Ventricular Septal Defect Repair:

What a parent should know about

device closure

Redmond P. Burke
The Congenital Heart Institute
Miami Children’s Hospital and
Arnold Palmer Hospital

PICS
2008
 How does my team decide on our
approach to each patient?
 Patients with VSD’s are
usually diagnosed by
pediatric cardiologists and
referred to our surgeons or
interventional cardiologists
for treatment.
 For the past several years, at
weekly program
conferences, we have
discussed every patient
presented for VSD closure.
 Our approach is to treat
each patient with the most
effective, and least
traumatic approach
available.
 Like you, we strive to make
Evidence Based Decisions
 “The Literature” is a nice guide, but
we use our own results for clinical
decision making whenever possible,
finding them to be more relevant.
 Our outcomes are reported on our
website at
www.pediatricheartsurgery.com
Current MCH surgical Results for VSD closure: 1995-2008

Total Cases (N) 387

Mortality (N) 1 0.25%
Transient CHB (N) 3 0.77%
Requiring Pacemaker (N) 1 0.25%
Median Weight (kg) 7.1
Median Age (days) 269 (4d-24yrs)
Median Post-op Stay
(days) 4

Includes:
Perimembranous VSD
Subarterial VSD
Supracrystal VSD
No instance of complete heart block in last 353 cases
This experience similar to GOS review of >2000 pts (.6% CHB)
Ann Thorac Surg. 2006 Sep;82(3):948-56; discussion 956-7.
 Is surgical heart block a real risk?
 Absolutely, but this risk is clearly surgeon
specific.
 Conduction disturbances (and most other
complications) can be viewed as a marker
of a surgeon’s gentleness, finesse,
technique, and experience.
 You might have a program where the risk
of surgical conduction problems and heart
block after VSD repair will lead you to
make different decisions than us.
Is the conduction system likely to be injured
during surgical repair?
 Terrifying history – AV node
injury was lethal in early surgical
experience. Surgeons are trained
to avoid any contact with the
septum during VSD repair
 Modern techniques – continuous
suture in the endocardium, no
touch technique on the septum
• Shallow stitching close to the
rim of the ventricular septal
defect eliminates injury to the
right bundle branch.
 Ann Thorac Surg
. 2004 Jun;77(6):2259-60; author reply 2260.
 No routine pacing wires, but easy
to do if needed
 Spontaneous cardioversion is the
rule in the OR
 If you’re seeing a lot of heart
block, you don’t need a new
approach, you need a new
surgeon.

Circulation. 2006;113:2775-2781.
 So is our typical patient with PMVSD a
candidate for device repair? No.
 Small baby 2.52
kg with FTT
 Large PMVSD
 Associated
lesions (50%)
 All pericardial
repair
 Never touch the
conduction area
 Visualize and
preserve the
aortic and
tricuspid valves
 Never put an
instrument across
the defect
 Never use
circulatory arrest
What information is available on
Device Closure? Not much.
 Pinto
 Kapoor
 Thanaopoulos
 Anil
 Li
 Carminati
 Arora
 Duronpisitkul
 Zabal
 Hijazi
 Walsh
 Pawelec-Woitalik

* Indicates prospective randomized study

Why do we have to be careful extrapolating
these early device results? They picked the
easy patients.
 The early device experience is in very
big patients with small defects, followed
for a short period of time
• 7.7y/25kg (Fu)
 In contrast, our surgical experience is in
small babies with big defects, followed
for decades:
• Our mean age/wt for surgical repair of
PMVSD is 9mo/7kg, the defects are usually
the size of the aortic valve annulus, and the
patients have FTT.
 As we have seen with ASD device
closure, sex, and surgery, size affects
performance
Is this experience with small defects in big patients misleading? Yes, I
think smaller patients with larger defects are a serious challenge to
device design and performance.
 Vascular access and catheter manipulation is easier.
 Older patients with small defects have had time to develop a
cushion of tricuspid tissue around the defect, creating a buffer from
the aortic valve. This is not the case in younger patients, where up
to half of the defect diameter is aortic valve annulus.

7yo , LOS 3d small defect 2 mo 4.2kg, LOS 5 days half the circumference
surrounded by fibrous scar of the defect is aortic valve annulus
 Are Surgical materials safe over time?
Absolutely.



It’s free
We have 5 decades of
Pericardial Patch
experience with the material,
and no uncertainty about long
term effects in the circulation.
 No erosion into adjacent
structures
 Anchored by continuous
suture, patch dehiscence is
very rare, embolization never
 Residual leak rare
 Each patch is customized to
the patient’s defect, very low
profile
 No long term anticoagulation
or antibiotic prophylaxis
Will device materials be safe over
time? No way to know, it will take
decades to find out.
PMVSD Device
Device closure is with
(Amplatzer)

Nitinol/fabric (cost - $4500 )
 Early studies are encouraging at
14 months (Kong)
 Anchoring with radial
pressure/double disc/fibrosis. Not
always stable, embolization
reported in several early series.
Retrieval is traumatic.
 Residual leak common early, with
subsequent closure over time
 The patient is forced to conform
to the available device size. You
must select from preset sizes and
shapes.
 Will devices require
anticoagulation or long term
antibiotics?
 My gut feeling
 If you gave me any available device, and
asked me to place it in a PM VSD under
direct vision, with the heart arrested, and
I could suture it in the best possible
position, so that it didn’t touch the aortic
valve, the tricuspid valve or the
conduction system, and completely closed
the defect…
 I couldn’t do it. (I could do it with a
pericardial patch though, pretty damn fast
too.)
 Do devices work anywhere in the
ventricular septum?

 Sure
 Picture a 39 week female born at
2.18 kg with a small PMVSD and a
large muscular VSD, and coarctation
with arch hypoplasia
 Repair at day of life 4.
 We choose a hybrid procedure, Surgical arch
repair, and Device Closure of the Muscular Defect,
we’re not closed minded about this stuff.
 So what’s my greatest concern? Devices
could destroy the aortic valve.
 Most PMVSD are contiguous
with the aortic valve annulus.
 PMVSD device engineers face a
conundrum - how to secure a
device in a high pressure flow
zone with a low profile on the
high pressure side (to avoid aortic
valve injury) without increasing
radial force (risk to conduction
and aortic valve).
 What will be the long term effects
of subvalvar turbulence and/or
device abrasion on the aortic
annulus or leaflets?
 ASD devices in proximity to the
aorta have eroded into the aorta
(Chun, 2003)
 What is the surgical experience with
foreign material under the aortic valve?
 Subaortic stenosis after VSD
repair is a rare progressive lesion
(Cicini) We have seen several
patients with subaortic
obstruction and aortic
insufficiency from fibrous
reaction to Dacron VSD patches.
We now use pericardium
exclusively.
 Our experience with Subaortic
membrane suggests that creating
turbulence and fibrosis under the
aortic valve can progressively
damage the valve, and necessitate
valve replacement.
Typical proximity of PMVSD to Aortic Valve
observed during surgery: 17 Month old
How close is the aortic valve with a small defect?
Very close.
 Is there misperception of the
conduction system anatomy?

EP studies might
give the impression
that there is a
conduction area that
can be avoided by
device placement
What’s the real Achille’s Heel for device
closure in the membranous septum?
The risk of Permanent Heart Block.
Anatomic studies show discrete conduction
bundles just under the endocardium, along
the margin of a PMVSD
A device in
contact with
the margin of a
PMVSD, will be
in contact with
the His Bundle
 Why is the conduction system likely to be
damaged during and after device closure?
 Early device experience suggests
the conduction system will be
injured frequently. (Zhonghua,
Kapoor, Fu, Carminati)
 Technique of dual wires and stiff
sheath across the septum applies
direct uncontrolled pressure
trauma to the septum (violating
surgical principles)
 The PMVSD device is then
implanted directly on the
conduction area with unmeasured
and uncontrolled radial and
compressive force
 This creates the potential for
early (pressure) and late (fibrotic)
injury to the conduction system
 Late CHB at 5 months and 1 year
after device placement has been
reported. (Caminiti)
How do we explain the
delayed onset of CHB
seen after device
closure?

Chronic fibrosis of the AV

node is a mechanism for
CHB and has been
related to compression

JACK L. TITUS
Anatomy of the Conduction
System
Circulation, Jan 1973; 47: 170 -
177
 Will the Tricuspid Valve be injured by PMVSD
device closure?
 During surgical repair,
tricuspid valve chords are
preserved.
 The TV septal leaflet chords
are always near the margin of
a PMVD and will always be in
contact with the larger RV
occluder disc. Over time, the
discs could damage the TV
leaflets and chords creating
TS or TI. 5 y/o with Hx of VSD. TEE postop, no TR.
 Acute TV chord rupture has
been reported during device
closure of PMVSD. (Fu)
 With all the attention on the
left side of the septum to
avoid the aortic valve and
conduction system, the TV
will take a beating.
 Does surgical closure of PMVSD create
LVOT turbulence or obstruction?
 Typical surgical repair: 1 mo, 2.52kg,
pericardial patch repair of PMVSD, discharged
home on POD 7.

Preop echo, PMVSD, no turbulence Postop echo, no VSD, no turbulence

subAS or AI under aortic valve. subAS or AI
 Is LVOT turbulence and obstruction more
likely to occur with PMVSD Device Closure?
 Based on the device design
requirements, devices are
likely to protrude into the
LVOT and create
turbulence
 This could create
immediate LVOTO, or late
LVOTO with fibrous
ingrowth and device shape
changes
 Surgical Treatment will
require device removal,
which will create complete
heart block

Simone Rolim, et al, Arq. Bras. Cardiol.

v.86 n.2 São Paulo fev. 2006
 Is procedural trauma so much less than surgery
that we should accept these uncertainties
regarding device closure?
 Device closure in Cath Lab under
 Surgery is performed in OR GA/TEE
under GA/TEE  Fluoroscopy, subjects the body
 Bypass subjects the body to to Ionizing radiation, with no
inflammation, time related safe duration of exposure
 Small risk of cerebral  Small risk of cerebral
embolization embolization
 Incision creates a visible  Vascular access creates invisible
cosmetic injury unrelated to functional injuries to major
patient size blood vessels, (DVT, ischemia)
 Hospital stays from 2 to 5 worse in small patients – arterial
days. Patients usually occlusion in 16% (Kulkarni)
completely stable  Hospital stays from 1 to 5 days.
hemodynamically in the OR, Patients reported to be unstable
episodes of uncontrolled in OR due to
hypotension very rare. arrhythmia/hypotension/bleedin
 Hemodynamically significant g (Kapoor)
residual lesion is rare  Hemodynamically significant
residual lesion also pretty rare
 Conclusions
 Surgical closure of PMVSD is safe and effective.
 Early uncontrolled, non-randomized trials of
device closure for selected older patients with
small defects raise significant concerns about
potential short and long term injury to the Aortic
and Tricuspid valves, the left ventricular outflow
tract, and the conduction system.
 There is no convincing evidence to suggest that
device closure of PMVSD will produce less lifelong
trauma or be more effective than surgical closure.
Thank You