Thursday, December 22, 2011

E-Challenges & Clinical Decisions

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 three-dimensional echocardiography. Eur J Echocardiogr 10:569-571, 2009