(Hellenic Journal of Cardiology) HJC ñ 511
Hellenic J Cardiol 2009; 50: 511-522
unexplained left ventricular hypertrophy.1-3
Its phenotypic prevalence in the general
population has been estimated as 1:500,
which renders it the most common genetic
heart disease. It has been described as a
highly heterogeneous genetically trans-
mitted disease of the sarcomere that in-
volves more than 400 different mutations
in at least 10 different contractile proteins
cg3/index.html). This genetic complexity
leads to a wide diversity in cardiac mor-
phology, pathophysiological features, and
clinical manifestations, even in a single fa-
mily.2The clinical course and outcome
may vary greatly, with many patients hav-
ing hardly any or no discernible cardiovas-
cular symptoms, whereas others have pro-
found exercise limitation and recurrent ar-
rhythmias.4Approximately one third of the
patients with hypertrophic cardiomyopathy
have dynamic left ventricular outflow tract
(LVOT) obstruction at rest, caused by con-
tact between the anterior, or less commonly
the posterior, mitral valve leaflet and the in-
terventricular septum during systole (hy-
pertrophic obstructive cardiomyopathy,
HOCM).5-8In some patients this obstruc-
tion may be associated with thickening and
distortion of the mitral leaflets and occa-
ypertrophic cardiomyopathy is a
primary myocardial disorder de-
fined clinically by the presence of
sionally obstruction may be caused by a-
nomalous insertion of the papillary mus-
cle into the mitral leaflet.9Lately, it has
been resolved that most patients with hy-
pertrophic cardiomyopathy may have
LVOT obstruction under provocation with
the Valsalva manoeuvre or exercise (Fig-
Treatment of symptomatic patients
with HOCM should effectively reduce sym-
ptoms, improve functional capacity and
provide better quality of life.1,12The patho-
physiological target of any treatment is to
reduce the extent of the outflow tract gradi-
ent and improve diastolic filling. The clini-
cal significance of the outflow gradient has
been an issue of debate for many years, but
gradient is now accepted as an important
cause of limiting symptoms in some pa-
tients.8,12Medical therapy, with the admin-
istration of negatively inotropic drugs, e.g.
beta blockers,13-15verapamil14-16or disopy-
ramide,17-20is always the first line of treat-
ment.1,12However, a considerable number
of patients with marked LVOT obstruction
continue to have severe symptoms regard-
less of any medical therapy.21Such patients
have traditionally been referred for surgical
myectomy/myotomy, which has been the
gold standard treatment for decades. In
highly experienced centres, the initially high
postoperative mortality rates have been re-
duced to <1-2%.22-26Surgery has provided
Alcohol Septal Ablation in Hypertrophic
ANGELOS G. RIGOPOULOS1, FOTIOS PANOU1, DIMITRIOS TH. KREMASTINOS1,
12nd Department of Cardiology, University of Athens Medical School, Attikon University Hospital, Athens, Greece;
2Medizinische Klinik 1, Leopoldina-Krankenhaus, Schweinfurt, Germany
November 24, 2008;
July 30, 2009.
Angelos G. Rigopoulos
2nd Department of
University of Athens
11632 Athens, Greece
long-term symptomatic relief in a substantial propor-
tion of patients.22,25
Percutaneous transluminal septal myocardial ab-
lation (PTSMA) by means of alcohol-induced occlu-
sion of a septal branch has emerged as a novel inter-
ventional treatment option during the last decade.27
It is less invasive than surgery and aims directly to re-
duce the hypertrophied interventricular septum with
consequent expansion of the LVOT and reduction of
the LVOT gradient.28This is achieved through a cir-
cumscribed infarction of the area supplied by the oc-
cluded septal branch.
The idea that permanent ischaemic damage to the
basal septum could be beneficial in HOCM came af-
ter preliminary studies had shown that temporary bal-
loon occlusion of the first larger septal branch result-
ed in substantial resting outflow gradient reduction in
some patients.27,29After the description of a similar
technique for treating ventricular arrhythmias,30Sig-
wart was the first to report a successful non-surgical
myocardial reduction after occlusion of the septal
branch using 96% alcohol.27
The original technique of PTSMA was based on
the injection of alcohol in the first septal branch
through the central lumen of an over-the-wire balloon
catheter positioned and inflated inside the target septal
branch. Subsequently, the technique was further re-
fined, with the addition of several modifications, in or-
der to improve the identification of the most appropri-
ate target septal perforator branch.27,31,32 The main ob-
jective in performing PTSMA should be to achieve an
optimal haemodynamic result with minimal complica-
tions.33The generally accepted technique, which is per-
formed by most groups across the world, is described in
sufficient detail below.28,33
As a prerequisite in all patients without a perma-
nent pacemaker, a temporary pacemaker should be
placed transvenously in the right ventricular apex, be-
cause of the risk of atrioventricular conduction distur-
bances following alcohol injection. Once an aortic valve
gradient has been excluded, a special pigtail catheter,
with holes only in its distal part and not on the shaft
(Cordis), is introduced and remains positioned in the
A.G. Rigopoulos et al
512 ñ HJC (Hellenic Journal of Cardiology)
Figure 1. Left ventricular outflow tract (LVOT) gradient recording in the catheterisation laboratory during the Valsalva manoeuvre.
The initial LVOT gradient at rest is below 30 mmHg and during Valsalva the LVOT obstruction increases: the left ventricular systolic
pressure is increased while the aortic pressure decreases. In addition, the aortic pressure curve gradually turns to a “spike and dome”
configuration (arrow), typical of significant LVOT obstruction. Ao – aortic pressure; LV – left ventricular pressure.
left ventricular apex, providing constant pressure
recording. A coronary angioplasty guide catheter is
then positioned at the ostium of the left coronary ar-
tery. Left Judkins catheters can normally be used in
most patients, although special catheters for extra back-
up are sometimes needed in cases of complex aortic
root or coronary anatomy. The guide catheter serves
also for pressure measurement in the ascending aorta
and therefore the LVOT gradient is recorded con-
stantly throughout the procedure, both at rest and
during provocative manoeuvres (Valsalva manoeuvre,
extrasystolic beat) (Figure 2a).
All patients receive intravenous weight-adjusted
heparin and early analgesic medication (preferably
with opiates) before the alcohol injection.
Baseline coronary angiography allows the identi-
fication of usually one or more target septal branches.
The most often chosen target septal branch is the first
septal branch, as it is expected to perfuse the basal part
of the interventricular septum.34After introduction of
an angioplasty guidewire into the target septal branch
(Figure 3a), an over-the-wire balloon catheter with a
short balloon (<1 cm in length) is advanced and in-
flated in the proximal part of the septal branch. The
Concerto®balloon catheter (OCCAM International
BV), which is specially manufactured for PTSMA, is
provided with a radiopaque marker at the proximal end
of the balloon, thus allowing exact positioning in the
septal branch and preventing balloon positioning in the
left anterior descending artery (Figure 3b). It is avail-
able in diameters of 1.5 to 2.5 mm, which in practice
include all possible septal branch diameters. Selection
of a slightly oversized balloon compared to the septal
branch diameter ensures tight sealing of the branch
with inflation of the balloon at the nominal pressure.
Injection of a small amount of angiographic contrast
dye (1-2 ml) through the guidewire lumen of the in-
flated balloon catheter provides angiographic demon-
stration of the supply area of the septal branch and
excludes the possibility of reflux into the left anterior
descending artery (Figure 3c). In addition, any possi-
ble collateral vessels can be identified before the in-
jection of alcohol.35
The first septal branch may have an unpredictably
variable anatomy and perfusion bed, which can also
involve other structures apart from the basal septum,
such as the papillary muscle or the right ventricular
free wall.36For this reason, echocardiographic moni-
toring of the procedure was introduced, which aims to
verify the correct target and avoid alcohol injection
Alcohol Septal Ablation
(Hellenic Journal of Cardiology) HJC ñ 513
Figure 2. Haemodynamically recorded left ventricular outflow tract gradient at rest and post-extrasystole before (a)
and after (b) percutaneous septal ablation. Ao – aortic pressure; LV – left ventricular pressure.
into an unsuitable area.32,37Consequently, prior to
any alcohol injection, 1-2 ml of an echocardiographic
contrast agent is administered through the central lu-
men of the balloon catheter under real-time two-di-
mensional echocardiographic and colour Doppler
monitoring. Among several agents that have been used
worldwide, the one with the largest experience is Levo-
vist®(Schering, Berlin, Germany).38If the target septal
branch is optimal, injection of the echo-contrast medi-
um results in complete opacification of the target sep-
A.G. Rigopoulos et al
514 ñ HJC (Hellenic Journal of Cardiology)
Figure 3. Angiographic demonstration of the technique of alcohol septal ablation. Left coronary angiography
shows the target septal branch (arrow), typically originating from the left anterior descending artery, in right
anterior oblique projection. An angioplasty guidewire is already inserted inside the septal branch (a). Optimal
positioning of the balloon catheter (arrow) in the proximal part of the septal artery without compromise of the
left anterior descending artery. The radiopaque marker at the proximal part of the balloon verifies the exact
positioning (b). Injection of angiographic contrast dye through the central lumen of the inflated balloon
catheter (arrow) determines the supply area of the septal branch and excludes leakage in the left anterior de-
scending artery or other coronary vessels (c). Final demonstration of the septal artery stump (arrow) after alco-
hol-induced occlusion (d). GC – left coronary artery guide catheter; PC – pigtail catheter; PM – temporary
tal area adjacent to Doppler maximal flow accelera-
tion and involving the area of mitral valve contact
during the systolic anterior motion of the mitral valve,
without, on the other hand, opacification of any other
cardiac structure (Figure 4). All standard echo-
cardiographic views (apical 2- and 4-chamber, para-
sternal short- and long-axis, subcostal) are examined
and compared with baseline stored echocardiograms.
Once contrast echocardiography has convincingly
shown that the chosen septal branch is optimal, 2 (-4)
ml of >95% alcohol in 1 ml portions are slowly inject-
ed through the central lumen of the over-the-wire bal-
loon catheter. Injection of alcohol is performed under
ongoing fluoroscopy so that any possible balloon dislo-
cation that would carry a risk of subsequent alcohol
misplacement will be noticed immediately. Echocardio-
Alcohol Septal Ablation
(Hellenic Journal of Cardiology) HJC ñ 515
Figure 4. Myocardial contrast echocardiography during alcohol
septal ablation. All steps of the procedure are shown in the 5-
chamber apical view. At the beginning, the anatomy of the heart is
presented and the target septal area is identified (a). Injection of
Levovist® in the target septal branch opacifies the basal part of
the septum, verifying the optimal choice of the septal branch (b).
A more sustained opacification of the basal septum after alcohol
injection signifies a good alcohol depot (c). LA – left atrium; LV –
left ventricle; RV – right ventricle.
graphy is repeated after alcohol injection in order to
identify the alcohol impregnation of the target septal
area.38The amount of injected alcohol depends prin-
cipally on the echocardiographically estimated size of
the contrasted septal area and less on the acute haemo-
dynamic effect. This has gradually led to the use of
lower alcohol doses over the years.39It is estimated
that 1 ml of alcohol should be enough for every 10 mm
of echocardiographically measured septal thickness.38
In search of the minimum dose of alcohol that can pro-
duce an optimal haemodynamic result, alcohol injec-
tion of <2 ml seems to be equally effective as larger
doses.40,41Ultra low doses of ~1 ml have also been
used with comparable results.42This signifies the im-
portance of correct and precise identification and tar-
geting of the myocardial area that will be ablated.
In order to avoid alcohol spilling in the left anterior
descending artery, the balloon catheter is deflated and
removed at least ten minutes after the last alcohol injec-
tion.43A final angiographic control excludes left coro-
nary artery damage and verifies septal branch occlusion
(Figure 3d), while final haemodynamic measurements
confirm the immediate result of septal ablation (Figure
2b). Subsequently, the patient is transferred to the
coronary care unit for haemodynamic and rhythm mon-
itoring, which is required for at least 48 hours. The tem-
porary pacemaker lead remains in place for at least 24
hours and usually can be removed if no conduction ab-
normalities appear during that time.
Apart from PTSMA, several other acronyms for
alcohol septal ablation that have appeared in the lit-
erature correspond to different techniques. TASH
(Transcoronary Ablation of Septal Hypertrophy) re-
lies only on the haemodynamic response during bal-
loon inflation and alcohol injection in the angiogra-
phically recognised target septal branch and the proce-
dure does not involve echocardiographic guiding.44,45
NSRT (Nonsurgical Septal Reduction Therapy) em-
ploys echocardiographic guidance using angiographic
contrast dye to delineate the septal area to be ablated
and also involves dobutamine provocation for the
baseline evaluation of patients.46NSMR (Nonsurgical
Myocardial Reduction) also relies on the haemody-
namic result of temporary balloon inflation in the
(usually more than one) septal branches that would
Indications and contraindications
The clinical indications for PTSMA refer to highly
symptomatic patients, in classes ≥ New York Heart
Association (NYHA) III or Canadian Cardiovascular
Society III despite optimal drug therapy, or with severe
side effects that preclude optimal medication.5The
haemodynamic indication requires a significant ob-
struction either at rest or under provocation. The ab-
solute gradient level criteria were originally set higher
than is currently accepted as an indication (≥30 mmHg
at rest or ≥60 mmHg under provocation).5,12,33It should
be emphasised that gradient provocation should only
be tried with exercise or physiological manoeuvres such
as Valsalva, or after an extrasystolic beat.10,11Dobuta-
mine infusion for gradient generation is clearly not rec-
ommended in symptomatic patients with HOCM.5In
individual patients with less severe symptoms interven-
tional treatment can be considered if they have a high
LVOT gradient (as above) and additional findings,
such as recurrent exercise-induced syncope, abnormal
blood pressure response at exercise, paroxysmal atrial
fibrillation, and/or objectively verified reduction of
exercise capacity.33,48These considerations are sup-
ported by actual data that have shown a correlation be-
tween a resting gradient of more than 30 mmHg and
both HOCM-related death and progressive heart fail-
ure.8,49It is also particularly important to mention that
a considerable number of patients may gradually get
used to their lower than normally expected exercise ca-
pacity and tend to underestimate their symptoms, thus
failing to receive optimal treatment. At the present
time, however, interventional treatment is contraindi-
cated in symptomatic patients with a low LVOT gradi-
ent or asymptomatic patients with preserved exercise
Morphological indications for echocardiography-
guided septal ablation include patients with subaortic as
well as midventricular obstruction.50The geometry of
the left ventricular wall should suggest that lessening of
the septal thickness would abolish obstruction. Patients
with a history of previous, haemodynamically unsuc-
cessful, surgical myectomy can also be treated.51Exis-
tence of concomitant cardiac diseases indicating
surgery—e.g. extensive coronary artery disease, valvular
disease, and anatomical ailments of the mitral valve or
papillary muscles responsible for gradient formation or
mitral regurgitation—should not be treated interven-
tionally, but rather referred for surgical therapy.9,33It
must be noted, however, that a combined percutaneous
treatment (PCI and PTSMA) can be performed in indi-
vidual patients with single vessel disease amenable to
balloon dilatation and stenting.52
To ensure the safety and efficacy of the proce-
dure, alcohol injection should not be attempted un-
A.G. Rigopoulos et al
516 ñ HJC (Hellenic Journal of Cardiology)
der certain circumstances. Such contraindications in-
clude the failure of myocardial contrast echocardiog-
raphy to identify a target septal branch, the echocar-
diographic contrast opacification of any cardiac struc-
ture other than the target septal area,53or insecure
balloon positioning that bears the risk of alcohol re-
flux during injection. Furthermore, alcohol injection
should be avoided if there is any suspicion of collater-
al flow that could lead to infarction far from the tar-
get septal area.35,54
Based on the reported results, symptomatic HOCM
patients have been classified by L. Faber according to
the indication and the expected efficacy of PTSMA as
ideal, possible and poor candidates (Table 1).
Alcohol septal ablation is generally well tolerated by
patients. Most feel a slight chest discomfort at the time
of alcohol injection, which may persist for several hours
in some cases.
It is generally agreed upon by most reports that
about 90% of the treated patients have an acute LVOT
gradient reduction (Figure 5).27,28,31,32,38,44,55-61
Younger patients seem to have less gradient reduc-
tion than older patients,45,62,63probably because they
have greater septal thickness and additional structur-
Table 1. Classification of candidates for percutaneous translumi-
nal septal myocardial ablation (PTSMA) according to indications
and reported results. (Proposed by L. Faber, as presented in Euro
Ideal PTSMA candidate:
Subaortic SAM-related LVOT obstruction ± SAM-related mitral
Basal septum thickness >18 mm, <30 mm
Possible PTSMA candidate:
Subaortic SAM-related LVOT obstruction ± SAM-related mitral
Basal septum thickness >30 mm
Midventricular obstruction or combined LVOT and midventricu-
Poor PTSMA candidate:
Marked elongation of mitral valve leaflet(s)
Severe mitral regurgitation due to primary mitral valve deformity
(unrelated to SAM)
Excessively fibrotic septum with massive thickness (>40 mm)
Unfavourable left ventricular geometry
Anomalous papillary muscle insertion in the mitral valve leaflet
Isolated apical flow acceleration
LVOT – left ventricular outflow tract; SAM – septal anterior motion.
al deformities, such as abnormal papillary muscles, that
might make some contribution to the gradient forma-
tion.33Even so, patients with an insufficient acute result
may have further gradient reduction at follow up due to
post-infarction remodelling and shrinkage of the ablat-
ed septal area.33,64Unlike the immediate result of surgi-
cal myectomy, a remodelling process has been de-
scribed in some patients after PTSMA, which lasts up
to 12 months and results in further thinning of the sep-
tum with ongoing gradient reduction.65,66It is therefore
prudent to allow for that time course before the treat-
ment is deemed ineffective and any decision about re-
peat intervention is made.67Furthermore, this remodel-
ling process seems to extend to the entire left ventricu-
lar myocardium, leading to regression of left ventricular
hypertrophy.28,32,60,68-70Indeed, total left ventricular
mass decreases after septal ablation and this reduction
exceeds that of septal mass, as has been shown by using
contrast-enhanced magnetic resonance imaging.70As in
surgical myectomy,71these findings can be regarded as
a result of the elimination (or at least reduction) of the
Patients show significant symptomatic improve-
ment after treatment (Figure 6).31,32,38,55,60,61,65,72NYHA
class is significantly lower after 3 months, with ongoing
improvement during the first year.31,60,61,72Exercise ca-
pacity and peak oxygen consumption are improved
The symptomatic improvement is based on changes
in cardiac physiology observed at follow up. Parallel
to the LVOT reduction, the systolic anterior motion
Alcohol Septal Ablation
(Hellenic Journal of Cardiology) HJC ñ 517
van Dockum (65)
LVOT gradient (mmHg)
Figure 5. Haemodynamic improvement after alcohol septal abla-
tion. Chart shows the reduction in left ventricular outflow tract
(LVOT) gradient reported in published studies with short-term
follow up (1-48 months). Each study is represented by a line of a
of the mitral valve and the resulting mitral regurgita-
tion are constantly reduced. On the other hand, the
systolic pulmonary artery pressure has been shown to
decrease after successful alcohol septal ablation.32,44
The observed reduction of left atrial dimensions
could suggest an expected lower long-term incidence
of atrial fibrillation.38,64,73This is in accordance with
the sustained improvement of left ventricular dias-
tolic function during follow up.73Myocardial blood
flow improves and myocardial perfusion is enhanced,
which could explain in part the reduction of anginal
Most complications of the procedure may occur
in the catheterisation laboratory or during the early
post-interventional period. Earlier series have shown
in-hospital death as the most significant complication
observed to date, with an earlier rate of up to 4% that
has now fallen to around 1.5%.44,76,77Growing experi-
ence has led to a reduction in mortality and complica-
tion rates.33,78Reports of delayed occurrence of com-
plete heart block up to 10 days after the intervention
need special mention, as they emphasise the need for
close arrhythmic monitoring for several days follow-
ing the intervention.79,80
After the introduction of myocardial contrast
echocardiography, the need for permanent pacemak-
er implantation due to permanent heart block was re-
duced to less than 5%, a rate that is comparable to
post-myectomy results.22,23Furthermore, the develop-
ment of complete heart block after septal ablation
can be predicted using a score that has been intro-
duced by Faber et al.81This score is based on the as-
Figure 6. Symptomatic improvement after alcohol septal ablation.
Chart shows the New York Heart Association (NYHA) class re-
duction reported in published studies. Each study is represented
by a line of a different colour.
sessment of electrocardiographic (QRS duration, PQ
duration, atrioventricular block occurrence and per-
sistence or recovery, heart rate) as well as haemody-
namic variables (baseline gradient) and myocardial
enzyme kinetics (peak SGOT time-point). A low
score (<8) predicts low-risk pacemaker dependency
and facilitates discharge from hospital, while a higher
score (8-12) warrants prolonged monitoring of the
patient, and a very high score (>12) is in favour of
early pacemaker implantation.82Right bundle-branch
block occurs in about 50% of patients27,44,60,72,83and is
associated with a better haemodynamic result.84In
contrast, after surgical myectomy many patients de-
velop left bundle-branch block (LBBB).23,65,85This
discrepancy can be explained by the different mecha-
nism for atrioventricular conduction tissue injury by
alcohol septal ablation and surgical myectomy.86It is
worth mentioning, however, that a patient with a pre-
existing LBBB has a higher risk of complete heart
block after PTSMA.87
A most feared complication is iatrogenic reflux of
alcohol into the left anterior descending artery, caus-
ing vessel occlusion and anterolateral ischaemia.43,55
This can be avoided, however, by the routine use of a
slightly oversized balloon compared to the septal
artery diameter, which should be kept inflated for at
least ten minutes after the last alcohol injection.28,33
Importance of echocardiographic guidance
Since its original appraisal, echocardiographic guid-
ance with myocardial contrast echocardiography has
become an indispensable part of the procedure.32,37,59
It has been clearly demonstrated that echocardio-
graphic guidance had a crucial impact on the selec-
tion of the ablated area in a significant proportion of
patients.28,38Echocardiographic contrast also enables
the identification of an atypically originating septal
branch as target vessel.28Most importantly, alcohol
misplacement can be avoided by changing the target
vessel after echo-contrast visualisation of wrong sep-
tal areas or other cardiac structures, such as papillary
muscles or ventricular free walls, thus preventing a
catastrophic remote infarction.88As the anatomy and
the perfusion bed of the septal branches are highly
unpredictable,36the choice of the first larger septal
branch for alcohol septal ablation without any my-
ocardial echocardiographic contrast validation could
lead to failure to reach the target area, or even more
It is expected that advances in cardiac imaging in
the future may provide non-invasive estimation of the
underlying histological substrate of the septal my-
ocardium before treatment, thus allowing better pa-
tient selection.90Predominance of fibrotic over mus-
cle tissue in the basal septum may be a reason for a
less significant haemodynamic result after PTSMA.
Thus, detection of unfavourable histology, together
with elongation of the mitral leaflets, may be helpful
in the future to exclude patients from PTSMA on the
grounds that their haemodynamic result is likely to be
Long-term results from the first patients who were
treated with PTSMA are now available and show that
this treatment is both safe and effective.64,69The im-
pressive ongoing symptomatic improvement is ac-
companied by an increase of exercise capacity in ob-
jective measurements.28,38,47,55,69In fact, the favour-
able effect of alcohol septal ablation on symptoms
and exercise capacity appears unremitting in longer-
term reports.64,91Echocardiographic measurements
during follow up present continuing and growing re-
duction of the LVOT gradients.28,61,64,69,77After a mean
follow up of 58 ± 14 months most patients showed
complete elimination of the outflow tract gradient.64
This should be appraised as an expression of post-in-
terventional remodelling following an induced septal
infarction. These findings emphasise the sense of effi-
cacy in our strategy at inducing septal necrosis by al-
cohol injection: the amount of scarred tissue should
be limited to the extent that can offer haemodynamic
benefit.33In fact, injection of much lower alcohol dos-
es than in the early years (<2 ml or even <1 ml), has
shown comparable results to those of the earlier strat-
egy of aiming at total abolition of the gradient during
Indeed, the generation of an intra-myocardial scar
has been a main issue of concern regarding the long-
term outcome of patients after septal ablation, due to
anxiety about a potentially higher risk of malignant ven-
tricular arrhythmias.92Ventricular arrhythmias have
been reported as an in-hospital complication, possibly
due to ischaemia, but they have rarely been described
during follow up.64,69,77,93-95In fact, no increased risk of
malignant arrhythmias after the procedure has been
shown in patients with an already implanted ICD be-
cause of an estimated high risk of sudden death.93,96
Furthermore, a decrease in the occurrence of syncope
has been reported after alcohol septal ablation.64,97It is
A.G. Rigopoulos et al
518 ñ HJC (Hellenic Journal of Cardiology)
plausible that, contrary to what happens in patients
with myocardial infarction due to coronary artery dis-
ease, the incidence of significant ventricular arrhyth-
mias after alcohol septal ablation is rare. As the exis-
tence of severe LVOT obstruction itself is an inde-
pendent risk factor for sudden cardiac death and ap-
propriate ICD discharges,98the reduction of LVOT
gradient and left ventricular hypertrophy after PTSMA
may be beneficial. Moreover, it seems that necrosis
produced by alcohol has entirely different morpho-
logic characteristics than necrosis after coronary is-
chaemia, which might also be extended to differences
in electrophysiological behaviour.99
Long-term follow up of the first 100 patients treat-
ed has shown an excellent 96% survival at 8 years, while
survival without severe symptoms, atrial fibrillation,
stroke or ICD implantation was 74%.64Recently pub-
lished data from a larger cohort of 347 patients has
shown 94% survival after 5 years and 87% after 10
years, which is comparable to the results of large myec-
Surgical and percutaneous treatments for septal re-
duction in HOCM have not been compared in ran-
domised trials. It is doubtful, however, that such a tri-
al can ever be performed.100Non-randomised com-
parison between alcohol septal ablation and myecto-
my has shown that both therapeutic modalities offer a
significant reduction of LVOT obstruction and symp-
tomatic improvement.65,101,102It is prudent, therefore,
to take account of the benefits and drawbacks of each
therapeutic method when deciding on treatment for
LVOT obstruction. This decision has to take into
consideration clinical, morphological, and technical
aspects, as well as the merit of each treatment modal-
ity for the individual patient. Although successful
combined percutaneous treatment of coexistent
HOCM and coronary artery disease has been report-
ed,52it should be considered that surgery primarily in-
corporates the ability to deal with HOCM and coexis-
tent cardiac diseases, such as coronary artery disease
and valvular disease. In patients with HOCM and mi-
tral regurgitation the presence or not of pathological
findings on the mitral valve apparatus should deter-
mine the preferred treatment option. In view of the
emerging long-term results, surgery and percuta-
neous septal ablation should be regarded as alterna-
tive treatment options in HOCM, in terms of safety
and efficacy. The individual decision in each patient
should realise the intention to achieve optimal re-
sults. This also means that the individual experience
of the centre should be taken into consideration when
dealing with such a heterogeneous disease. Further-
more, it is essential that symptomatic treatment of
patients with HOCM should be part of an integrated
treatment approach that includes the assessment and
management of risk factors for sudden death, as well
as adjustment of treatment to lifestyle parameters
and quality of life requirements.
1. Spirito P, Seidman CE, McKenna WJ, Maron BJ. The man-
agement of hypertrophic cardiomyopathy. N Engl J Med.
1997; 336: 775-785.
2. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hyper-
trophic cardiomyopathy. Clinical spectrum and treatment.
Circulation. 1995; 92: 1680-1692.
3. Rigopoulos A, Anastasakis A. Hypertrophic cardiomyopathy:
recent aspects and knowledge of the last decade. Hellenic J
Cardiol. 2000; 41: 212-234.
4. Georgakopoulos D, Tolis V. Hypertrophic cardiomyopathy
in children, teenagers and young adults. Hellenic J Cardiol.
2007; 48: 228-233.
5. Maron BJ, McKenna WJ, Danielson GK, et al. American Col-
lege of Cardiology/European Society of Cardiology clinical ex-
pert consensus document on hypertrophic cardiomyopathy. A
report of the American College of Cardiology Foundation Task
Force on Clinical Expert Consensus Documents and the Euro-
pean Society of Cardiology Committee for Practice Guidelines.
J Am Coll Cardiol. 2003; 42: 1687-1713.
6. Maron BJ. Hypertrophic cardiomyopathy: a systematic re-
view. JAMA. 2002; 287: 1308-1320.
7. Wigle ED, Sasson Z, Henderson MA, et al. Hypertrophic
cardiomyopathy. The importance of the site and the extent of
hypertrophy. A review. Prog Cardiovasc Dis. ; 28: 1-83.
8. Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventric-
ular outflow tract obstruction on clinical outcome in hyper-
trophic cardiomyopathy. N Engl J Med. 2003; 348: 295-303.
9. Maron BJ, Nishimura RA, Danielson GK. Pitfalls in clinical
recognition and a novel operative approach for hypertrophic
cardiomyopathy with severe outflow obstruction due to anom-
alous papillary muscle. Circulation. 1998; 98: 2505-2508.
10. Maron MS, Olivotto I, Zenovich AG, et al. Hypertrophic car-
diomyopathy is predominantly a disease of left ventricular
outflow tract obstruction. Circulation. 2006; 114: 2232-2239.
11. Shah JS, Esteban MTT, Thaman R, et al. Prevalence of exer-
cise-induced left ventricular outflow tract obstruction in symp-
tomatic patients with non-obstructive hypertrophic cardiomy-
opathy. Heart. 2008; 94: 1288-1294.
12. Fifer MA, Vlahakes GJ. Management of symptoms in hyper-
trophic cardiomyopathy. Circulation. 2008; 117: 429-439.
13. Frank MJ, Abdulla AM, Canedo MI, Saylors RE. Long-term
medical management of hypertrophic obstructive cardiomy-
opathy. Am J Cardiol. 1978; 42: 993-1001.
14. Haberer T, Hess OM, Jenni R, Krayenbühl HP. [Hypertrophic
obstructive cardiomyopathy: spontaneous course in compari-
son to long-term therapy with propranolol and verapamil]. Z
Kardiol. 1983; 72: 487-493.
Alcohol Septal Ablation
(Hellenic Journal of Cardiology) HJC ñ 519
15. Harrison DC, Braunwald E, Glick G, Mason DT, Chidsey
CA, Ross J. Effects of beta adrenergic blockade on the circu-
lation with particular reference to observations in patients
with hypertrophic subaortic stenosis. Circulation. 1964; 29:
16. Kaltenbach M, Hopf R, Kober G, Bussmann WD, Keller M,
Petersen Y. Treatment of hypertrophic obstructive cardiomy-
opathy with verapamil. Br Heart J. 1979; 42: 35-42.
17. Sherrid MV, Barac I, McKenna WJ, et al. Multicenter study
of the efficacy and safety of disopyramide in obstructive hy-
pertrophic cardiomyopathy. J Am Coll Cardiol. 2005; 45:
18. Pollick C. Muscular subaortic stenosis: hemodynamic and clini-
cal improvement after disopyramide. N Engl J Med. 1982; 307:
19. Kimball BP, Bui S, Wigle ED. Acute dose-response effects of
intravenous disopyramide in hypertrophic obstructive car-
diomyopathy. Am Heart J. 1993; 125: 1691-1697.
20. Sherrid M, Delia E, Dwyer E. Oral disopyramide therapy for
obstructive hypertrophic cardiomyopathy. Am J Cardiol. 1988;
21. Maron BJ. Appraisal of dual-chamber pacing therapy in hy-
pertrophic cardiomyopathy: too soon for a rush to judgment?
J Am Coll Cardiol. 1996; 27: 431-432.
22. Woo A, Williams WG, Choi R, et al. Clinical and echocardio-
graphic determinants of long-term survival after surgical
myectomy in obstructive hypertrophic cardiomyopathy. Cir-
culation. 2005; 111: 2033-2041.
23. Schulte HD, Gramsch-Zabel H, Schwartzkopff B. [Hyper-
trophic obstructive cardiomyopathy: surgical treatment]. Sch-
weiz Med Wochenschr. 1995; 125: 1940-1949.
24. Robbins RC, Stinson EB. Long-term results of left ventricu-
lar myotomy and myectomy for obstructive hypertrophic car-
diomyopathy. J Thorac Cardiovasc Surg. 1996; 111: 586-594.
25. Heric B, Lytle BW, Miller DP, Rosenkranz ER, Lever HM,
Cosgrove DM. Surgical management of hypertrophic ob-
structive cardiomyopathy. Early and late results. J Thorac
Cardiovasc Surg. 1995; 110: 195-206; discussion 206-208.
26. Schoendube FA, Klues HG, Reith S, Flachskampf FA, Han-
rath P, Messmer BJ. Long-term clinical and echocardio-
graphic follow-up after surgical correction of hypertrophic
obstructive cardiomyopathy with extended myectomy and re-
construction of the subvalvular mitral apparatus. Circulation.
1995; 92: II122-127.
27. Sigwart U. Non-surgical myocardial reduction for hypertrophic
obstructive cardiomyopathy. Lancet. 1995; 346: 211-214.
28. Seggewiss H. Current status of alcohol septal ablation for pa-
tients with hypertrophic cardiomyopathy. Curr Cardiol Rep.
2001; 3: 160-166.
29. Kuhn H, Gietzen F, Leuner C, Gerenkamp T. Induction of
subaortic septal ischaemia to reduce obstruction in hyper-
trophic obstructive cardiomyopathy. Studies to develop a new
catheter-based concept of treatment. Eur Heart J. 1997; 18:
30. Brugada P, de Swart H, Smeets JL, Wellens HJ. Transcoro-
nary chemical ablation of ventricular tachycardia. Circula-
tion. 1989; 79: 475-482.
31. Seggewiss H, Gleichmann U, Faber L, Fassbender D, Sch-
midt HK, Strick S. Percutaneous transluminal septal myocar-
dial ablation in hypertrophic obstructive cardiomyopathy:
acute results and 3-month follow-up in 25 patients. J Am Coll
Cardiol. 1998; 31: 252-258.
32. Faber L, Seggewiss H, Gleichmann U. Percutaneous translu-
minal septal myocardial ablation in hypertrophic obstructive
cardiomyopathy: results with respect to intraprocedural my-
ocardial contrast echocardiography. Circulation. 1998; 98:
33. Seggewiss H, Rigopoulos A, Faber L, Ziemssen P. Alcohol
septal ablation. In: Maron BJ, editor. Diagnosis and manage-
ment of hypertrophic cardiomyopathy. Malden, Mass.; Ox-
ford: Blackwell Futura; 2004: p. 259-278.
34. Angelini P. The “1st septal unit” in hypertrophic obstructive
cardiomyopathy: a newly recognized anatomo-functional en-
tity, identified during recent alcohol septal ablation experi-
ence. Tex Heart Inst J. 2007; 34: 336-346.
35. Rigopoulos A, Sepp R, Palinkas A, Ungi I, Kremastinos DT,
Seggewiss H. Alcohol septal ablation for hypertrophic ob-
structive cardiomyopathy: collateral vessel communication
between septal branches. Int J Cardiol. 2006; 113: e67-69.
36. Singh M, Edwards WD, Holmes DR, Tajil AJ, Nishimura
RA. Anatomy of the first septal perforating artery: a study
with implications for ablation therapy for hypertrophic car-
diomyopathy. Mayo Clin Proc. 2001; 76: 799-802.
37. Faber L, Seggewiss H, Fassbender D, et al. Guiding of percu-
taneous transluminal septal myocardial ablation in hyper-
trophic obstructive cardiomyopathy by myocardial contrast
echocardiography. J Interv Cardiol. 1998; 11: 443-448.
38. Faber L, Seggewiss H, Welge D, et al. Echo-guided percuta-
neous septal ablation for symptomatic hypertrophic obstruc-
tive cardiomyopathy: 7 years of experience. Eur J Echocar-
diogr. 2004; 5: 347-355.
39. Kuhn H, Lawrenz T, Lieder F, et al. Survival after transcoro-
nary ablation of septal hypertrophy in hypertrophic obstruc-
tive cardiomyopathy (TASH): a 10 year experience. Clin Res
Cardiol. 2008; 97: 234-243.
40. Veselka J, Procházková S, Duchonová R, et al. Alcohol sep-
tal ablation for hypertrophic obstructive cardiomyopathy:
Lower alcohol dose reduces size of infarction and has compa-
rable hemodynamic and clinical outcome. Catheter Cardio-
vasc Interv. 2004; 63: 231-235.
41. Veselka J, Duchonová R, Páleníckova J, et al. Impact of
ethanol dosing on the long-term outcome of alcohol septal ab-
lation for obstructive hypertrophic cardiomyopathy: a single-
center prospective, and randomized study. Circ J. 2006; 70:
42. Veselka J, Zemánek D, Tomasov P, Duchonová R, Lin-
hartová K. Alcohol septal ablation for obstructive hyper-
trophic cardiomyopathy: ultra-low dose of alcohol (1 ml) is
still effective. Heart Vessels. 2009; 24: 27-31.
43. Ruzyllo W, Chojnowska L, Demkow M, et al. Left ventricu-
lar outflow tract gradient decrease with non-surgical myocar-
dial reduction improves exercise capacity in patients with hy-
pertrophic obstructive cardiomyopathy. Eur Heart J. 2000;
44. Gietzen FH, Leuner CJ, Raute-Kreinsen U, et al. Acute and
long-term results after transcoronary ablation of septal hy-
pertrophy (TASH). Catheter interventional treatment for hy-
pertrophic obstructive cardiomyopathy. Eur Heart J. 1999;
45. Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C,
Kuhn H. Transcoronary ablation of septal hypertrophy for hy-
pertrophic obstructive cardiomyopathy: feasibility, clinical ben-
efit, and short term results in elderly patients. Heart. 2004; 90:
46. Lakkis NM, Nagueh SF, Kleiman NS, et al. Echocardiogra-
phy-guided ethanol septal reduction for hypertrophic ob-
A.G. Rigopoulos et al
520 ñ HJC (Hellenic Journal of Cardiology)
structive cardiomyopathy. Circulation. 1998; 98: 1750-1755.
47. Boekstegers P, Steinbigler P, Molnar A, et al. Pressure-guid-
ed nonsurgical myocardial reduction induced by small septal
infarctions in hypertrophic obstructive cardiomyopathy. J Am
Coll Cardiol. 2001; 38: 846-853.
48. Veselka J. Alcohol septal ablation for hypertrophic obstruc-
tive cardiomyopathy: a review of the literature. Med Sci Monit.
2007; 13: RA62-68.
49. 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.
50. Seggewiss H, Faber L. Percutaneous septal ablation for hy-
pertrophic cardiomyopathy and mid-ventricular obstruction.
Eur J Echocardiogr. 2000; 1: 277-280.
51. Faber L, Welge D, Hering D, et al. Percutaneous septal abla-
tion after unsuccessful surgical myectomy for patients with
hypertrophic obstructive cardiomyopathy. Clin Res Cardiol.
2008; 97: 899-904.
52. Seggewiss H, Faber L, Meyners W, Bogunovic N, Odenthal
HJ, Gleichmann U. Simultaneous percutaneous treatment in
hypertrophic obstructive cardiomyopathy and coronary artery
disease: a case report. Cathet Cardiovasc Diagn. 1998; 44: 65-
53. Alfonso F, Isla LP, Seggewiss H. Contrast echocardiography
during alcohol septal ablation: friend or foe? Heart. 2005; 91:
54. Parham WA, Kern MJ. Apical infarct via septal collateraliza-
tion complicating transluminal alcohol septal ablation for hy-
pertrophic cardiomyopathy. Catheter Cardiovasc Interv.
2003; 60: 208-211.
55. Knight C, Kurbaan AS, Seggewiss H, et al. Nonsurgical septal
reduction for hypertrophic obstructive cardiomyopathy: out-
come in the first series of patients. Circulation. 1997; 95:
56. Lakkis N, Kleiman N, Killip D, Spencer WH 3rd. Hypertro-
phic obstructive cardiomyopathy: alternative therapeutic op-
tions. Clin Cardiol. 1997; 20: 417-418.
57. Bhargava B, Agarwal R, Kaul U, Manchanda SC, Wasir HS.
Transcatheter alcohol ablation of the septum in a patient of
hypertrophic obstructive cardiomyopathy. Cathet Cardiovasc
Diagn. 1997; 41: 56-58.
58. Kornacewicz-Jach Z, Gil R, Woltarowicz A, et al. Early results
of alcohol ablation of the septal branch of coronary artery in pa-
tients with hypertrophic obstructive cardiomyopathy. Pol Heart
J. 1998; 48: 105.
59. Nagueh SF, Lakkis NM, He ZX, et al. Role of myocardial
contrast echocardiography during nonsurgical septal reduc-
tion therapy for hypertrophic obstructive cardiomyopathy. J
Am Coll Cardiol. 1998; 32: 225-229.
60. Seggewiss H, Faber L, Gleichmann U. Percutaneous translu-
minal septal ablation in hypertrophic obstructive cardiomy-
opathy. Thorac Cardiovasc Surg. 1999; 47: 94-100.
61. Faber L, Meissner A, Ziemssen P, Seggewiss H. Percuta-
neous transluminal septal myocardial ablation for hyper-
trophic obstructive cardiomyopathy: long term follow up of
the first series of 25 patients. Heart. 2000; 83: 326-331.
62. Seggewiss H, Faber L, Ziemssen P, et al. Age related acute
results in percutaneous septal ablation in hypertrophic ob-
structive cardiomyopathy. J Am Coll Cardiol. 2000; 35 (Suppl
A): 188A (abstract).
63. Faber L, Welge D, Fassbender D, Schmidt HK, Horstkotte
D, Seggewiss H. One-year follow-up of percutaneous septal
ablation for symptomatic hypertrophic obstructive cardiomy-
opathy in 312 patients: predictors of hemodynamic and clini-
cal response. Clin Res Cardiol. 2007; 96: 864-873.
64. 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.
65. Qin JX, Shiota T, Lever HM, et al. Outcome of patients with
hypertrophic obstructive cardiomyopathy after percutaneous
transluminal septal myocardial ablation and septal myectomy
surgery. J Am Coll Cardiol. 2001; 38: 1994-2000.
66. Rivera S, Sitges M, Azqueta M, et al. [Left ventricular re-
modeling in patients with hypertrophic obstructive cardiomy-
opathy treated with percutaneous alcohol septal ablation: an
echocardiographic study]. Rev Esp Cardiol. 2003; 56: 1174-
67. Yoerger DM, Picard MH, Palacios IF, Vlahakes GJ, Lowry
PA, Fifer MA. Time course of pressure gradient response af-
ter first alcohol septal ablation for obstructive hypertrophic
cardiomyopathy. Am J Cardiol. 2006; 97: 1511-1514.
68. Mazur W, Nagueh SF, Lakkis NM, et al. Regression of left
ventricular hypertrophy after nonsurgical septal reduction
therapy for hypertrophic obstructive cardiomyopathy. Circu-
lation. 2001; 103: 1492-1496.
69. 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. German.
70. van Dockum WG, Beek AM, ten Cate FJ, et al. Early onset
and progression of left ventricular remodeling after alcohol
septal ablation in hypertrophic obstructive cardiomyopathy.
Circulation. 2005; 111: 2503-2508.
71. Curtius JM, Stoecker J, Loesse B, Welslau R, Scholz D. Chang-
es of the degree of hypertrophy in hypertrophic obstructive car-
diomyopathy under medical and surgical treatment. Cardiolo-
gy. 1989; 76: 255-263.
72. 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.
73. Jassal DS, Neilan TG, Fifer MA, et al. Sustained improve-
ment in left ventricular diastolic function after alcohol septal
ablation for hypertrophic obstructive cardiomyopathy. Eur
Heart J. 2006; 27: 1805-1810.
74. Soliman OII, Geleijnse ML, Michels M, et al. Effect of suc-
cessful alcohol septal ablation on microvascular function in
patients with obstructive hypertrophic cardiomyopathy. Am J
Cardiol. 2008; 101: 1321-1327.
75. Pedone C, Biagini E, Galema TW, Vletter WB, ten Cate FJ.
Myocardial perfusion after percutaneous transluminal septal
myocardial ablation as assessed by myocardial contrast echocar-
diography in patients with hypertrophic obstructive cardiomy-
opathy. J Am Soc Echocardiogr. 2006; 19: 982-986.
76. 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 functional class III or IV, and outflow obstruction
only under provocable conditions. Circulation. 2002; 106: 454-
77. Alam M, Dokainish H, Lakkis N. Alcohol septal ablation for
hypertrophic obstructive cardiomyopathy: a systematic review
of published studies. J Interv Cardiol. 2006; 19: 319-327.
78. Pauschinger M, Keren A. Increasing evidence for the safety
and efficacy of alcohol septal ablation during medium- and
Alcohol Septal Ablation
(Hellenic Journal of Cardiology) HJC ñ 521
long-term follow-up. Clin Res Cardiol. 2007; 96: 851-855. Download full-text
79. Kern MJ, Holmes DG, Simpson C, Bitar SR, Rajjoub H. De-
layed occurrence of complete heart block without warning af-
ter alcohol septal ablation for hypertrophic obstructive car-
diomyopathy. Catheter Cardiovasc Interv. 2002; 56: 503-507.
80. Reinhard W, Ten Cate FJ, Scholten M, De Laat LE, Vos J.
Permanent pacing for complete atrioventricular block after
nonsurgical (alcohol) septal reduction in patients with ob-
structive hypertrophic cardiomyopathy. Am J Cardiol. 2004;
81. Faber L, Seggewiss H, Welge D, et al. [Predicting the risk of
atrioventricular conduction lesions after percutaneous septal
ablation for obstructive hypertrophic cardiomyopathy]. Z
Kardiol. 2003; 92: 39-47. German.
82. Faber L, Welge D, Fassbender D, Schmidt HK, Horstkotte
D, Seggewiss H. Percutaneous septal ablation for sympto-
matic hypertrophic obstructive cardiomyopathy: managing the
risk of procedure-related AV conduction disturbances. Int J
Cardiol. 2007; 119: 163-167.
83. Coakley E, Steinberg DH, Tibrewala A, et al. Effect of alco-
hol septal ablation in patients with hypertrophic cardiomy-
opathy on the electrocardiographic pattern. Am J Cardiol.
2008; 102: 621-624.
84. McCann GP, Van Dockum WG, Beek AM, et al. Extent of
myocardial infarction and reverse remodeling assessed by
cardiac magnetic resonance in patients with and without right
bundle branch block following alcohol septal ablation for ob-
structive hypertrophic cardiomyopathy. Am J Cardiol. 2007;
85. Williams WG, Wigle ED, Rakowski H, Smallhorn J, LeBlanc
J, Trusler GA. Results of surgery for hypertrophic obstructive
cardiomyopathy. Circulation. 1987; 76: V104-108.
86. Talreja DR, Nishimura RA, Edwards WD, et al. Alcohol sep-
tal ablation versus surgical septal myectomy: comparison of
effects on atrioventricular conduction tissue. J Am Coll Car-
diol. 2004; 44: 2329-2332.
87. Qin JX, Shiota T, Lever HM, et al. Conduction system abnor-
malities in patients with obstructive hypertrophic cardiomy-
opathy following septal reduction interventions. Am J Cardi-
ol. 2004; 93: 171-175.
88. Faber L, Seggewiss H, Ziemssen P, Gleichmann U. Intrapro-
cedural myocardial contrast echocardiography as a routine
procedure in percutaneous transluminal septal myocardial
ablation: detection of threatening myocardial necrosis distant
from the septal target area. Catheter Cardiovasc Interv. 1999;
89. Mayer SA, Anwar A, Grayburn PA. Comparison of success-
ful and failed alcohol septal ablations for obstructive hyper-
trophic cardiomyopathy. Am J Cardiol. 2003; 92: 241-242.
90. Efthimiadis GK, Spanos GP, Giannakoulas G, et al. Hyper-
trophic cardiomyopathy with late enhancement of the non-
hypertrophied left ventricular segments. Hellenic J Cardiol.
2008; 49: 114-116.
91. Malek LA, Chojnowska L, Klopotowski M, et al. Long term
exercise capacity in patients with hypertrophic cardiomyopa-
thy treated with percutaneous transluminal septal myocardial
ablation. Eur J Heart Fail. 2008; 10: 1123-1126.
92. Maron BJ, Dearani JA, Ommen SR, et al. The case for surgery
in obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol.
2004; 44: 2044-2053.
93. Lawrenz T, Obergassel L, Lieder F, et al. Transcoronary ab-
lation of septal hypertrophy does not alter ICD intervention
rates in high risk patients with hypertrophic obstructive car-
diomyopathy. Pacing Clin Electrophysiol. 2005; 28: 295-300.
94. Seggewiss H, Faber L, Ziemssen P. Alcohol septal ablation
for hypertrophic obstructive cardiomyopathy. Cardiol Rev.
1999; 7: 316-323.
95. Boltwood CM, Chien W, Ports T. Ventricular tachycardia
complicating alcohol septal ablation. N Engl J Med. 2004;
96. Cuoco FA, Spencer WH 3rd, Fernandes VL, et al. Implan-
table cardioverter-defibrillator therapy for primary preven-
tion of sudden death after alcohol septal ablation of hyper-
trophic cardiomyopathy. J Am Coll Cardiol. 2008; 52: 1718-
97. Veselka J, Honek T. Early remodelling of left ventricle and im-
provement of myocardial performance in patients after percu-
taneous transluminal septal myocardial ablation for hyper-
trophic obstructive cardiomyopathy. Int J Cardiol. 2003; 88:
98. Elliott PM, Gimeno JR, Tomé MT, et al. Left ventricular
outflow tract obstruction and sudden death risk in patients
with hypertrophic cardiomyopathy. Eur Heart J. 2006; 27: 1933-
99. Raute-Kreinsen U. Morphology of necrosis and repair after
transcoronary ethanol ablation of septal hypertrophy. Pathol
Res Pract. 2003; 199: 121-127.
100. Olivotto I, Ommen SR, Maron MS, Cecchi F, Maron BJ. Sur-
gical myectomy versus alcohol septal ablation for obstructive
hypertrophic cardiomyopathy. Will there ever be a random-
ized trial? J Am Coll Cardiol. 2007; 50: 831-834.
101. Nagueh SF, Ommen SR, Lakkis NM, et al. Comparison of
ethanol septal reduction therapy with surgical myectomy for
the treatment of hypertrophic obstructive cardiomyopathy. J
Am Coll Cardiol. 2001; 38: 1701-1706.
102. Firoozi S, Elliott PM, Sharma S, et al. Septal myotomy-myecto-
my and transcoronary septal alcohol ablation in hypertrophic
obstructive cardiomyopathy. A comparison of clinical, haemo-
dynamic and exercise outcomes. Eur Heart J. 2002; 23: 1617-
A.G. Rigopoulos et al
522 ñ HJC (Hellenic Journal of Cardiology)