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Transcript
Percutaneous Septal
Myocardial Ablation
(PASMA)
经皮间隔支化学消融治疗肥厚梗阻性心肌病
Cardiovascular Institute & Fu Wai Hospital
Chinese Academy of Medical Science
You Shi Jie MD
2010.7. 23 GuiYang
Introduction
 Treatment of symptomatic patients with HOCM aims to
reduce symptoms, improve function capacity and provide
better quality life.
 Aims directly to reduce the hypertrophied interventricular
septum with consecutive expansion of the LV outflow tract
and reduction of the LV outflow tract gradient and
improve distolic function LV.
 First choice druges treatment. At least 10% of patients with
marked outflow tract obstruction have severe symptoms,
which are unresponsive to medical therapy.
 HOCM Myectomy
 DDD-PM
 ICD
 PTSMA
Hypertrophic cardiomyopathy
Epidemiological characteristics
 Hypertrophic cardiomyopathy incidence of
0.2% (1:500), 0.16% in our country .
 The vast majority of patients with no symptoms,
 25% of outflow tract obstruction occurred
 only about 5-10% of patients with drug
treatments fail or cause serious side effects of
drugs effective dose.
 Require treatment or surgical intervention in
patients treated with only very few parts.
Pathophysiologic and clinical
characteristics of HOCM





Ventricular hypertrophy
Left ventricular outflow tract pressure gradient
Myocardial ischemia-angina pectoris.
Arrhythmia - ventricular tachycardia, fibrillation .
Clinical manifestations: dizziness, amaurosis,
syncope, exertional shortness of breath, angina
pectoris, heart disfunction and sudden death.
 Generally considered: more severe hypertrophy,
outflow tract obstruction near the LVOT sit, the
more higher the obstructive pressure gradient were
the more obvious clinical symptoms and the greater
the potential threat.
The natural course of outflow tract
obstruction
 Level –any ages.
 there is a big difference in Natural history
 The natural course not sure.
 The more cardiac hypertrophy, the higher the
pressure gradient, the greater the risk of sudden
death.
 The outflow tract pressure gradient of the clinical
importance of the issue remains controversial, but
it is generally considered an important clinical
process indicators.
 Nnual mortality rate of 2-4%, the incidence of
sudden death ≤1%
The symptoms
Whether the obstruction produced the clinical
symptoms? not only with the degree of outflow
tract obstruction and outflow tract pressure
gradient, as well as the obstruction site. But also
with ventricular diastolic function and the
adequacy of venous return is also closely related.
Increase the heart before and after load and
myocardial contractility often cause noticeable
clinical symptoms. Therefore, it will become more
apparent after exercise . The patients should be
treatment.
Diastolic dysfunction
♦ All patients had diastolic dysfunction –
♦ How the pressure gradient and symptoms
♦ And the extent and distribution of the
hypertrophy has nothing to do.
♦ Whether normal or small ventricular cavity, due
to increased heart weight, ventricular volume
reduction, myocardial fibrosis, leaving ventricular
stiffness increased, compliance decreased and
caused the diastolic function damage. Pulmonary
venous pressure and end-diastolic pressure were
increased and heart disfunction.
systolic function
 Systolic function is normal or supranormal in HCOM
 Both obstruction and non-obstruction, Systolic
dysfunction occurs in small subset (10-15%)
 Result of progressive impairment of systolic function.
 This transformation: wall thinning, cavity dilation,
and fibrosis, increased mortality 11% (annual ) and
risk of SCD.
 Conventional UCG, M-mode, or EF, fractional
shortening preserved despite impaiment long-axis
function
 Tissue Doppler image (TD)-derived systolic velocities:
in the basal inferoseptal and anterolateral wall
routinely in all patients on subsequent scans.
Myocardial ischemia
• Myocardial ischemia, the symptoms of angina
pectoris are:
• High-power so that left ventricular myocardial
oxygen consumption increased;
• Cardiac contraction strength of oppression the
large myocardial coronary artery;
• Intramyocardial small coronary artery stenosis
and intimal thickening abnormalities, leading to
cardiac hypertrophy and coronary artery oxygen
required due to an imbalance of oxygen supply.
Arrhythmia and sudden death
 HOCM of patients with abnormal myocardial
cells and the arrangement of disorder provides a
basis for the arrhythmia.
 However, abnormal myocardial arrangement
and spontaneous arrhythmias and ventricular
fibrillation threshold, the precise relationship is
unclear.
 About 25% of patients may have non-sustained
ventricular tachycardia, the arrhythmia is
sudden death of a good predictor, and negative
predictive accuracy is 97%.
Risk factors for sudden death
• High-risk:
1 Sudden death occurred in a successful
rescue
2 continuous monomorphic ventricular
tachycardia
Clinical risk factors:
1 non-sustained ventricular tachycardia
2 movement abnormal blood pressure
response ( ≥ 25mmHg)
3 unexplained syncope
4 early-onset family history of sudden
death
5 severe left ventricular hypertrophy>
30mm
The purpose of the treatment PTMSA
 Treatment of symptomatic patients with HOCM
 The PTMSA treatment of HOCM is a obstruction
by blocking a the supply blood of parts of the
septal hypertrophy of myocardial and myocardial
injury in the region, leading to the area of
myocardial necrosis, myocardial contractile
function disappeared, Widened the left ventricular
outflow tract, while lowering the outflow tract
obstruction and the cardiac output increase. And
improve clinical symptoms and hemodynamics.
PTSMA indication (1)
Clinical indication
Symptomatic patients

Drug refractory severe said effects medical
treatment

Functional class III or IV

Functional class II with objective limitation or
risk factors

Recurrent exercise-induced syncopes

Failure of prior myectomy or DDD-PM

Comorbitiy with increased surgical risk.
PTSMA indication (2)
Hemodynamic indication in symptomatic patients
 The pressure gradient at rest > 50mmHg or > 100mmHg
with provocation.
 In 2008 ESC meeting, Seggewise that LV gradient ≧30
mmHg at rest or Provocable LV gradient ≧ 60 mmHg.
 Valsalva
 Post extrasystole.
 No dobutamine gradients (Drugs)
(There is no information that reduce the LVOT pressure to
reduce sudden death, but the LVOT> 30mmHg and increased
risk of death directly related to, New Eng l J Med 2003; 348:295-303)
Hypertrophic Cardiomyopathy
Survival According to Outflow Tract Gradient
BJ Maron et al; JAMA 281:650-655, 1999
PTSMA indication (3)
Morophologic indication
Echocariography
Subaorrtic SAM-associated gradient
Mid-cavitary gradient
Caution: papillary muscle involvement:
MCE
No prolonged mitral leaflets
Coronary angiography
suitable septal branch.
Outflow tract obstruction sign
in Echocardiograph
• M-mode echocardiogram in obstructive hypertrophic
cardiomyopathy showing systolic anterior motion of the mitral valve
(SAM) (arrows indicating septum and mitral valve leaflet contact)
Morphologic of HOCM
New classfication of HOCM
Methods: they were classified
into 4 types according to the
echocardiographic results:
Type I :local subaortic
obstruction of HOCM;
Type II: predominant in
midventicular obstruction;
Type III: diffuse septal
hypertrophic obstruction in
outflow tract and
midventicular obstruction;
Type IV: multiposition
hypertrophic obtruction.
1.asymmetrical septal hypertrophy (ASH), 2.Idiopathic
hypertrophic subaortic stenosis (IHSS), 3.Apical or
Japanese HCM. In this form of nonobstructive HCM,
the thickest part of the left ventricle is at the tip or apex
of the pump .4. the obstruction is not in the outflow
tract but in the middle of the ventricle. A tunnel leads
into a dilated apical portion, called an aneurysm, which
has thin walls.
Our classfication in PTSMA
Our typing in the I-type and Maron in the Ityping was the same as suitable for PTSMA
treatment and Maron's II-type includes the
type II and type III of our model, it is
suitable PTSMA treatment. Therefore, our
IV-type classification is the first made by
ultrasound imaging features of HOCM,
according to its characteristics in line with
PTSMA treatment.
Target vessel
 Select ablation of regional importance,
particularly in the target vessel is not clear who
the septal branch
The first septal branch of the size and
distribution are great variation
 20% of patients first branch was supplied the free
wall of right ventricle
 40% of patients with subaortic of septal is not
completely supported by the first septal branch
 5% of patients can not determine the target vessel
of the region
Contrast echocardiography method
in the target vesse choice
1. Injection of a small amount of dye (1-2ml)
through the guidewire lumen of the
inflated balloon catheter angiographically
2. Prior to alcohol injection 1-2ml of echo
contrast medium is administered through
the central lumen of the balloon catheter
under UCG. determines the supply area of
the target septal branch. Ensure that no
areas involving non-obstructive, such as
the papillary muscles and ventricular free
wall and other parts.
Myocardial - Contrast - Echo in HOCM
Exclude LAD leakage
Avoid LAD ballooning
Septal Ablation in HOCM
Myocardial - Contrast - Echo
Levovist 
Alcohol 
Shadow 
In the interval of contrast agent injected into
the branch to observe the distribution of
vascular contr
Levovist shadow
Echo sequence: Subaortic septum
as targetbregion in typical SAMassociated, subaortic obstraction,
( D dotted line) ,
E test injection of the echo contrast
agent in balloon of the the first setal
branch of a forward branch of
position highlighting be basal half of
septum plus a RV papillary muscle
(white arrows) .
After superselective balloon of
other branch of first
septal branch.
Correct
opacification.
Septal Ablation in HOCM
Acute Results / Ablation Technique
MCE
N=222
No MCE
n=30
P
Septal branches (n)
1.0±0.1
1.3±0.2
<0.0001
Alcohol (ml)
2.9±0.9
3.9±2.4
<0.0001
Balloon size (mm)
1.9±0.4
2.4±0.2
<0.0001
CK max (U/l)
534±248
745±420
<0.001
62±30
96±62
<0.0001
CK-MB max (U/l)
H. Seggewiss et al, 49th Scientific Sessions ACC, 2000
Septal Ablation in HOCM
Acute Results / Ablation Technique
MCE, n=222
No MCE, n=30
86
Patients (%)
80
70
60
p<0.01
45
40
p<0.05
18
20
17
5
0
LVOTG-Reduction
>50%
AVB III° 15 Min.
after PTSMA
DDD-PM
H. Seggewiss et al, 49th Scientific Sessions ACC, 2000
keys of Technology of PTSMA
The key technology:
 identification The pressure gradient at subaortic and left
ventricular
 identification suitable of target septal branches.
 Must be inserted temporary pacemaker (to prevent the
conduction block).
 Simultaneous monitoring of aortic and left ventricular
pressure.
 Heparin ( to prevent catheter induced thrombosis).
 Analgesic
 Guiding catheter: supporting flexible and low injury
 Suitable Over-the-wire balloon catheter
The keys of Technology PTSMA





Intraoperative ultrasound monitoring
Contrast echocardigraphy
Pay close attention to the pressure gauge
under fluoroscopy (observation balloon expansion of state).
Injection of alcohol dose and speed
 determine whether should injury (catheter or alcohol) and
the interval branch block (necrosis state) conditions
 1 (with complications) or 2 septal branches ablation did
not significantly reduce the pressure, and no increase
alcohol dose
 Remove balloon should be emptying alcohol of the balloon
catheter and stagnation injection alcohol
A 51-year-old woman’s LVOT gradient was
monitored continuously just before the
balloon occlusion . (PG=80mmHg)
LV
AO
Her LVOT gradient 10 minutes after
septal ablation (PG=12mmHg)
LV
AO
A 36-year-old man’s LVOT gradient
tested by Doppler echocardiography
before PTSMA (PG=219mmHg)
His LVOT gradient 6 months after
PTSMA (PG=15mmHg)
PG120mmHg before procedure
PG=40mmHg after injection of 4.8 ml
alchohol
Great attention
Echocardiography showed ventricular
septal hypertrophy over 30 mm in HOCM,
necessary to performeing PTSMA should be
very cautious and careful. May be there
were a thick septal branch, and control wide,
and collateral-rich septal branch of support,
treatment had a higher risk and improve the
clinical symptoms and hemodynamics have
difficulties, so surgery mytomce may be a
better choice.
It is very big septal branch > 2.5mm and too long.
There is quite danger to PTMSA
PTSMA contraindications
 No significant pressure gradient in hypertrophic
cardiomyopathy or very diffuse obstructive.
 Merge other needs surgery heart disease
Mitral valve abnormalities and their own form
of papillary muscles involved in the formation of
pressure gradient, or mitral valve prolapse and
regurgitation.
 Contrast echocardiography can not determine
target vessel or the obstruction of regional no
suitable target vessel.
 Target vessel supply to non-obstruction other
regions such as: papillary muscle, free wall, etc.
 Not suitable Over-the-wire balloon.
PTSMA complications (1)
 Hospital mortality rate :1-2%
 DDD-pacemaker :2-10%
 Myocardial infarction
Reason: alcohol leakage into the parts of
inappropriate, collateral branch opening , alcohol
into the inappropriate parts cause no-reflow, LAD
/ LM / RCA injury
 Emergency surgery
Reason: coronary artery injury, acute mitral
regurgitation (papillary muscle rupture )
 Bundle branch block: about 50% and RBBBbased
PTSMA complications (2)
 Height or III °-AVB
Factors: whether the method of application of
myocardial contrast echocardiography.
Dose of alcohol and speed.
 Left anterior descending artery dissection,
coronary thrombosis, ventricular fibrillation and
ventricular tachycardia, acute mitral
regurgitation, right ventricular infarction, left
ventricular free wall infarction.
PTSMA shortcomings
 Injury of the left coronary artery required
emergency bypass or stent
 Can not enter the target septal branch
 Can not determine the target branch of support
 For mitral and papillary muscle anomalies and
abnormal septal hypertrophy the best choice the
surgery
 Mitral valve injury required emergency surgery .
 Permanent conduction block occurs treatment
should be PM
PTSMA limitations
 Some young patients to reduce the pressure
gradient effect is not satisfactory, the
possible reasons:
The septal branch with good collateral
circulation.
The vessel can not thorough or incomplete
ablation (remaining smaller branches), selfrevascularization.
 A higher degree of septal hypertrophy, a
higher degree of fibrosis, Parts of the septal
ablation scar formation poor.
PTSMA in
Fuwai Hospital
• From Dec 2000 to May 2009 , 171
patients underwent PTSMA in
Fuwai Hospital.
• Procedure success was achieved in
141 patients,success rate was 82.6%.
Patient Characteristics
Characteristics
Patients (n=171)
Age (yrs)
45.37±17.71
Men/women
122/49
(71.35%/28.65%)
Symptoms
Dyspnea
93 (54.39%)
Angina
73 (42.69%)
Syncope
76 (44.44%)
NYHA functional class(II/III/IV)
136(79.53%) /32(18.72%)/ 3(1.75%)
Family history
42 (24.6%)
Medication
Beta-blockers
106 (62%)
Verapamil
52 (30.4%)
Diltiazem
38 (22.2%)
Amiodanone
13 (7.6%)
Results of PTSMA
PTSMA (n=171)
p
Septal thickness
(pre-PTSMA)
22.67±5.35mm
Septal thickness
(post-PTSMA 3days)
20.68±4.61mm
NS
Septal thickness
(post-PTSMA 6months)
16.77±4.39mm
<0.05
LVOTPG
(pre-PTSMA)
97.58±38.23mmHg
LVOTPG
(post-PTSMA 3days)
52.36±35.7mmHg
<0.001
LVOTPG
(post-PTSMA 6months)
47.26±38.62mmHg
<0.001
LA Diameter
(pre-PTSMA)
43.78±7.33mm
LA Diameter
(post-PTSMA 3days)
42.41±7.52mm
NS
LA Diameter
(post-PTSMA 6months)
32.76±15.58mm
<0.05
Complications in our patients
In-hospital death
• Up to May 2009 , two patients died in those 171
patients(1.17%) who underwent PTSMA in
Fuwai Hospital. One was because of alcohol
leakage to the Left anterior decending artery,
another occurred drug-induced liver injury .
Complete heart block
• Transitory trifascicular blocks occurred at a rate
of 52.05%(89 patients).
• Only one patient (0.59%) underwent permanent
pacemaker implantation due to permanent
complete AV block.
Complications in our patients
• One patient (0.59%) occurred ventricular
fibrillation , but he recovered well after the
procedure.
• Right bundle branch block occurred at a
rate of 48.54%(83 in 171 patients).
• No dissections of the LM and LAD .
• No emergency CABG
• Acute mitral regurgitation also did not
occur.
Follow-up in our patients by echo
 Left ventricular outflow tract pressure gradient was
continued to a significant decrease is an important
feature:
Compared with the acute phase, 56% of patients 3
months resting and stimulate the pressure gradient will
continue to decline further; Compared with 3-month
period, 43 % of patients one year the pressure gradient is
still further reduced.
 After 3 months 40% of patients with pressure gradient
completely reduced, a year later this value was promoted
to 62% .
 43 months later, 90% of the patients of the pressure
gradient completely eliminated by echocardiographic
CONCLUSIONS
♦ PTSMA is an effective non-surgical procedure
for symptomatic patients and associated with
LVOTO in HOCM because of its low risk and its
significant hemodynamic and symptomatic
improvement.
♦ Ablation area should be appropriate, as small as
possible, to avoid a large scar formation.
♦ Echocardiographic observations plays an
important role in that will help to finalize define
the choice of septal ablation and the ablation
efficacy and reduce risks and Long-term followup of treatment efficacy .
Advice
Who have no symptoms or mild
symptoms of the patient, determined
not to consider the line to reduce
outflow tract obstruction of any
therapeutic intervention measures
(including surgical and interventional
treatment)!!!