural infarction as a result of PTSMA will shrink during the following months.15,51 In accordance, the LVOT cross-sec-tional area gradually increases during the first months after PTSMA.53,54 On the other hand, the remodeling process also affects the left ventricular free wall, with left ventricular mass decreasing disproportionally to the reduction caused by the ablated area only.55 A reduction in free wall thickness has also been described after myectomy, implying that the increased afterload in HOCM may boost left ventricular hypertrophy, which can be subsequently lessened with effective reduction of the LVOT gradient.56

Changes in coronary blood flow after PTSMA have been investigated with various methods. Invasive assessment of coronary flow reserve shows an immediate improvement after PTSMA as a result of the reduced contraction load of the left ventricle.57 In accordance with this, an MRI study has shown that the resting blood flow in the LAD artery decreases at 1 month and 6 months after PTSMA compared with base-line.58 This reduction is associated with a decrease in the LVOT gradient and has no relation to the scarred tissue mass. Myocardial flow reserve has been estimated with myocardial contrast echocardiography to be significantly improved after PTSMA, although it does not reach the level of healthy con-trols.59,60

Acutely after PTSMA, the systolic function of left ventricle is reduced. The end-systolic and end-diastolic volumes are increased and ejection fraction decreases.61 The diastolic function, however, improves significantly, with reductions of end-diastolic pressure, diastolic stiffness and tau. At 6 months, changes in the pressure – volume loops indicate

Tabl

e 2.

Lo

ng

-Ter

m F

ollo

w-u

p A

fter

Alc

oh

ol S

epta

l Ab

lati

on

Stu

dy

No

. of

pat

ien

tsA

ge

(yea

rs)

Pri

or

DD

D

(%)

Pri

or

ICD

(%

)

Pac

emak

er

in-h

osp

ital

(%

)

Nee

d f

or

new

p

acem

aker

(%

)

Mea

n

follo

w-u

p

(yea

rs)

In-h

osp

ital

m

ort

alit

y (%

)

Lo

ng

-te

rm

mo

rtal

ity

Red

o

pro

ced

ure

s (%

)

Mye

cto

my

(%)

Su

rviv

alS

urv

ival

w

ith

ou

t sy

mp

tom

s

Seg

gew

iss

et a

l (20

07)3

210

052

.7±

15.7

5　0

8　 8

.54.

8±1.

21　

　　3　

96%

at 8

yea

rs

74%

Wel

ge e

t al (

2008

)34

347

54±

157　

27　

8.4

4.8±

2.9

1　　　

8　5　

392

%

74%

Sor

ajja

et a

l (20

08)3

313

864

±21

10.1

520

　　　23

.92.

2±2.

81.

48　

4　88

% a

t 4 y

ears

76.4

%

Kuh

n et

al (

2008

)36

329

58±

155

17　　　

2.1

1.8

7　13

　　　91

.1%

Fer

nand

es e

t al (

2008

)35

619

53.9

±15

.015

.6 8

.2 9

.74.

6±2.

56　

　　18

　　　14

.125

89%

at 8

yea

rs

Kw

on e

t al (

2008

)37

55

63±

1320

　　25

.531

.88±

10　

　　24

　　　 5

.5 5

76%

at 1

0 ye

ars

Nos

ewor

thy

et a

l (20

09)8

9 8

99　

95.

0±2.

38　

8　10

ten

Cat

e et

al (

2010

)86

91

54±

150　

04　

5.4±

2.5

2　　　

11　　　

Lyne

et a

l (20

10)3

8 1

20　

0　　　

16.6

16.6

73%

at 1

0 ye

ars

DD

D, d

ual c

ham

ber

paci

ng; I

CD

, im

plan

tabl

e ca

rdio

vert

er d

efibr

illat

or.



preserved myocardial contractility, with improvement of the active and passive diastolic properties of the left ventri-cle.62 Echocardiographic indices of diastolic function remain improved at 1- and 2-year follow-up in patients with success-ful PTSMA, indicating a sustained favorable hemodynamic result.63 As a consequence, the left atrial pressure and volume decrease in the first 3 months after PTSMA, with a simultaneous increase in left atrial ejection fraction that correlates with the LVOT gradient reduction.64

Electrophysiological Changes After Alcohol Septal Ablation

Despite the fact that only a small artery is occluded, PTSMA induces significant ECG changes. New anterior ST elevation and new Q waves may appear immediately after the proce-dure in some patients and QRS duration may be prolonged.65 The appearance of a new right bundle branch block is the commonest change occurring in approximately half of the patients treated. The right ventricular bundle branch is con-tained in the part of the basal septum that is ablated, thus is

Figure 3. Collateralization between septal branches. (a) Left coronary angiography shows the target septal branch (white arrow). Injection of angiographic contrast dye through the central lumen of the inflated balloon cath-eter can determine the supply area of the septal branch and exclude leakage into the left anterior descending artery. The red arrow shows the collateral retrograde flow to a dis-tal septal branch. Injection of alcohol at this point would probably cause spillage into the distal left anterior descending artery, generat-ing a remote infarction. Instead, a second angioplasty guidewire is inserted in the sec-ond septal branch and a monorail balloon is inflated in this branch, thus obviating any mis-placement of alcohol (b).



often prone to injury during PTSMA.66 Conduction abnor-malities may appear as 1st-degree atrioventricular block in approximately 50% or as complete heart block requiring a permanent pacemaker in 10% of patients.67

Clinical OutcomeEver since the first patients were treated, numerous reports have shown success in ≥90% of those treated with the echocar-diography-guided technique, with effective reduction of both resting and provocable LVOT gradients.9,11,31–33,41,46–48,55,66–74 Diminished LVOT obstruction is related to symptomatic relief and improved exercise capacity.41,73,75

During follow-up there is a sustained and constant hemo-dynamic improvement, with further reduction after the first year of the LVOT gradient, which is almost eliminated in most patients after several years.32 Relief of obstruction is permanent and does not reappear after successful treatment. Regular echocardiographic evaluation has shown an ongoing left ventricular remodeling process, with reduction of both septal and posterior wall thicknesses. Increases left ventricu-lar dimensions, however, do not exceed normal limits, alle-viating initial concerns about possible negative effects. The SAM with mitral regurgitation is also reduced with time,32 and pulmonary artery pressure decreases after successful per-cutaneous septal ablation.31,70 Consistent with the hemody-namic improvement, there is also an increasing improvement in clinical status during follow-up, as regards functional class, symptomatic relief and reduction of syncopal episodes.32,33 Increased exercise capacity and peak oxygen consumption provide objective confirmation of the clinical benefit.32,73

In a pooled analysis of 42 studies published between 1996 and 2005 involving 2,959 patients, the mean procedure-related (in-hospital) mortality was 1.5%.67 A noteworthy 6.6% of patients have needed redo procedures, and 2.0% were ulti-mately referred for myectomy. Results of longer follow-up, however, confirm the safety and efficacy of alcohol septal ablation (Table 2).32–38 In a cohort of the first 100 patients treated the overall survival was 96% at 8 years, and 74% of patients remained free of severe symptoms, atrial fibrillation, stroke or ICD implantation.32 A larger cohort of 347 patients, also treated with the echocardiography-guided technique, has shown 94% survival after 5 years and 87% after 10 years.34 It should also be mentioned that long-term results from a cohort of 55 high-risk patients, not eligible for surgical treat-ment, has shown a rather impressive 76% survival at 10 years, with only 1 patient dying of confirmed cardiac cause.37 Long-term mortality in this cohort was associated only with old age at the time of treatment. Reported data from a series of patients treated with percutaneous septal ablation in a highly esteemed myectomy center has shown 88% survival at 4 years, which was comparable to the outcome of an age- and gender-matched, but probably less sick, group of patients who underwent surgical myectomy.33

ComplicationsComplication rates have decreased during the past decade, probably because of the increasing experience of the opera-tors. Procedure-associated mortality, reported to range from 0% to 4%,67 is clearly less in the latest cohort compared with the early cohort of patients treated by several groups.34,36 In fact, in the Leopoldina Hospital Registry, a series of >650 patients have been treated without any hospital deaths.

Conduction abnormalities remain the most frequent ad-

verse reaction, but they are mostly temporary, necessitating the use of a temporary pacemaker for the procedure and obli-gating careful rhythm monitoring throughout the hospital stay.76 The need for permanent pacing has been shown to be related to several predicting factors, such as female sex, bolus alcohol injection, occlusion of more than 1 septal branch, preexisting left bundle branch block and first degree atrioven-tricular block.77 A scoring system, based on the assessment of the ECG (ie, QRS duration, PQ duration, atrioventricular block occurrence and persistence or recovery, heart rate) as well as hemodynamic variables (baseline gradient) and myo-cardial enzyme kinetics (time-point of peak alanine amino-transferase), has also been proposed for the prediction of permanent pacemaker dependency after the intervention.78 Nonetheless, less than 10% of patients will eventually need a permanent pacemaker.79

Damage to the coronary arteries with the guidewire or bal-loon inflation is a rare complication and can be avoided with increasing experience and use of proper equipment.35 Alcohol leakage to the LAD artery is also uncommon, but can be disastrous for the patient.41,80 The use of a slightly oversized balloon catheter, with slow and watchful injection of alcohol and deflation of the balloon at least 10 min after the last alco-hol injection will effectively prevent retrograde alcohol flow to the LAD artery,31 and meticulous angiographic demon-stration of the target septal branch before alcohol injection will reveal the existence of collateralization between septal branches (Figure 3).32

The myocardial scar caused by percutaneous septal abla-tion has aroused concern of a potentially increased risk for malignant ventricular arrhythmias.81,82 This theoretical con-sideration has not been supported so far by either the long follow-up data or by analysis of data from patients who already had an ICD implanted at the time of intervention. Ventricular arrhythmias have been reported in the early post-procedural phase, possibly as an effect of ischemia.67,83–85 With the exception of 1 study,86 long-term follow-up data have described ventricular arrhythmias as a rare event.32–35 In contrast, no increased risk of malignant arrhythmias after the procedure has been shown in patients who already had an ICD implanted because of a previously estimated high risk of sudden death.87,88 In fact, it seems that a less successful hemodynamic outcome may be associated with a higher arrhythmic risk, with the risk of arrhythmia increasing as the post-interventional gradient increases.89

The advent of myocardial contrast echocardiography during percutaneous septal ablation has been shown to improve the hemodynamic result and decrease the complication risk.31,73 Use of the proper contrast agent enables better imaging qual-ity, thus ensuring the safety of the procedure, which could be also applied to treat patients with midventricular obstruc-tion or who had undergone a previously unsuccessful surgical attempt.90,91 The precise identification of the target septal region has permitted injection of less alcohol without com-promising the hemodynamic result.74,75,92

Although it is evident that complications decrease with increasing experience, the upper range of reported complica-tions is unacceptably high.67 Proper training and institutional organization should ensure the safety of alcohol septal abla-tion, and a deep understanding and extensive experience in clinical assessment and treatment of HOCM patients should be a prerequisite for institutions that offer alcohol septal abla-tion.



Conclusions and PerspectiveIn the past decade it can be shown that septal ablation in symptomatic patients with HOCM resulted in ongoing relief of clinical symptoms in more than 90% of the patients. Hos-pital mortality can be reduced to nearly 0% in experienced centers with knowledge of the special problems and com-plexities that can emerge in the postinterventional period. Therefore, the need for permanent pacemaker implantation in less than 10% of patients treated is in fact the most signifi-cant complication.

In the future, only randomized trials will show whether septal ablation or myectomy is the gold standard for symp-tomatic relief in HCM patients with significant obstruction.

References 1. Elliott P, McKenna WJ. Hypertrophic cardiomyopathy. Lancet

2004; 363: 1881 – 1891. 2. Maron BJ, McKenna WJ, Danielson GK, Kappenberger LJ, Kuhn

HJ, Seidman CE, et al. American College of Cardiology/European Society of Cardiology clinical expert consensus document on hyper-trophic cardiomyopathy: A report of the American College of Car-diology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol 2003; 42: 1687 – 1713.

3. Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser JR, Losi MA, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med 2003; 348: 295 – 303.

4. Fifer MA, Vlahakes GJ. Management of symptoms in hypertrophic cardiomyopathy. Circulation 2008; 117: 429 – 439.

5. Hamada M, Shigematsu Y, Inaba S, Aono J, Ikeda S, Watanabe K, et al. Antiarrhythmic drug cibenzoline attenuates left ventricular pressure gradient and improves transmitral Doppler flow pattern in patients with hypertrophic obstructive cardiomyopathy caused by midventricular obstruction. Circ J 2005; 69: 940 – 945.

6. Ozaki K, Sakuma I, Mitsuma K, Suzuki T, Tsuchida K, Takahashi K, et al. Effect of cibenzoline and atenolol administration on dynamic left ventricular obstruction due to sigmoid-shaped septum. Circ J 2008; 72: 2087 – 2091.

7. Maron BJ. Appraisal of dual-chamber pacing therapy in hyper-trophic cardiomyopathy: Too soon for a rush to judgment? J Am Coll Cardiol 1996; 27: 431 – 432.

8. Maron BJ. Surgical myectomy remains the primary treatment option for severely symptomatic patients with obstructive hypertrophic cardiomyopathy [Controversies in Cardiovascular Medicine]. Circu-lation 2007; 116: 196 – 206; discussion 206.

9. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995; 346: 211 – 214.

10. Seggewiss H. Percutaneous transluminal septal myocardial ablation: A new treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J 2000; 21: 704 – 707.

11. Seggewiss H. Current status of alcohol septal ablation for patients with hypertrophic cardiomyopathy. Curr Cardiol Rep 2001; 3: 160 – 166.

12. Maron BJ, Maron MS, Wigle ED, Braunwald E. The 50-year his-tory, controversy, and clinical implications of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy from idiopathic hypertrophic subaortic stenosis to hypertrophic cardiomyopathy: From idiopathic hypertrophic subaortic stenosis to hypertrophic cardiomyopathy. J Am Coll Cardiol 2009; 54: 191 – 200.

13. Ommen SR, Nishimura RA. What causes outflow tract obstruction in hypertrophic cardiomyopathy? Heart 2009; 95: 1725 – 1726.

14. Maron BJ, Nishimura RA, Danielson GK. Pitfalls in clinical recog-nition and a novel operative approach for hypertrophic cardiomy-opathy with severe outflow obstruction due to anomalous papillary muscle. Circulation 1998; 98: 2505 – 2508.

15. Angelini P. The “1st septal unit” in hypertrophic obstructive car-diomyopathy: A newly recognized anatomo-functional entity, iden-tified during recent alcohol septal ablation experience. Tex Heart Inst J 2007; 34: 336 – 346.

16. Singh M, Edwards WD, Holmes DR Jr, Tajil AJ, Nishimura RA. Anatomy of the first septal perforating artery: A study with implica-tions for ablation therapy for hypertrophic cardiomyopathy. Mayo Clin Proc 2001; 76: 799 – 802.

17. Rigopoulos A, Sepp R, Palinkas A, Ungi I, Kremastinos DT,

Seggewiss H. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: Collateral vessel communication between septal branches. Int J Cardiol 2006; 113: e67 – e69.

18. Ross J Jr, Braunwald E, Gault JH, Mason DT, Morrow AG. The mechanism of the intraventricular pressure gradient in idiopathic hypertrophic subaortic stenosis. Circulation 1966; 34: 558 – 578.

19. Kizilbash AM, Heinle SK, Grayburn PA. Spontaneous variability of left ventricular outflow tract gradient in hypertrophic obstructive cardiomyopathy. Circulation 1998; 97: 461 – 466.

20. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy: Clinical spectrum and treatment. Circulation 1995; 92: 1680 – 1692.

21. Maron MS, Olivotto I, Zenovich AG, Link MS, Pandian NG, Kuvin JT, et al. Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction. Circulation 2006; 114: 2232 – 2239.

22. Brockenbrough EC, Braunwald E, Morrow AG. A hemodynamic technic for the detection of hypertrophic subaortic stenosis. Circu-lation 1961; 23: 189 – 194.

23. Maron BJ, Casey SA, Poliac LC, Gohman TE, Almquist AK, Aeppli DM. Clinical course of hypertrophic cardiomyopathy in a regional United States cohort. JAMA 1999; 281: 650 – 655.

24. Kubo T, Kitaoka H, Okawa M, Hirota T, Hayato K, Yamasaki N, et al. Clinical impact of atrial fibrillation in patients with hypertro-phic cardiomyopathy: Results from Kochi RYOMA Study. Circ J 2009; 73: 1599 – 1605.

25. Autore C, Bernabo P, Barilla CS, Bruzzi P, Spirito P. The prognos-tic importance of left ventricular outflow obstruction in hypertro-phic cardiomyopathy varies in relation to the severity of symptoms. J Am Coll Cardiol 2005; 45: 1076 – 1080.

26. Elliott P, Gimeno J, Tome M, McKenna W. Left ventricular outflow tract obstruction and sudden death in hypertrophic cardiomyopathy. Eur Heart J 2006; 27: 3073; author reply 3073 – 3074.

27. Sigwart U, Grbic M, Essinger A, Rivier J. L’effect aigu d’une occlusion coronarienne par ballonet de la dilatation transluminale. Schweiz Med Wochenschr 1982; 45: 1631 (in French).

28. Come PC, Riley MF. Hypertrophic cardiomyopathy: Disappearance of auscultatory, carotid pulse, and echocardiographic manifestations of obstruction following myocardial infarction. Chest 1982; 82: 451 – 454.

29. Brugada P, de Swart H, Smeets JL, Wellens HJ. Transcoronary chemical ablation of ventricular tachycardia. Circulation 1989; 79: 475 – 482.

30. Kuhn H, Gietzen F, Leuner C, Gerenkamp T. Induction of subaortic septal ischaemia to reduce obstruction in hypertrophic obstructive cardiomyopathy: Studies to develop a new catheter-based concept of treatment. Eur Heart J 1997; 18: 846 – 851.

31. Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomy-opathy: Results with respect to intraprocedural myocardial contrast echocardiography. Circulation 1998; 98: 2415 – 2421.

32. Seggewiss H, Rigopoulos A, Welge D, Ziemssen P, Faber L. Long-term follow-up after percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Clin Res Cardiol 2007; 96: 856 – 863.

33. Sorajja P, Valeti U, Nishimura RA, Ommen SR, Rihal CS, Gersh BJ, et al. Outcome of alcohol septal ablation for obstructive hyper-trophic cardiomyopathy. Circulation 2008; 118: 131 – 139.

34. Welge D, Seggewiss H, Fassbender D, Schmidt HK, Horstkotte D, Faber L. Long-term follow-up after percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Dtsch Med Wochenschr 2008; 133: 1949 – 1954 (in German).

35. Fernandes VL, Nielsen C, Nagueh SF, Herrin AE, Slifka C, Franklin J, et al. Follow-up of alcohol septal ablation for symptomatic hyper-trophic obstructive cardiomyopathy: The Baylor and Medical Uni-versity of South Carolina experience 1996 to 2007. JACC Cardio-vasc Interv 2008; 1: 561 – 570.

36. Kuhn H, Lawrenz T, Lieder F, Leuner C, Strunk-Mueller C, Obergassel L, et al. Survival after transcoronary ablation of septal hypertrophy in hypertrophic obstructive cardiomyopathy (TASH): A 10 year experience. Clin Res Cardiol 2008; 97: 234 – 243.

37. Kwon DH, Kapadia SR, Tuzcu EM, Halley CM, Gorodeski EZ, Curtin RJ, et al. Long-term outcomes in high-risk symptomatic pa-tients with hypertrophic cardiomyopathy undergoing alcohol septal ablation. JACC Cardiovasc Interv 2008; 1: 432 – 438.

38. Lyne JC, Kilpatrick T, Duncan A, Knight CJ, Sigwart U, Fox KM. Long-term follow-up of the first patients to undergo transcatheter alcohol septal ablation. Cardiology 2010; 116: 168 – 173.

39. Faber L, Seggewiss H, Fassbender D, Strick S, Gleichmann U. Guiding of percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy by myocardial contrast



echocardiography. J Interv Cardiol 1998; 11: 443 – 448.40. Veselka J, Duchonova R, Palenickova J, Zemanek D, Tiserova M,

Linhartova K, et al. Impact of ethanol dosing on the long-term out-come of alcohol septal ablation for obstructive hypertrophic cardio-myopathy: A single-center prospective, and randomized study. Circ J 2006; 70: 1550 – 1552.

41. Ruzyłło W, Chojnowska L, Demkow M, Witkowski A, Kusmierczyk-Droszcz B, Piotrowski W, et al. Left ventricular outflow tract gra-dient decrease with non-surgical myocardial reduction improves exercise capacity in patients with hypertrophic obstructive cardio-myopathy. Eur Heart J 2000; 21: 770 – 777.

42. Rigopoulos AG, Panou F, Kremastinos DT, Seggewiss H. Alcohol septal ablation in hypertrophic obstructive cardiomyopathy. Hellenic J Cardiol 2009; 50: 511 – 522.

43. Lever HM. Selection of hypertrophic cardiomyopathy patients for myectomy or alcohol septal ablation. Anadolu Kardiyol Derg 2006; 6(Suppl 2): 27 – 30.

44. Seggewiss H, Faber L, Meyners W, Bogunovic N, Odenthal HJ, Gleichmann U. Simultaneous percutaneous treatment in hypertro-phic obstructive cardiomyopathy and coronary artery disease: A case report. Cathet Cardiovasc Diagn 1998; 44: 65 – 69.

45. Baggish AL, Smith RN, Palacios I, Vlahakes GJ, Yoerger DM, Picard MH, et al. Pathological effects of alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Heart 2006; 92: 1773 – 1778.

46. Yoerger DM, Picard MH, Palacios IF, Vlahakes GJ, Lowry PA, Fifer MA. Time course of pressure gradient response after first alcohol septal ablation for obstructive hypertrophic cardiomyopa-thy. Am J Cardiol 2006; 97: 1511 – 1514.

47. 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-month follow-up in 25 patients. J Am Coll Cardiol 1998; 31: 252 – 258.

48. Seggewiss H, Faber L, Gleichmann U. Percutaneous transluminal septal ablation in hypertrophic obstructive cardiomyopathy. Thorac Cardiovasc Surg 1999; 47: 94 – 100.

49. Lakkis NM, Nagueh SF, Dunn JK, Killip D, Spencer WH 3rd. Nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy: One-year follow-up. J Am Coll Cardiol 2000; 36: 852 – 855.

50. Mazur W, Nagueh SF, Lakkis NM, Middleton KJ, Killip D, Roberts R, et al. Regression of left ventricular hypertrophy after nonsur-gical septal reduction therapy for hypertrophic obstructive cardio-myopathy. Circulation 2001; 103: 1492 – 1496.

51. Aqel RA, Hage FG, Zohgbi GJ, Tabereaux PB, Lawson D, Heo J, et al. Serial evaluations of myocardial infarct size after alcohol septal ablation in hypertrophic cardiomyopathy and effects of the changes on clinical status and left ventricular outflow pressure gra-dients. Am J Cardiol 2008; 101: 1328 – 1333.

52. van Dockum WG, ten Cate FJ, ten Berg JM, Beek AM, Twisk JW, Vos J, et al. Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopa-thy: Evaluation by contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol 2004; 43: 27 – 34.

53. Schulz-Menger J, Strohm O, Waigand J, Uhlich F, Dietz R, Friedrich MG. The value of magnetic resonance imaging of the left ventricu-lar outflow tract in patients with hypertrophic obstructive cardio-myopathy after septal artery embolization. Circulation 2000; 101: 1764 – 1766.

54. Sitges M, Qin JX, Lever HM, Bauer F, Drinko JK, Agler DA, et al. Evaluation of left ventricular outflow tract area after septal reduction in obstructive hypertrophic cardiomyopathy: A real-time 3-dimen-sional echocardiographic study. Am Heart J 2005; 150: 852 – 858.

55. van Dockum WG, Beek AM, ten Cate FJ, ten Berg JM, Bondarenko O, Gotte MJ, et al. Early onset and progression of left ventricular remodeling after alcohol septal ablation in hypertrophic obstruc-tive cardiomyopathy. Circulation 2005; 111: 2503 – 2508.

56. Curtius JM, Stoecker J, Loesse B, Welslau R, Scholz D. Changes of the degree of hypertrophy in hypertrophic obstructive cardio-myopathy under medical and surgical treatment. Cardiology 1989; 76: 255 – 263.

57. Jaber WA, Yang EH, Nishimura RA, Sorajja P, Rihal CS, Elesber A, et al. Immediate improvement in coronary flow reserve after alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy. Heart 2009; 95: 564 – 569.

58. van Dockum WG, Knaapen P, Hofman MB, Kuijer JP, ten Cate FJ, ten Berg JM, et al. Impact of alcohol septal ablation on left anterior descending coronary artery blood flow in hypertrophic obstructive cardiomyopathy. Int J Cardiovasc Imaging 2009; 25: 511 – 518.

59. Pedone C, Biagini E, Galema TW, Vletter WB, ten Cate FJ. Myo-cardial perfusion after percutaneous transluminal septal myocardial ablation as assessed by myocardial contrast echocardiography in patients with hypertrophic obstructive cardiomyopathy. J Am Soc Echocardiogr 2006; 19: 982 – 986.

60. Soliman OI, Geleijnse ML, Michels M, Dijkmans PA, Nemes A, van Dalen BM, et al. Effect of successful alcohol septal ablation on microvascular function in patients with obstructive hypertrophic cardiomyopathy. Am J Cardiol 2008; 101: 1321 – 1327.

61. Steendijk P, Meliga E, Valgimigli M, Ten Cate FJ, Serruys PW. Acute effects of alcohol septal ablation on systolic and diastolic left ventricular function in patients with hypertrophic obstructive cardiomyopathy. Heart 2008; 94: 1318 – 1322.

62. Meliga E, Steendijk P, Valgimigli M, ten Cate FJ, Serruys PW. Effects of percutaneous transluminal septal myocardial ablation for obstructive hypertrophic cardiomyopathy on systolic and diastolic left ventricular function assessed by pressure-volume loops. Am J Cardiol 2008; 101: 1179 – 1184.

63. Jassal DS, Neilan TG, Fifer MA, Palacios IF, Lowry PA, Vlahakes GJ, et al. Sustained improvement in left ventricular diastolic func-tion after alcohol septal ablation for hypertrophic obstructive car-diomyopathy. Eur Heart J 2006; 27: 1805 – 1810.

64. Hage FG, Karakus G, Luke WD Jr, Suwanjutah T, Nanda NC, Aqel RA. Effect of alcohol-induced septal ablation on left atrial volume and ejection fraction assessed by real time three-dimensional trans-thoracic echocardiography in patients with hypertrophic cardiomy-opathy. Echocardiography 2008; 25: 784 – 789.

65. Kazmierczak J, Kornacewicz-Jach Z, Kisly M, Gil R, Wojtarowicz A. Electrocardiographic changes after alcohol septal ablation in hy-pertrophic obstructive cardiomyopathy. Heart 1998; 80: 257 – 262.

66. Talreja DR, Nishimura RA, Edwards WD, Valeti US, Ommen SR, Tajik AJ, et al. Alcohol septal ablation versus surgical septal myec-tomy: Comparison of effects on atrioventricular conduction tissue. J Am Coll Cardiol 2004; 44: 2329 – 2332.

67. Alam M, Dokainish H, Lakkis N. Alcohol septal ablation for hyper-trophic obstructive cardiomyopathy: A systematic review of pub-lished studies. J Interv Cardiol 2006; 19: 319 – 327.

68. Knight C, Sigwart U. Non-surgical ablation of the ventricular sep-tum for the treatment of hypertrophic cardiomyopathy. Heart 1996; 76: 92.

69. Lakkis NM, Nagueh SF, Kleiman NS, Killip D, He ZX, Verani MS, et al. Echocardiography-guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation 1998; 98: 1750 – 1755.

70. Gietzen FH, Leuner CJ, Raute-Kreinsen U, Dellmann A, Hegselmann J, Strunk-Mueller C, et al. Acute and long-term results after trans-coronary ablation of septal hypertrophy (TASH): Catheter inter-ventional treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J 1999; 20: 1342 – 1354.

71. Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C, Kuhn H. Role of transcoronary ablation of septal hypertrophy in patients with hypertrophic cardiomyopathy, New York Heart Association func-tional class III or IV, and outflow obstruction only under provocable conditions. Circulation 2002; 106: 454 – 459.

72. Faber L, Seggewiss H, Welge D, Fassbender D, Ziemssen P, Schmidt HK, et al. Predicting the risk of atrioventricular conduction lesions after percutaneous septal ablation for obstructive hypertro-phic cardiomyopathy. Z Kardiol 2003; 92: 39 – 47 (in German).

73. Faber L, Seggewiss H, Welge D, Fassbender D, Schmidt HK, Gleichmann U, et al. Echo-guided percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: 7 years of experience. Eur J Echocardiogr 2004; 5: 347 – 355.

74. Veselka J, Prochazkova S, Duchonova R, Bolomova-Homolova I, Palenickova J, Tesar D, et al. Alcohol septal ablation for hyper-trophic obstructive cardiomyopathy: Lower alcohol dose reduces size of infarction and has comparable hemodynamic and clinical outcome. Catheter Cardiovasc Interv 2004; 63: 231 – 235.

75. Faber L, Welge D, Fassbender D, Schmidt HK, Horstkotte D, Seggewiss H. One-year follow-up of percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy in 312 patients: Predictors of hemodynamic and clinical response. Clin Res Cardiol 2007; 96: 864 – 873.

76. Reinhard W, ten Cate FJ, Scholten M, De Laat LE, Vos J. Perma-nent pacing for complete atrioventricular block after nonsurgical (alcohol) septal reduction in patients with obstructive hypertrophic cardiomyopathy. Am J Cardiol 2004; 93: 1064 – 1066.

77. Chang SM, Nagueh SF, Spencer WH 3rd, Lakkis NM. Complete heart block: Determinants and clinical impact in patients with hyper-trophic obstructive cardiomyopathy undergoing nonsurgical septal reduction therapy. J Am Coll Cardiol 2003; 42: 296 – 300.



78. Faber L, Welge D, Fassbender D, Schmidt HK, Horstkotte D, Seggewiss H. Percutaneous septal ablation for symptomatic hyper-trophic obstructive cardiomyopathy: Managing the risk of proce-dure-related AV conduction disturbances. Int J Cardiol 2007; 119: 163 – 167.

79. Fifer MA. Most fully informed patients choose septal ablation over septal myectomy [Controversies in Cardiovascular Medicine]. Cir-culation 2007; 116: 207 – 216; discussion 216.

80. Antolinos Perez MJ, de la Morena Valenzuela G, Gimeno Blanes JR, Cerdan Sanchez Mdel C, Hurtado Martinez JA, Valdes Chavarri M. Balloon rupture and alcohol leakage into the left anterior de-scending coronary artery during percutaneous septal ablation for hypertrophic obstructive cardiomyopathy. Rev Esp Cardiol 2005; 58: 872 – 874 (in Spanish).

81. Kimmelstiel CD, Maron BJ. Role of percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Circulation 2004; 109: 452 – 456.

82. Maron BJ. Surgery for hypertrophic obstructive cardiomyopathy: Alive and quite well. Circulation 2005; 111: 2016 – 2018.

83. Seggewiss H, Faber L, Ziemssen P. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Cardiol Rev 1999; 7: 316 – 323.

84. Boltwood CM Jr, Chien W, Ports T. Ventricular tachycardia com-plicating alcohol septal ablation. N Engl J Med 2004; 351: 1914 – 1915.

85. Antoun P, El Masry H, Breall JA. Sudden cardiac death complicat-ing alcohol septal ablation: A case report and review of literature. Catheter Cardiovasc Interv 2009; 73: 956 – 959.

86. ten Cate FJ, Soliman OI, Michels M, Theuns DA, de Jong PL, Geleijnse ML, et al. Long-term outcome of alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy: A word of caution. Circ Heart Fail 2010; 3: 362 – 369.

87. Lawrenz T, Obergassel L, Lieder F, Leuner C, Strunk-Mueller C, Meyer Zu Vilsendorf D, et al. Transcoronary ablation of septal hypertrophy does not alter ICD intervention rates in high risk pa-tients with hypertrophic obstructive cardiomyopathy. Pacing Clin Electrophysiol 2005; 28: 295 – 300.

88. Cuoco FA, Spencer WH 3rd, Fernandes VL, Nielsen CD, Nagueh S, Sturdivant JL, et al. Implantable cardioverter-defibrillator therapy for primary prevention of sudden death after alcohol septal ablation of hypertrophic cardiomyopathy. J Am Coll Cardiol 2008; 52: 1718 – 1723.

89. Noseworthy PA, Rosenberg MA, Fifer MA, Palacios IF, Lowry PA, Ruskin JN, et al. Ventricular arrhythmia following alcohol septal ablation for obstructive hypertrophic cardiomyopathy. Am J Cardiol 2009; 104: 128 – 132.

90. Seggewiss H, Faber L. Percutaneous septal ablation for hyper-trophic cardiomyopathy and mid-ventricular obstruction. Eur J Echocardiogr 2000; 1: 277 – 280.

91. Faber L, Welge D, Hering D, Butz T, Oldenburg O, Seggewiss H, et al. Percutaneous septal ablation after unsuccessful surgical myec-tomy for patients with hypertrophic obstructive cardiomyopathy. Clin Res Cardiol 2008; 97: 899 – 904.

92. Veselka J, Zemanek D, Tomasov P, Homolova S, Adlova R, Tesar D. Complications of low-dose, echo-guided alcohol septal ablation. Catheter Cardiovasc Interv 2010; 75: 546 – 550.

93. Kuhn H, Gietzen FH, Leuner C, Schafers M, Schober O, Strunk-Muller C, et al. Transcoronary ablation of septal hypertrophy (TASH): A new treatment option for hypertrophic obstructive car-diomyopathy. Z Kardiol 2000; 89(Suppl 4): IV41 – IV54.

94. Boekstegers P, Steinbigler P, Molnar A, Schwaiblmair M, Becker A, Knez A, et al. Pressure-guided nonsurgical myocardial reduction induced by small septal infarctions in hypertrophic obstructive car-diomyopathy. J Am Coll Cardiol 2001; 38: 846 – 853.


A Decade of Percutaneous Septal Ablation in Hypertrophic Cardiomyopathy

Documents

Transcript of A Decade of Percutaneous Septal Ablation in Hypertrophic Cardiomyopathy