Feroze Mahmood, MD
Madhav Swaminathan, MD
Section Editors
Coronary Artery Disease, Acute Myocardial Infarction, and a Newly Developing Ventricular Septal Defect: Surgical Repair or Percutaneous Closure?
Mona Kulkarni, MD, Antonio Hernandez Conte, MD, MBA, Aaron Huang DO, Lorraine Lubin MD, Takahiro Shiota MD, FACC, FASE, Saibal Kar, MD
Division of Cardiothoracic Anesthesiology and Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA
M.K. and A.H. are Cardiothoracic Anesthesiology Fellows.
Address reprint requests to Antonio Hernandez Conte, MD, MBA, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Suite 8211, Loas Angeles, CA 90048. E-mail: antonio.conte@cshs.org
KEY WORDS: postmyocardial infarction, ventricular septal defect, percutaneous closure devices, Amplatzer
A
52-YEAR-OLD MAN presented to an outside hospital with a chief complaint of
severe shortness of breath with severe coughing; the patient had been experiencing
weakness, dizziness, chest tightness, and mild shortness of breath at home for
a total of four days before his arrival. Upon admission to the outside
hospital, the patient was diagnosed via an electrocardiogram with an acute
inferior wall myocardial infarction, and he immediately underwent cardiac
catheterization, which revealed an occluded right coronary artery. He had a
successful percutaneous intervention with stenting of the right coronary
artery. On the same day postprocedure, the patient was found to be in heart
failure with clinical evidence of cardiogenic shock. A transthoracic
echocardiogram (TTE) revealed a postmyocardial infarction (MI) ventricular
septal defect (VSD). An intra-aortic balloon pump was inserted to optimize
emodynamics, and the patient was placed in the intensive care unit without the
need for intubation. An immediate transfer was
arranged, and the patient arrived at the authors' facility later that
evening. The time from admission to the initial hospital followed by coronary
intervention, the identification of the VSD, and the subsequent transfer to the
authors' facility was less than 24 hours. The patient's past medical history
was significant for morbid obesity, non-insulin-dependent diabetes, and Valley
fever. The patient was a nonsmoker without any pertinent family history and
denied any previous surgical procedures. The patient's medications included
aspirin, eptifibatide, and furosemide. A bedside TTE performed at the authors'
institution revealed a basal VSD measuring approximately 1 cm in diameter by 1
cm in length. Additional findings included preserved left ventricular function
with a left ventricular ejection fraction of 55% and normal right ventricular
function; the left ventricle displayed basal inferior hypokinesis. The gradient
across the VSD was 45 mmHg with left-to-right flow and a right ventricular
systolic pressure of 40 mmHg. There were no other associated valvular
abnormalities. Fifty hours after the admission to the authors' facility and
based on the echocardiographic findings and clinical scenario, the treatment
modality was agreed upon by consensus among the medical intensivist, cardiac
surgeon, and interventional cardiologist. It was decided that the patient would
undergo percutaneous closure of the VSD. The preprocedure laboratory studies
were unremarkable. The patient was taken to the interventional cardiology
suites, and after the placement of standard monitors with the insertion of an
arterial catheter, general anesthesia was induced with etomidate and
rocuronium; the airway was secured without difficulty. Anesthesia was
maintained with sevoflurane and cisatracurium.
Intraoperative
Transesophageal Echocardiographic Findings
An
intraoperative transesophageal echocardiogram (TEE) was performed using a
Philips iE33 ultrasound system with a x7-2 t transesophageal echocardiographic
probe (Philips Medical Systems, Andover, MA). The noteworthy findings included
the following: (1) normal ventricular function with a left ventricular ejection
fraction of 55%; (2) no evidence of a VSD was notable in the standard
midesophageal 4-chamber and 2-chamber views; (3) in the transgastric short-axis
view at 0-degrees, a VSD was evident measuring approximately 1.1 cm in diameter
and 1 cm in length with left-to-right flow and the presence of an inferior left
ventricular aneurysm (Fig 1); (4) inserting the TEE probe deeper in the
transgastric short-axis view, displayed a continued VSD 1 cm in length; (5) the
right ventricle was moderately dilated with mildly reduced right ventricular
function; and (6) there was moderate tricuspid regurgitation.
Fig 1 Transgastric transesophageal echocardiographic images showing (A) left ventricular aneurysm (arrow) with (B) the VSD (arrow) after MI. RV, right ventricle; LV, left ventricle.
Discussion
The
following challenges were met in this case:
1.
Should the VSD closure proceed percutaneously as planned, or should the patient
undergo surgical repair? If yes to percutaneous closure, what are the
limitations? If yes to surgical repair, what are the implications and risks in
the operative and postoperative course?
2.
How should the percutaneous closure be performed in the context of the
described anatomy and the selection of occluder device size(s)?
3.
What are the risks and complications associated with deployment of multiple
occluder devices?
Optional
The
following options were considered: (1) percutaneous closure with the use of one
occluder device with potential residual VSD, (2) percutaneous closure with the
deployment of two occluder devices with possible residual VSD or no residual
VSD, and (3) sternotomy with open surgical repair of the VSD with
cardiopulmonary bypass.
Strategy
After extensive discussion with the medical
intensivist, interventional cardiologist, cardiac surgeon, echocardiologist, and anesthesiologist, a
decision was made to proceed with deployment of at least one and possibly two
Amplatzer (AGA Medical Corp, Plymouth, MN) occluder devices. The final decision
to initiate percutaneous closure was based primarily on the anatomy of the VSD,
which appeared to have a sigmoidal or serpiginous structure, as well as the
adjacent inferior left ventricular aneurysm. An Amplatzer occluder could be
deployed in either one of two distinct segments of the VSD with anticipated
partial obliteration of the VSD.
Rationale
The
use of the Society of Thoracic Surgeons risk scoring/calculator system does not
support the calculation of risk mortality or morbidity and mortality in the
setting of complex cardiac procedures. Unless the patient undergoes coronary
artery bypass graft surgery and/or valve surgery, the Society of Thoracic
Surgeons risk scoring estimation cannot be performed.1 Therefore, for this
patient, it was very difficult to estimate the risk of mortality or the overall
morbidity/mortality of a percutaneous procedure for the repair of the VSD
versus open surgical repair of the VSD. However, factors to be considered
included a recent MI (<6 days prior) with a VSD coupled with a left
ventricular aneurysm. In addition, cardiogenic shock with the use of an
intra-aortic balloon pump for hemodynamic stabilization also should be
considered when performing a risk analysis; the overall risk can be estimated
to be very high. Although the use of occluder devices for the closure of VSDs
has been fairly well established as an acceptable method of ameliorating
smaller VSDs, its efficacy in closing larger VSDs still is not established.
Evidence indicates that the percutaneous closure of larger VSDs with one
occluder, even with a residual defect, may allow significant hemodynamic
stabilization and myocardial fibrosis to form so that a surgical repair of any
residual VSD may be performed at a later time. After the deployment of an
initial occluder device, a substantial residual shunt remained (Fig 2);
therefore, the decision to deploy a second Amplatzer occluder was entertained.
After deployment of the second occluder device, a small residual VSD shunt
remained (Fig 3). There is a paucity of literature describing the use of two
Amplatzer occluder devices to close a VSD; therefore, the long-term ramifications
of double-device deployment are relatively unknown. Regardless of the
intervention performed, the time from VSD diagnosis to intervention is a
significant predictor of morbidity and mortality, and rapid intervention in
this case was critical.
Fig 2 The transgastric view after the first closure device implantation with significant residual VSD blood flow (arrow).
Fig 3 Three-dimensional transesophageal echocardiographic images displaying double Amplatzer occluder devices with a small residual shunt (arrow).
Postoperative
Course
The
patient tolerated the procedure well without any evidence of anesthetic or
procedural-related complications. During the procedure and postoperatively, the
patient did not require any inotropic agents or pressors. After the procedure,
the patient was transferred to the intensive care unit in stable condition and
remained intubated. On postoperative day 2, the patient was extubated, and the
intra-aortic balloon pump and the pulmonary artery catheter were removed. A
follow-up TTE on postoperative day 2 revealed evidence of a very small (<0.5
cm) residual VSD with no significant gradient. The dual Amplatzer occluders
were well seated with no evidence of a rocking motion.
Conclusions
This
case highlights how an acute MI can lead to the formation of a VSD as well as
an inferior left ventricular aneurysm. Although the VSD was initially estimated
via TTE to be fairly small (1 cm x 1 cm), the intraoperative TEE revealed a
complex VSD with aserpiginous anatomic structure. Although larger VSDs traditionally
are corrected with the deployment of one Amplatzer occluder or corrective
cardiac surgery with anticipated residual VSD, this defect was able to be
corrected with the deployment of two Amplatzer occluder devices. The use of an
Amplatzer occluder device for the closure of post-MI VSDs dates back to 1998,
and several centers have reported results from small series of Amplatzer
interventions.2-4 In addition, the results from a US registry assessing
immediate and midterm outcomes from the use of Amplatzer devices for post-MI
VSDs were released in 2004.5 The use of 2-dimensional TEE coupled with
3-dimensional TEE in assessing VSD occluder placement has been shown
previously, and the authors also determined a 3-dimensional TEE to be very
helpful in delineating the VSD anatomy in addition to guiding occluder site
placement and deployment.6 In light of this patient's recent MI and cardiogenic
shock, the decision to proceed with a percutaneous procedure was deemed to pose
less morbidity and mortality compared with traditional surgical repair, and
this approach led to a successful therapeutic outcome.
References
1.
Society of Thoracic Surgeons Online Risk Calculator, 2011.
http://www.sts.org/quality-research-patient-safety/quality/risk-calculator-and-models/risk-calculator.
Accessed April 30, 2011
2.
E.M. Lee, D.H. Roberts, Walsh: Transcatheter closure of a residual
postmyocardial infarction ventricular septal defect with the Amplatzer septal
occluder. Heart 80:522-524, 1998
3.
J.A. Goldstein, I.P. Casserly, D.T. Balzer, et al: Transcatheter closure of
recurrent postmyocardial infarction ventricular septal defects utilizing the
Amplatzer postinfarction VSD device: A case series. Catheter Cardiologic Intv
59:238-243, 2003
4.
J. Ahmed, P.N. Ruygrok, N.J. Wilson, et al: Percutaneous closure of
post-myocardial infarction ventricular septal defects: A single centre
experience. Heart Lung Circ 17:119-123, 2008
5.
R. Holzer, D. Balzer, Z. Amin, et al: Transcatheter closure of postinfarction
ventricular septal defects using the new Amplatzer muscular VSD occluder:
Results of a U.S. registry. Catheter Cardiovasc Interventions 61:196-201, 2004
6.
D.G. Halpern, G. Perk, C. Ruiz, et al: Percutaneous closure of a
post-myocardial infarction ventricular septal defect guided by real-time
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