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

 

E-Challenges & Clinical Decisions

Feroze Mahmood, MD

Madhav Swaminathan, MD

Section Editor

CARDIAC ANESTHESIA FELLOW'S EDUCATION
Dalia A. Banks, MD
Section Editor

Fate of Mitral Regurgitation After Aortic Valve Replacement for Aortic Stenosis

Haider Javed Warraich, MD, Geoffery Hayward, MD, Robina Matyal, MD, Salid Shahul, MD, and Balachundar Subramaniam, MD, MPH

Department of Anesthesia, Critical Care and Pain Medicine Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Address Reprint Requests to Haider Javed Warraich, MD, Cardiovascular Anesthesia Research Fellow, CC 454, 1 Deaconess Road, Beth Israel Deaconess Medical Center, Boston MA 02215. E-mail: hwarraiac@bidmc.harvard.edu

Key words: aortic valve replacement, mitral regurgitation, aortic stenosis

A 75-YEAR-OLD MAN with dizziness and shortness of breath underwent a balloon valvuloplasty performed for critical aortic stenosis. After experiencing minimal symptomatic relief, the patient presented to the authors' tertiary care center with worsening symptoms 2 weeks after the procedure. The patient's history was significant for congestive heart failure, type-2 diabetes mellitus, coronary artery disease, chronic atrial fibrillation, and hypertension, and he had undergone a coronary artery bypass graft procedure in 1992. Because of a lack of symptomatic improvement after balloon valvuloplasty and persistence of decompensated congestive heart failure, despite his high risk, it was decided to perform aortic valve replacement (AVR).

After an uneventful induction of general anesthesia, a pre-cardiopulmonary bypass (CPB) transesophageal echocardiographic (TEE) examination was performed; an AV area of 0.5 cm2(critical <0.8 cm2) was calculated with the continuity equation with a peak transaortic valvular gradient of 54 mmHg (normal <20 mmHg) with a mean gradient of 38 mmHg (moderate 25-40 mmHg) and mild aortic insufficiency. The left ventricular (LV) ejection fraction was 45% to 50%, and the LV end-diastolic diameter was 6.1 cm with normal LV wall thickness. Right ventricular function was normal with no hypertrophy.

Fig 1 The prebypass TEE examination from the midesophageal 4-chamber view shows severe MR. (Inset) Midesophageal long-axis view.

Echocardiographic Findings

TEE interrogation of the mitral valve (MV) revealed moderate-to-severe (3+) mitral regurgitation (MR) (Fig 1andVideo 1[supplementary videos are available online]), with vena contracta of 6 mm (severe >=5.5mm) and mildly thickened leaflets; there was no structural abnormality of the MV. The echocardiographic challenge was to rule in or out the presence of any organic/structural cause of MR. A 3-dimensional en face view of the MV from the left atrial perspective revealed failure of coaptation between the A3 and P3 segments of the mitral leaflets (Video 2). There was no evidence of any structural abnormality. The left atrium was dilated with a long-axis dimension of 6.4 cm (normal <4.0 cm). A discussion was initiated with the surgeons regarding different therapeutic options, which included double valve replacement, AVR with MV repair, and AVR alone.

Clinical Challenge

The clinical challenge was to weigh the increased risk of concomitant MV surgery during AVR and to accurately predict the effect of AVR on the severity of MR.

Surgical Decision

After weighing the pros and cons, it was decided to perform AVR alone. A 21-mm Edwards pericardial tissue valve was used. After successful valve replacement and separation from CPB, post-CPB transesophageal echocardiography showed a well-seated bioprosthetic AV. The AV area was noted to be 1.5 cm2with trace central regurgitation and no paravalvular leak. The LV ejection fraction improved to 50-55%, and MR improved to moderate (2+) (Fig 2 and Video 3). A follow-up transthoracic echocardiogram 2 months after surgery revealed MR to still be moderate (2+).

Fig 2 The postbypass TEE examination shows improvement of the MR grade to moderate severity.

E-CHALLENGES & CLINICAL DECISIONS

Feroze Mahmood, MD

Madhav Swaminathan, MD

Section Editors

CARDIAC ANESTHESIA FELLOWS EDUCATION

Dalia A. Banks, MD, FASE

Aortic Stenosis and Coronary Artery Disease ... and a Challenging Aorta

Brandi A. Bottiger, MD, Robert D. Davis, MD, Robert C. Swift MD, Madhav Swaminathan MD, FASE, FAHA

Departments of Anesthesiology and Surgery, Duke University Health System, Durham, NC

Address reprint requests to Madhav Swaminathan, MD, FASE, FAHA, Department of Anesthesiology, Division of Cardiothoracic Anesthesiology and Critical Care Medicine, Box 3094/5691F HAFS Building, Duke University Health System, Durham, NC 27710. E-mail: swami001@mc.duke.edu

Key words: aortic stenosis, coronary artery disease

A 77-YEAR-OLD man presented to an outside hospital with the chief complaint of chest pain that radiated to his jaw. He had a known history of coronary artery disease for which he had coronary stents placed 6 years previously. He was diagnosed with a non-ST elevation myocardial infarction and after stabilization was transferred to the authors' facility for further evaluation and management. Transthoracic echocardiography showed preserved left ventricular systolic function with an estimated ejection fraction of >55%, a grade I diastolic relaxation abnormality, normal wall motion, mild left ventricular hypertrophy, and a moderately stenosed aortic valve (45 mmHg peak and 24-mmHg mean transvalvular gradient) with thickened, calcified leaflets. Coronary angiography at the transferring hospital showed severe 3-vessel disease.

His past medical history was significant for hypertension, hyperlipidemia, tobacco abuse (65-pack-year history), and carotid artery disease with previous left carotid endarterectomy. He denied complications with anesthesia for his past surgeries. Based on his presentation and imaging studies, the patient was scheduled for coronary artery bypass graft (CABG) surgery and aortic valve replacement (AVR) on cardiopulmonary bypass (CPB).

Preoperative laboratory studies were unremarkable except for anemia (hemoglobin, 10.0 g/dL) and an elevation in creatinine (1.6 mg/dL). He was on a heparin infusion. He was taken to the operating room, and after placement of appropriate monitors, general anesthesia was induced uneventfully and the airway was secured in typical fashion.

Intraoperative Transesophageal Echocardiographic Findings

An intraoperative transesophageal echocardiographic (TEE) examination was performed on an ie-33 ultrasound system with an X7-2t TEE probe (Philips Medical Systems, Andover, MA). The principal findings were the following: (1) preserved left ventricular systolic function, (2) estimated ejection fraction of >55%, (3) a thickened and mildly calcified aortic valve with turbulent flow by color-flow Doppler (Fig 1,left panel), (4) a peak transvalvular gradient of 37 mmHg with a mean gradient of 22 mmHg (Fig 1, right panel), and (5) severe atherosclerotic disease of the descending aorta and aortic arch with multiple atheromatous plaques (Fig 2). Calcified plaques in the ascending aorta also were noted. The surgeon determined by manual palpation that there was dense calcification of the ascending aorta in the region where manipulation (ie, cannulation, cross-clamping, proximal anastomosis, and aortotomy) was planned, the so-called "porcelain aorta" (see supplementary video available online).

Discussion

The following challenges were met in this case.

1. Should the aortic valve be replaced? If yes, how should the surgery be conducted? If no, what are the

implications of residual aortic stenosis on postoperative outcome?

2. How should the CABG surgery be conducted? Should it be on-pump CABG surgery? What are the possible

cannulation sites? Where are the possible proximal anastomotic sites? Should it be off-pump CABG surgery?

Where are the possible proximal anastomotic sites? What are the advantages versus the disadvantages of off-

pump CABG surgery?

3. What are the risks of perioperative stroke with a calcified aorta?

Options

The following options were considered: (1) CABG surgery and AVR with right axillary cannulation for arterial access instead of direct aortic cannulation; (2) CABG surgery, AVR, and ascending aorta with root replacement under deep hypothermic circulatory arrest; (3) CABG surgery only on CPB with right axillary cannulation for arterial access instead of direct aortic cannulation; and (4) off-pump CABG surgery only with minimal aortic manipulation.

Strategy

After extensive discussions among the referring cardiologist, surgeon, and Anesthesiologist, a decision was made not to replace the aortic valve and proceed with off-pump CABG surgery. The patient had 3 coronary bypass grafts performed, including a left internal mammary artery to the left anterior descending, and saphenous vein grafts to the first marginal and right posterior lateral first branch. One saphenous vein graft was anastomosed to the proximal ascending aorta using a minimally invasive technique (Heartstrings II; Maquet Cardiovascular LLC, Wayne, NJ) without the need for a partial aortic cross-clamp. The proximal anastomosis of the second vein graft was performed on the first vein graft, thereby allowing for only a single aortic proximal anastomotic site.

Fig 1 The image on the left shows the midesophageal aortic valve long-axis view with color-flow Doppler across the aortic valve indicating turbulent transvalvular flow. The image on the right represents continuous wave spectral Doppler across the aortic valve in the deep transgastric long-axis view. The measurements are described in the text.

Rationale

According to the Society of Thoracic Surgeons (STS) risk score, his calculated overall mortality risk was 5.1%, morbidity or mortality risk was 34.2%, and stroke risk was 3.9% for CABG surgery and AVR. Without the AVR procedure, his risks for the same outcomes were 3.5%, 26.1%, and 2.4%, respectively. However, the STS risk calculator does not account for the severity of aortic stenosis or a porcelain aorta. This was also balanced with the risk of progression of aortic stenosis without surgical intervention. Given the patient's age and comorbidities, combined with the high risk of morbidity and mortality accompanying the AVR, it was believed that the aortic valve should not be replaced. First, there likely would be limited reduction in the transvalvular gradient from a prosthetic valve and therefore limited benefit in this patient with a mean gradient of 22 mmHg. Second, with close postoperative follow-up, the aortic stenosis could be monitored, and, if required, a percutaneous replacement could be feasible in the future. The off-pump approach was chosen to eliminate cannulation and limit aortic manipulation to reduce the stroke risk. Although the STS risk calculator does not account for the off-pump technique to reduce risk, aortic manipulation in this case was believed to be the most significant factor rather than CPB itself. The potential risk was that the patient may not tolerate surgical handling of the heart or beating-heart surgery and CPB may need to be initiated emergently. A "no-touch" technique of vein graft anastomosis was used to minimize aortic manipulation while retaining the quality of revascularization.

Fig 2 The descending aorta is shown simultaneously in the short-axis (SAX) and long-axis (LAX) views. Significant atheromatous disease is indicated by the arrows in the image.

Postoperative Course

The patient tolerated the procedure well without any complications or the need for inotropic support. After the procedure, he was transferred to the postoperative cardiac surgical intensive care unit in stable condition. In the immediate postoperative period, he continued to do quite well and had a routine discharge 5 days after surgery.

Summary

In summary, this case highlights how a heavily calcified aorta, which was initially detected with transesophageal echocardiography, limited the management of a patient with combined aortic valve stenosis and coronary artery disease. These findings led to a complete change in surgical plan guided by a multidisciplinary discussion of all possible approaches and their implications. Fortunately, the patient had an uneventful in-hospital course as planned. A video summarizing the case including TEE video clips is also presented.