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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3737_Библиотеки_им_академика_М_И_Перельмана
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Percutaneous Closure ofPost-myocardial Infarction Ventricular Septal Rupture
https://t.me/med1917
233
VSD [5]. Despite the high mortality with surgery,
the current American College of Cardiology of
American Heart Association Guidelines recommend surgical repair regardless of hemodynamic
status [6].
Transcatheter device closure of PMI-VSD has
been attempted in lieu of surgery in the acute,
subacute and chronic phase as an alternative to
surgery and has been reported in case reports and
small case series. A larger case series of 29
patients undergoing attempted transcatheter
PMI-VSD closure showed 25/29 acute successes
but with a mortality of 72% overall. Most of these
procedures however were done in patients in the
acute phase with 16 patients in shock and all on
IABP support [7]. Another study of 17 patient
had 12 acute successes with a survival of 65%.
Only 5 of the 17 however were on IABP and most
of the survivors were those >3weeks out from
MI [8].
Overall, the data is inconclusive favoring surgical or transcatheter closure in the acute phase
but it is clear that there is a high risk of mortality
for those patients in shock needing mechanical
support and that waiting for some time after the
acute insult is preferable if the patient’s condition
can tolerate this.
There are several choices for devices for PMIVSD closure. Initial experience with the
Cardioseal device described by Landzberg and
Lock in 1998 was unsatisfactory except for the
smallest defects [9]. Development of braided
nitinol devices of the Amplatzer family (now a
part of Abbott Laboratories) was met with better
success. The Amplatzer muscular VSD occluder
designed for congenital VSDs comes in a range
of sizes from 6 through 18mm in 2mm increments. The central waist is 7mm long and the
disks are equal in size and 8mm larger than the
central waist. Abbott also makes a specic device
for PMI-VSD [10]. The PMI-VSD occluder is
available in sizes from 16 through 24mm with
the disks 10mm larger than the central waist and
a central waist length of 10mm. The PMI-VSD
occluder was available for several years only on
an emergency use basis however the device has
now received an HDE approval making access to
the device somewhat less cumbersome in the
United States. One of the problems with the PMIVSD occluder is that even the largest size may
not be sufciently large for many of the hemodynamically signicant lesions. For larger PMIVSD defects, the Amplatzer Septal Occluder
provides a much larger range of sizes with waist
diameters up to 38 mm with a left-sided disk
12–14mm larger than the central waist and a central waist that is 4 mm long. Occlutech and
Ceraex make similarly designed devices available outside the US. For small defects, the
Amplatzer Duct Occluder II and the Amplatzer
Vascular plugs can also be considered.
Location of the defect and proximity to the AV
valves is important in determining the feasibility
of transcatheter closure. The device disks cannot
be in contact with the AV valves or it will cause
regurgitation or perforate the leaet. Patients
who have other lesions that require surgical intervention such as pseudoaneurysm or mitral
chordal rupture with ail, or those who require
surgical coronary revascularization are also not
good candidates for transcatheter PMI-VSD closure. The defect always appears smaller by echocardiography than the needed occluder size
because the edges of the defect are necrotic and
soft and so anticipating needing to oversize the
device by at least 1.5 × compared to the defect
size by echocardiography is expected. Larger
defects more than 10–15mm are also much more
challenging and prone to failure or
complications.
The surgical team felt this patient was a surgical candidate for closure. Her young age and premorbid status (she was living on her own
independently) favored a surgical approach but
her comorbidities (smoking, diabetes, prior
stroke, recent myocardial infarction) made the
surgical team cautious. A primary transcatheter
closure was discussed. Given the relatively small
apparent size of the VSD it was felt that primary
transcatheter closure was feasible. However, the
basal location of the defect and the proximity to
the mitral valve made us cautious that we would
not be able to signicantly oversize the defect
without risk of interference with the mitral valve.
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Heart Team Decision
The decision was made to proceed for primary
transcatheter closure.
Intraprocedural Imaging Modalities
andMeasurements
Cath Procedure #1
The access for PMI-VSD closure will depend on
the VSD location and the planned device selection. For most larger VSDs, it is preferable to
cross the VSD from the LV side as crossing from
the RV side is more difcult and the catheter and
device can become ensnared in the tricuspid
apparatus and RV trabeculations. Additionally, it
is preferable to open the LV disk of the device
and pull it ush with the septum to create the best
seal. After crossing the VSD from the LV side,
the wire and catheter are typically easily advanced
to the pulmonary artery. The wire can then be
snared in the pulmonary artery from a venous
approach and exteriorized. The delivery sheath is
then advanced over the exteriorized wire from the
venous approach through the RA, RV and VSD to
the LV where the LV disk is opened, pulled ush
with the septum and the RV disk is then formed.
For apical VSDs, an internal jugular vein
approach is the least tortuous whereas for basal
VSDs, a femoral approach is easier.
Access was obtained in the right femoral vein
(9 Fr) and right femoral artery (6 Fr). The VSD
was rst imaged by TEE and the defect appeared
to be in the basal septum close to the mitral and
tricuspid valves and ~1.3cm in diameter (Figs.4
and 5). An LV angiogram was performed showing the basal defect and the size measured
~10mm by angiography (Fig.6). The VSD was
crossed retrograde with a 6 Fr JR4 catheter
(Fig.7). A 260 cm 0.035 wire was then passed
through the catheter and advanced to the pulmonary artery. The wire was then snared in the right
pulmonary artery with a 30 mm Gooseneck
snare (Fig.8) and exteriorized out the right fem-
J. Raviv and B. Love
Fig. 4 Transesophageal echo showing basal VSD measuring 1.3 cm. RV right ventricle, LV left ventricle, MV
mitral valve. Note VSD proximity to mitral valve
Fig. 5 TEE of PMI-VSD showing color ow from L to
R.Note proximity to TV (tricuspid valve)
oral vein (Fig.9). Care needs to be taken when
pulling the wire through the heart to also advance
the wire and keep the catheter in place on the
wire until it is pulled through the heart to avoid
the wire acting like a saw and damaging the
heart.
Percutaneous Closure ofPost-myocardial Infarction Ventricular Septal Rupture
https://t.me/med1917
Fig. 8 The wire has passed from the LV through the VSD
Fig. 6 LV angiogram showing basal VSD with ow to
RV
to the RV and out to the right pulmonary artery (RPA). A
30 mm Gooseneck snare has been advanced form the
femoral artery and the wire is snared in the RPA.Other
shadows on the image include the TEE probe, the intraaortic balloon pump and the Swan-Ganz catheter in the main
pulmonary artery
235
Fig. 7 Angiogram of catheter crossing VSD from LV to
RV and wire out to pulmonary artery (to PA)
In this patient, we did not have easy availability of the PMI-VSD occluder. Given the anticipated size of the defect however, we thought the
largest mVSD occluder would provide a good t.
Fig. 9 The snare catheter has pulled the wire out the femoral vein. Arrows denote the complete wire loop from
femoral artery, aorta, LV, VSD, RV, RA, IVC, femoral
vein
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J. Raviv and B. Love
Fig. 10 Deployment of 18 mm Amplatzer mVSD
occluder. The LV disk (26 mm in diameter) is gently
pulled ush against the septum and the waist is in the VSD
A 9 Fr Amplatzer delivery sheath was
advanced over the wire from the femoral vein
through the RA, RV, VSD, LV to the ascending
aorta. The dilator and wire were removed. An
18mm mVSD occluder was then advanced and
the LV disk and connecting waist opened in the
LV and pulled gently against the septum (Fig.10).
However, the defect was obviously larger and not
as rigid as we had anticipated and the VSD ow
was able to easily push the LV disk (26 mm)
through the VSD to the RV (Fig.11). The device
was recaptured in the RV.
We considered recrossing and placing a larger
device but the proximity to the mitral valve gave us
pause. Given that the 26 mm disk of the device
could easily pass through the defect, we anticipated
that we would need a device with at least a 30mm
waist. That meant choosing an Amplatzer Septal
Occluder that has a larger disk:central waist ratio
and we were concerned that would risk interference with the mitral valve. An ad-hoc heart team
meeting with the patient on the table was convened
and we decided the patient would be better-off with
a surgical approach. The sheaths were removed and
patient taken back to the ICU with the balloonpump still in-place, intubated in stable condition.
Fig. 11 The defect margins were too friable to hold the
device and the 18mm mVSD occluder prolapsed through
the VSD to the RV where it was recaptured and removed
Surgical Procedure
The following day the patient was taken for surgical VSD closure. On bypass, a longitudinal
incision was made in the LV lateral to the posterior descending coronary artery. The VSD was
identied and 2–0 pledgeted Ethibond sutures
were used to secure a bovine pericardial patch.
Given the extent of RV dysfunction, a surgical
tricuspid ring was also placed, and the left atrial
appendage was clipped. A small residual VSD
was seen by TEE post-operatively.
Post-surgical Course
The patient had a difcult post-operative course.
She initially weaned from inotropic support but
when the balloon pumped was removed, her lactate increased, and she required reinsertion of the
IABP and reinitiation of inotropes. She developed renal failure and required hemodialysis. By
post-op day 15 it was clear that she was not progressing with medical management. A TEE
showed a signicant residual VSD with maintained LV function (Fig.12).
Percutaneous Closure ofPost-myocardial Infarction Ventricular Septal Rupture
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Fig. 12 2 weeks after attempted surgical closure, TEE
shows a residual VSD 1.6cm
Fig. 14 The VSD was crossed as outlined for attempt #1
and a complete wire loop created. A 24mm Amplatzer
sizing balloon was advanced from the femoral vein and
the VSD was balloon-sized with a compliant balloon with
a waist of 19mm
237
Fig. 13 LV angiogram shows the LV, VSD and RV.Note
the tricuspid ring placed at the time of surgery
The heart team reconvened, and we decided
that another more aggressive attempt at transcatheter PMI-VSD closure was warranted.
Cath Procedure #2
On post-op day 17 the patient was brought back
to the cath lab. Access was obtained in the RFV
(12 Fr) and RFA (6 Fr). Angiography from the
LV showed a large VSD (Fig.13). The VSD was
crossed retrograde in a similar fashion to attempt
#1 and the wire snared in the pulmonary artery
and exteriorized. This time, balloon sizing with a
24mm Amplatzer sizing balloon was performed.
The balloon waist measured 19 mm (Fig. 14).
Given the prior difculty with the device pulling
through the defect, we decided we needed a
device with a waist ~1.5 × the size of the defect.
A 30 mm Amplatzer Septal Occluder was chosen. This device has a central waist measuring
30mm and a left disk that is 44mm and a right
atrial disk that is 42mm. The femoral sheath was
upsized to a 16 Fr short sheath and a 12 Fr
Amplatzer delivery sheath passed from the femoral vein through the defect and out the aorta. The
left disk was opened in the LV and pulsed ush
against the septum (Fig.15). TEE showed the left
disk to be close to, but not touching the mitral
valve (Fig.16). The right disk was then uncovered. Initially the RV disk had a “cobra-head”
shape that can occur when there is insufcient
room for the disk to form or when there is torque
on the device, however the device was stable and
was unscrewed from the delivery cable and
released (Fig. 17). Over the course of the next
5min, the right disk slowly reoriented to a more
nominal shape.
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Fig. 15 A 30 mm Amplatzer Septal Occluder was
advanced through a 12 Fr delivery sheath. The Left disk
was opened in the LV and pulsed ush against the
septum
Fig. 16 TEE during
deployment of the
30mm Amplatzer Septal
Occluder shows the L
disk ush against the
septum. The superior
aspect of the left disk is
close to but doesn’t
touch the mitral valve
annulus
J. Raviv and B. Love
Repeat hemodynamics were much improved
with a Qp/Qs of 1.2:1 with a small residual VSD
through the device fabric by angiography
(Fig. 18) and TEE. TEE also conrmed no
increase in tricuspid regurgitation (Fig.19).
Post Procedural Assessment
The patient improved considerably after the
transcatheter VSD closure. The IABP was able to
be removed 2days later and she weaned off all
inotropic support. He renal function did not
recover and she required a tunneled dialysis catheter. At the time of tunneled dialysis catheter
placement 2 weeks after device placement, her
hemodynamics were repeated showing a Qp/Qs
of 1.14:1 and a wedge pressure of 11 mmHg.
Fluoroscopy showed the disks to have reformed
Percutaneous Closure ofPost-myocardial Infarction Ventricular Septal Rupture
https://t.me/med1917
Fig. 17 The right-risk of the 30mm Amplatzer occluder
took a “cobra-head” deformity but we chose to release the
device as it was stable
Fig. 19 TEE post-deployment showing the LV disk ush
against the septum. Minimal tricuspid regurgitation
239
Fig. 18 After 5min, the device recongured and the R
sided disk was better expanded. LV angiogram shows
some residual ow through the fabric of the device. Note
the central waist appears to be completely ush against
the VSD margins so we expect the residual ow to diminish/disappear
to nominal shape (Fig.20). Transthoracic echocardiogram showed the device in stable position
across the septum with no signicant residual
shunt and no interference with the mitral or tri-
Fig. 20 Fluoroscopy 2 weeks later showing the device
has further conformed to its nominal shape
cuspid valves both with trace-mild regurgitation
only (Fig.21).
The patient was discharged to a rehabilitation
facility 3weeks post-device closure and successfully weaned off the ventilator and discharged
home 2months later.
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Fig. 21 Transthoracic echocardiogram 2 weeks after
placement of the 30 mm Amplatzer Septal Occluder to
close the large residual PMI-VSD.No signicant residual
shunt and no interference with AV valves
Clinical Controversies andClinical
Pearls
• Echo derived Qp:Qs are not accurate and
shunt calculations from oxygen saturations is
necessary to conrm shunt severity in post MI
VSD’s.
• Hemodynamic stabilization by dropping SVR
and increasing CO is key to decreasing left to
right shunt, supporting patient to the time of
PMI-VSD closure.
• PMI-VSD’s always appear smaller on echocardiography and sizing should be 1.5 times
larger than imaging predicts.
J. Raviv and B. Love
– The best outcomes for transcatheter PMI-
VSD closure occur after attempted surgical
closure or if the patient can be managed medically for several weeks to allow for the margins of the VSD to become better dened.
This may not be possible with large
PMI-VSDs.
– Specic devices for transcatheter PMI-VSD
closure are often too small for the largest,
hemodynamically signicant defects but other
off-label devices such as ASD Occluders can
be used.
Multimodality imaging comparison (table
format)
Modality Advantages Disadvantages
Transthoracic
echo
Transesophageal
echo
Angiography Better
CT angiography Excellent
Disclosures
Abbott Laboratories.
Can be easily
performed
bedside
Better
imaging of
VSD
visualization
of VSD size
denition of
VSD
Dr. Love is a proctor and consultant for
Often
underestimates
extent of VSD
More invasive
Tends to foreshorten
apex also
underestimating
extent of VSD
Invasive
Doesn’t visualize
adjacent structures
will e.g.: valves
Many patients have
renal dysfunction
increasing risk of
contrast nephropathy
Usually not able to
be performed in
patients in critical
care
Chapter Review Questions
Key Points
– PMI-VSD remains a difcult problem.
Surgical and transcatheter approaches for
hemodynamically signicant VSDs with
shock are difcult and continue to have a high
mortality.
An 84year old woman presents with shortness of
breath after 1week of chest pain. She is found to
have an evolving myocardial infarction. She has a
holosystolic murmur at the apex and an echocardiogram shows an LVEF of ~60% and an apical
post-MI VSD.The patient has cool extremities
and minimal urine output. A Swan-Ganz catheter
Percutaneous Closure ofPost-myocardial Infarction Ventricular Septal Rupture
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241
is placed and a pulmonary artery saturation is
82% with the patient breathing room air.
Thermodilution cardiac output is performed and
shows a CO of 7 LPM.PA pressure 50/22 (38).
1. Which of the statements is true:
A. We should be worried—the patient is in
shock
B. We should be reassured—the patient has
good cardiac output
C. We should be reassured—the patient has a
small VSD
D. We should be reassured—the patient has a
normal LVEFAnswer: A
Explanation: Cool extremities and low
urine output indicate shock. The high pulmonary artery saturation of 82% reects left to
right shunt secondary to what must be a signicant VSD.The mixed venous saturation is
best estimated by the SVC saturation would
be low in this patient. Thermodilution will
reect the PULMONARY ow—not the systemic ow. The LVEF is often higher than
expected in these patients owing to the low
afterload because the majority of the blood is
being ofoaded to the low resistance pulmonary circuit.
2. To calculate the pulmonary to systemic ow
ratio (Qp/Qs) we need the following additional data:
A. Right atrial and aortic saturation
B. SVC and aortic saturation
C. Pulmonary capillary wedge and aortic
saturations
D. Cannot calculate Qp/Qs in this scenario-
Answer: B
Explanation: In a patient with a large
post-MI VSD, the ratio of pulmonary:systemic
ow (Qp/Qs) can be calculated with the aid of
a pulmonary artery catheter. The formula is as
follows:
Qp/Qs = Aortic sat (%) − Mixed venous
sat (%)/Pulmonary vein sat (%) − Pulmonary
artery sat (%). The SVC saturation obtained
from the side port of an internal jugular vein
sheath is the best proxy for a mixed venous
saturation. Noteworthy to add that RA sampling can miss small left-to-right shunt due to
incomplete mixing of blood entering from
SVC, IVC and coronary sinus. The aortic saturation is the arterial saturation obtained from
an arterial line or pulse oximeter. The pulmonary vein saturation is the same as the aortic
saturation as there is no signicant right to left
shunt in this lesion, and the pulmonary artery
saturation is obtained from the pulmonary
artery catheter.
3. Medical optimization of this patient would be
best achieved with
A. Norepinephrine
B. Intraaortic balloon pump
C. Epinephrine
D. Inhaled nitric oxideAnswer: B
Explanation: Epinephrine and norepinephrine would increase the systemic
vascular resistance and worsen the shunting
and worsen systemic output. IABP lowers
the systemic resistance favoring systemic
ow. The pulmonary artery pressure is high
due to high left to right ow. Nitric oxide
would further lower the pulmonary vascular
resistance and worsen left to right shunt at
the VSD.
4. Contraindication for transcatheter post-MI
VSD closure in this patient would be
A. Renal failure
B. Defect size >10mm
C. Apical location
D. Mitral valve chordal rupture with severe
MRAnswer: D
Explanation: Additional defects that
require surgical repair are contraindications to
transcatheter PMI-VSD closure.
5. After successful VSD closure, the patient’s
LVEF compared to pre-closure would be
expected to
A. Remain the same
B. Increase
C. DecreaseAnswer: C
Explanation: With VSD closure, the lower
afterload of the pulmonary system is eliminated and the volume load on the left ventricle
decreases. Both the increase in afterload and
the decrease in preload will make the LVEF
decrease even though the cardiac muscle ability is unchanged.
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J. Raviv and B. Love
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