E-CHALLENGE & CLINICAL DECISIONS

Feroze Mahmood, MD

Madhav Swaminathan, MD

Section Editors

Severe Tricuspid Valve Regurgitation:  

A Case for Laminar Flow

Frederick C Cobey, MD, * Maria Fritock, MD, † … Frederick W. Lombard, MD, † … Donald D.Glower, MD, § Madhav Swaminathan, MD, FAHA, FASE‡

 * Georgetown University, the Washington Hospital Center, Washington, DC

†Department of Anesthesiology, Mayo Clinic, Rochester, MN

§Department of Surgery, Division of Thoracic Surgery, Duke University Health System, Durham, NC

 ‡Department of Anesthesiology, Division of Cardiothoracic, Anesthesiology and Critical Care Medicine, Duke University Health System, Durham, NC

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

Key Words:  tricuspid regurgitation, Doppler, laminar flow

A 67-YEAR-OLD WOMAN presented with progressive dyspnea limiting her ability to perform daily activities. Her past medical history was significant for hyperlipidemia and Hashimoto thyroiditis. Upon further workup, a transthoracic echocardiogram (TTE) was performed, which revealed severe mitral regurgitation (MR) with mild tricuspid regurgitation (TR). Subsequently, she was scheduled for mitral valve repair. After an uneventful induction of anesthesia, an intraoperative transesophageal echocardiogram (TEE) was performed using a matrix array transducer and images acquired on an IE33 ultrasound system (Philips Healthcare, Andover, MA). The examination showed biatrial enlargement and prolapse of both the mitral and tricuspid valves. The tricuspid annulus in diastole measured 4 cm in the midesophageal 4-chamber view. The diagnosis of severe MR and mild TR was confirmed. The surgeon proceeded as planned with a mitral valve repair via a minimally invasive port-access approach. After cardiopulmonary bypass (CPB), the TEE showed a satisfactory mitral repair. However, there was hemodynamic evidence of TR with right ventricular dysfunction and an underfilled left ventricle. The central venous pressure was elevated; there were large "v" waves on the pressure waveform. Although the echocardiographic examination clearly showed TR, there was no clearly defined turbulent jet, and, therefore, the TR could not be quantified simply using the vena contracta, the proximal isovelocity surface area, or the jet area. The systolic flow across the tricuspid valve was laminar (Fig 1)and had a low peak velocity of 0.9 m/s. Both hepatic venous systolic flow reversal and a dense triangular-shaped spectral Doppler tricuspid regurgitant flow pattern also were noted. 

Fig 1 The midesophageal right ventricle inflow-outflow view showing laminar regurgitant flow into the right atrium after the discontinuation of CPB after mitral valve repair.

Challenges 

How Should the Severity of TR Be Evaluated and Graded When a Regurgitant Jet Is Laminar?

In typical cases of TR with a turbulent flow regurgitation jet, the simplest, initial, and most common approach is to use color-flow Doppler to visualize the jet. The severity of TR may be graded by mapping the area of the color jet in the right atrium.1-3 Other established approaches include measurement of the vena contracta and proximal isovelocity surface area.2,4,5 However, TR jets are often ellipsoid, often eccentrically directed, and are difficult to accurately capture in a 3-dimensional space with 2-dimensional echocardiographic planes.6 These factors likely contribute to the significant overlap seen in TR severity grades and the underestimation of TR in 20% to 30% of severe cases evaluated with color-flow Doppler.2,7 When flow is laminar, the borders of a color jet can be so difficult to appreciate that even a large jet can be missed entirely.8 Regurgitant laminar flow in contrast to flow that is turbulent allows a much greater regurgitant volume for a given transvalvular pressure gradient. The lower energy loss of laminar flow likely results in a smaller pressure drop and sustained flow. The American Society of Echocardiography (ASE) guidelines for evaluating regurgitant valve lesions suggest integrating different parameters when evaluating TR severity to avoid such errors.7 Right-sided anatomic changes consistent with severe TR include enlarged cardiac chambers with a dilated tricuspid annulus, a lack of leaflet coaptation, paradoxic septal motion, and a distended venous system.7 The morphology of the spectral tracing also may be used, with a dense triangular pattern suggestive of severe TR. A high-velocity jet does not indicate severe TR, and, indeed, laminar jets generally are associated with velocities <2 m/s.7,9,10 Antegrade and retrograde spectral patterns may almost mirror each other relating to the "to-and-fro" flow across the valve.7,10 Hepatic venous systolic flow reversal is a sensitive indicator of severe TR and also should be present.7 If most of the ASE parameters suggest moderate-to-severe TR, even in the absence of a clearly visible turbulent jet, then the presence of a significantly incompetent valve needs to be considered.

How Should Unexpected Moderate-to-Severe TR in the Operating Room Be Managed?

Recently, there has been a paradigm shift in how TR is viewed and when it should be repaired, especially in the context of left-sided valve disease. Although there is general agreement that severe TR should be repaired, guidelines are less clear regarding moderate TR.11,12 The development of late significant TR after left-sided surgery is associated with a higher rate of cardiovascular death, repeat cardiac surgery, and congestive heart failure requiring hospital admission.13 Given such findings, a large meta-analysis concluded that tricuspid dilation may be the most important risk factor for late TR and that the valve should be repaired regardless of the regurgitant severity if significant dilation is present.12 New TR that is present immediately after CPB presents a different management dilemma because this may be related to myocardial stunning or coronary air embolization and may be recoverable.

Discussion

In the case presented, the decision was made not to repair the tricuspid valve given the lack of a firm preoperative diagnosis and the absence of a conventional turbulent jet that was difficult to quantify. The patient required significant inotropic support, and on the 3rd postoperative day a TTE confirmed the presence of a laminar tricuspid jet and worsening right ventricular function (Fig 2).The patient was taken back to the operating room for possible tricuspid valve repair. The intraoperative TEE confirmed the presence of laminar TR (Fig 3)with hepatic vein systolic flow reversal (Fig 4)that resolved after the tricuspid ring annuloplasty (Fig 5).Subsequently, the patient had an uneventful postoperative recovery and was discharged in a routine fashion. A summary of echocardiographic video clips and spectral Doppler images is provided in Video 1. Upon retrospective review of the echocardiographic images, certainly repairing both valves initially could have been considered given the dilated tricuspid annulus with a prolapsing valve. The TR jet seen on both the initial TTE and prebypass TEE was also laminar and arguably misinterpreted by 2 different echocardiographers. An early case series suggested that up to a quarter of severe tricuspid jets are laminar.9 Although this number seems high, it certainly is possible that laminar TR may be an under appreciated entity. 

Fig 2 The transthoracic apical 4-chamber view showing severe TR with a laminar jet in the right atrium on the 2nd postoperative day after mitral valve repair.

Fig 3 The midesophageal 4-chamber view confirming a large laminar jet of TR before tricuspid valve repair.

Fig 4 The pulsed-wave Doppler of hepatic vein flow showing systolic flow reversal (arrow).

Fig 5 The midesophageal 4-chamber view showing a satisfactory repair of the tricuspid valve without evidence of TR on color-flow Doppler.

Conclusions

The case presented highlights the difficulty in quantifying a TR jet that shows laminar flow. When this occurs immediately after CPB intraoperatively in the setting of mitral valve surgery, the issues become even more complex. Surgical decision making is also complicated after decannulation, especially in the minimally invasive approach. Given the growing body of evidence that early intervention may be indicated in cases of TR, especially in the setting of left-sided valve surgery and the possibility of laminar flow, vigilance for identifying such cases of "silent" regurgitation is warranted.9,12 

References

1. Y. Shapira, A. Porter, M. Wurzel, et al. Evaluation of tricuspid regurgitation severity: Echocardiographic and clinical correlation J Am Soc Echocardiogr 11:652-659, 1998

2. G. Grossmann, M. Stein, M. Kochs, et al. Comparison of the proximal flow convergence method and the jet area method for the assessment of the severity of tricuspid regurgitation Eur Heart J 19:652-659, 1998

3. F. Gonzalez-Vilchez, J. Zarauza, J.A. Vazquez de Prada, et al. Assessment of tricuspid regurgitation by Doppler color flow imaging: Angiographic correlation Int J Cardiol 44:275-283, 1994

4. S. Yamachika, C.L. Reid, D. Savani, et al. Usefulness of color Doppler proximal isovelocity surface area method in quantitating valvular regurgitation J Am Soc Echocardiogr 10:159-168, 1997

5. W.I. Yang, C.Y. Shim, M.K. Kang, et al. Vena contracta width as a predictor of adverse outcomes in patients with severe isolated tricuspid regurgitation J Am Soc Echocardiogr 24:1013-1019, 2011

6. J.M. Song, M.K. Jang, Y.S. Choi, et al. The vena contracta in functional tricuspid regurgitation: A real-time three-dimensional color Doppler echocardiography study J Am Soc Echocardiogr 24:663-670, 2011

7. W.A. Zoghbi, M. Enriquez-Sarano, E. Foster, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography J Am Soc Echocardiogr 16:777-802, 2003

8. S. Akamatsu, N. Ueda, E. Terazawa, et al. Mitral prosthetic dehiscence with laminar regurgitant flow signals assessed by transesophageal echocardiography Chest 104: 1911-1913, 1993

9. K. Yoshida, J. Yoshikawa, T. Akasaka, et al. Silent severe tricuspid regurgitation: A study by Doppler echocardiography J Cardiol 19:187-194, 1989

10. S. Minagoe, S.H. Rahimtoola, P.A. Chandraratna. Significance of laminar systolic regurgitant flow in patients with tricuspid regurgitation: A combined pulsed-wave, continuous-wave Doppler and two-dimensional echocardiographic study Am Heart J 119:627-635, 1990

11. R.O. Bonow, B.A. Carabello, K. Chatterjee, et al. Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 guidelines for the management of patients with valvular heart disease): Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons Circulation 2008:e523-e661, 2008

12. G. Bianchi, M. Solinas, S. Bevilacqua, et al. Which patient undergoing mitral valve surgery should also have the tricuspid repair? Interact Cardiovasc Thorac Surg 9:1009-1020, 2009

13. H. Song, M.J. Kim, C.H. Chung, et al. Factors associated with development of late significant tricuspid regurgitation after successful left-sided valve surgery Heart 95:931-936, 2009

Fig 1 The midesophageal right ventricle inflow-outflow view showing laminar regurgitant flow into the right atrium after the discontinuation of CPB after mitral valve repair. 

Fig 2 The transthoracic apical 4-chamber view showing severe TR with a laminar jet in the right atrium on the 2nd postoperative day after mitral valve repair.

Fig 3 The midesophageal 4-chamber view confirming a large laminar jet of TR before tricuspid valve repair.

Fig 4 The pulsed-wave Doppler of hepatic vein flow showing systolic flow reversal (arrow).

Fig 5 The midesophageal 4-chamber view showing a satisfactory repair of the tricuspid valve without evidence of TR on color-flow Doppler.

E-CHALLENGES & CLINICAL DECISIONS

Feroze Mahmood,MD

Madhav Swaminathan, MD

Section Editors

An Incidental Finding During Emergent Vascular Surgery:  How Far to Go?

Shanaz Ali, MD, Omair Shakil, MD, Tzong-Huei Chen, MD, Haider Javed Warraich, MD, and Robina Matyal, MD

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

Address reprint requests to Shanaz Ali, MD, Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, CC-470, Boston, MA 02215. E-mail: seali@bidmc.harvard.edu

Key words: Amplatzer device, transesophageal echocardiography, intracardiac thrombus

A 40-YEAR-OLD MAN presented to the authors' tertiary care center with an acute onset of pain in his left foot. He was otherwise hemodynamically stable, alert, and oriented. His past medical history was significant for multiple strokes and pulmonary emboli. On a previous admission for stroke workup 5 years earlier, he had a transthoracic echocardiogram that revealed an atrial septal defect (ASD). The defect was closed percutaneously with an Amplatzer device (AGA Medical Corporation, Plymouth, MN). Since the closure of the ASD, the patient had been free of embolic events. A physical examination in the emergency room revealed no palpable pulses in the

Figue 1.  Two-dimensional transesophageal echocardiogram:  The midesophageal 4-chamber view showing the Amplatzer device in the interatrial septum with 2 clots in the left atrium.

Fig 2.  Three-dimensional transesophageal echocardiogram:  the view throught the left atrial perspective of the mitral valve showing the Amplatzer device in the interatrial septum, with one clot attached to the inferior portion of the device and the smaller clot attached to the posterior wall of the left atrium.  (Color version of figure is available online.)

left lower extremity. A computed tomographic angiogram showed occlusion of the left common iliac artery. A heparin drip was initiated, vascular surgery service was consulted, and the patient was scheduled for an emergent thrombectomy under general anesthesia.

After an uneventful induction of general anesthesia, based on his history of multiple embolic events, the presence of an intracardiac device, and acute limb ischemia, a transesophageal echocardiographic (TEE) examination was performed using an IE-33 Ultrasound System Omni-III TEE Probe (Philips Medical Systems, Andover, MA).

Echocardiographic Findings

TEE interrogation revealed a well-seated septal occluder device across the interatrial septum. A color-flow Doppler study of the interatrial septum did not show any flow across the septum. The left atrium was mildly dilated. Two large echodensites were visualized in the left atrium, which appeared pedunculated and freely mobile with a homogenous consistency and a smooth surface. The larger density measured 2 x 3 cm, and the smaller density measured approximately 0.5 x 1.5 cm (Fig 1 and Video 1 [supplementary videos are available online].

Figure 3.  (A)  The Amplatzer device after removal from the patient.  (B)  Clots removed from the left atrium.  (Color version of figure is available online.)

Echocardiographic Challenge

On 2-dimensional TEE examination, the larger echodensity seemed attached to the Amplatzer device, whereas the other one seemed to be located just above the mitral annulus. To better delineate the spatial location, it was decided to do a real-time 3-dimensional transesophageal echocardiogram. The 3-dimensional transesophageal echocardiogram established that the larger density was clearly attached to the inferior edge of the septal device, whereas the smaller density, which on a 2-dimensional esophageal echocardiogram had appeared to be attached to the mitral annulus, was actually attached to the posterior wall of the left atrium (Fig 2 and Video 2).

Clinical Challenge

This case posed the following 2 clinical dilemmas to the team:
1. After establishing the presence of thrombi in the left atrium, the risk of embolization in the patient needed to be determined. Based on the patient's presentation and echocardiographic appearance of the thrombi (pedunculated and freely mobile), it was determined that the risk of embolization was significant.
2. The second challenge was whether to proceed to emergent cardiac surgery during the same anesthestic versus obtaining informed consent and proceeding urgently the following day. Would obtaining informed consent and delaying cardiac surgery place the patient at an increased risk for a catastrophic embolic event?

Intraoperative Decision

After discussion with the cardiac and vascular surgery teams, it was decided that the patient would require removal of the thrombi along with the possible removal of the Amplatzer device under cardiopulmonary bypass. The situation was discussed with the patient's next-of-kin, and it was decided to place the patient on a therapeutic heparin drip and proceed with cardiac surgery after obtaining informed consent. The patient was brought back to the operating room the next morning. After the initiation of cardiopulmonary bypass, the left atrium was opened, and two large thrombi were removed, one attached to the inferior aspect of the ASD closure device and the other attached to the posterior aspect of left atrium near the mitral valve annulus (Fig 3). The ASD closure device was removed and the defect closed with a core matrix patch. The patient had an uneventful postoperative recovery. A thorough workup was ordered to investigate the possibility of a hypercoagulable disorder, and the patient was found to have protein S and factor X deficiency. Subsequently, the patient was discharged with a prescription for coumadin in therapeutic doses.



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.

E-Challenges & Clinical Decisions

Feroze Mahmood, MD

Madhav Swaminathan, MD

Section Editors

Systolic Anterior Motion After Mitral Valve Repair and a Systolic Anterior Motion Tolerance Test

Gerard R. Manecke, MD, Liem C. Nguyen, MD, Adam D. Tibble, MD, Eugene Golts, MD, and Dalia Banks, MD

From the Department of Anesthesiology and Division of Cardiothoracic Surgery, University of California

San Diego Medical Center, San Diego, CA

Address reprint requests to Gerard R. Manecke, MD, Department of Anesthesiology, University of California San Diego, 200 West Arbor Drive, San Diego, CA 92103.

E-mail: gmanecke@ucsd.edu © 2010 Elsevier Inc. All rights reserved. 1053-0770/2405-0026$36.00/0 doi :10.1053/j.jvca.2010.07.021.

Key words: mitral valve repair, systolic anterior motion

A 62-YEAR-OLD MAN with an unremarkable medical history presented for mitral valve repair and single-vessel coronary artery bypass. He had experienced a 2-month period of increasing dyspnea on exertion, and his cardiologist noted a IV/VI systolic murmur. His lifestyle was sedentary; he performed basic chores and occasional climbing of a flight of stairs. He did not partake in regular exercise. A preoperative transthoracic echocardiogram showed moderate/severe mitral regurgitation (MR), thickened mitral leaflets, prolapse of the posterior mitral leaflet, a mildly dilated left atrium, and normal left ventricular function. Cardiac catheterization revealed an 85% lesion in the distal left anterior descending artery.

Intraoperative monitoring included a radial arterial catheter, pulmonary artery catheter, and transesophageal echocardiography (TEE). Anesthetic induction (midazolam/fentanyl/relaxant) and maintenance (isoflurane in oxygen) were uneventful. The pre-cardiopulmonary bypass (CPB) transesophageal echocardiographic findings were in agreement with those of the preoperative transthoracic echocardiogram (Fig 1 and Video 1 ^[supplementary videos are available online^]). Representative pre-CPB hemodynamics were as follows: heart rate, 72 beats/min; blood pressure (BP), 110/70 mmHg; cardiac output (CO), 4.5 L/min; pulmonary artery pressure (PAP), 28/14 mmHg; and central venous pressure (CVP), 6 mmHg.

The surgical procedure, via a midline sternotomy, consisted of a coronary bypass graft to the left anterior descending artery using the left internal mammary artery and mitral valve repair. The repair involved resection of a large, redundant P2 segment and placement of an annuloplasty ring (28-mm Carpentier-Edwards Physio Ring; Edwards Lifesciences, Irvine, CA). The anterior leaflet did not appear particularly redundant upon surgical inspection, so it was not resected.

Separation from CPB was accomplished easily, without the use of vasoactive medications. TEE before decannulation revealed only trace MR, and hemodynamics were favorable (heart rate, 80 beats/min; BP, 110/70 mmHg; PAP, 28/14 mmHg; CO, 5.5 L/min; CVP, 6 mmHg). However, systolic anterior motion (SAM) of the mitral leaflets was noted, with dynamic obstruction of the left ventricular outflow tract (LVOT) and turbulent aortic flow (Fig 2 and Video 2). After discussion with the surgeon,a provocative test was performed. This was performed while the great vessels were still cannulated, with the goal of determining if his SAM would be tolerated should he become hypovolemic, tachycardic, and vasodilated postoperatively. For 15 minutes, ventricular pacing at 120 beats/min was instituted, and nitroglycerin, 200 µg/min, and dopamine, 7 µg/kg/min, were administered.The BP dropped to 80/50 mmHg but was then maintained, CO was maintained at >5 L/min, PAP rose to 42/24 mm Hg, and the CVP remained at 6 mmHg. TEE revealed some worsening of the MR (moderate), and the LVOT obstruction appeared to worsen slightly, with the appearance of a "double envelope" on continuous-wave Doppler of the LVOT (Video 2). The decision then was made to discontinue the dopamine, nitroglycerin, and pacing. No further surgery was performed on the mitral valve, and the remainder of the operation was uneventful. His postoperative period was likewise uneventful, and he was discharged on the 9th postoperative day with a prescription for daily β-blockade therapy.

Discussion

SAM is not uncommon after mitral valve repair, having been reported to occur in 8.4% of cases.1 Anatomic risk factors for its development include a short coaptation-septal distance (C-sept)2; low anterior leaflet:posterior leaflet length ratio2; large, redundant leaflets3; and septal hypertrophy.3 Hemodynamic risks include highly contractile state, hypovolemia, tachycardia, and low afterload. This patient presented with all the anatomic risks, including short C-sept (2.24 cm) and low anterior:posterior ratio (0.75) before repair.2

SAM after mitral valve repair often is well tolerated, and, when initially present, may resolve after mitral valve repair.1 Indeed, patients with SAM from other causes are often asymptomatic (and undiagnosed) until an inciting injury results in hypovolemia and a high catecholamine state.4

The question was not if SAM was present but rather how well the patient would tolerate it under "SAM-aggravating" conditions. In the authors' experience, when severe SAM occurs after mitral repair, it can result in "wide-open" MR, LVOT obstruction, very high PAP, and hypotension, necessitating a return to CPB. In such cases, it is obvious that the valve must either be rerepaired or replaced. This patient presented a "gray-zone" situation in which hemodynamics were favorable after CPB, but the presence of SAM was clear.

A potentially useful test that may help in determining if a patient is at postoperative risk for SAM has been described by Crescenzi et al.5 This group treats intraoperative SAM with conservative measures (intravascular volume expansion and discontinuation of inotropes) as well as more aggressive ones (β-blockade, increasing afterload by manual compression of the ascending aorta). These authors suggest surgical revision of the repair if conservative measures fail to result in the resolution of SAM.

In contrast, the test the present authors propose, the "SAM tolerance test," is designed to determine, given that SAM is present, how well it will be tolerated postoperatively if SAM-aggravating conditions (hypovolemia, vasodilatation, and high contractile state) develop. The patient's condition deteriorated somewhat with this test, but he did not suffer hemodynamic collapse, severe hypotension, or require reinstitution of CPB. The test was performed with the great vessels still cannulated and before heparin reversal in case a return to CPB became necessary. Considering his sedentary lifestyle and his ability to tolerate (with some struggle) the "SAM tolerance test," the authors believe this patient very likely will tolerate SAM should it persist postoperatively. The authors strongly recommend that such patients receive chronic β-blocker therapy and be advised to remain well-hydrated and to report deteriorating exercise tolerance to their cardiologist immediately.

Readers are encouraged to view the online videos (Videos 1 and 2) and share their thoughts on the potential utility of this test at the JCVA online blog site.

Fig 1. Transesophageal echocardiographic midesophageal 4-chamber view with color-flow Doppler showing moderate/severe mitral regurgitation before mitral valve repair.

Fig 2. Transesophageal echocardiographic midesophageal long-axis view after mitral valve repair showing mitral leaflets entering the left ventricular outflow tract during systole. In Video 2, the aortic valve is noted to "flutter" during systole,suggesting turbulent flow.

Appendix

Supplementary data

Supplementary data associated with this article can be found, in the online version, at doi :10.1053/j.jvca.2010.07.021.

References

1. Brown ML, Abel MD, Click RL, et al: Systolic anterior motion after mitral valve repair: Is surgical intervention necessary? J Thorac Cardiovasc Surg 133:136-143, 2007

2. Maslow AD, Regan MM, Haering JM, et al: Echocardiographic predictors of left ventricular outflow tract obstruction and systolic anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease. J Am Coll Cardiol 34:2096-2104, 1999

3. Tewari P, Basu R: Left ventricular outflow tract obstruction after mitral valve replacement.Anesth Analg 106:65-66, 2008

4. Luckner G, Margreiter J, Jochberger S, et al: Systolic anterior motion of the mitral valve with left ventricular outflow tract obstruction: Three cases of acute perioperative hypotension in noncardiac surgery. Anesth Analg 100:1594-1598, 2005

5. Crescenzi G, Landoni G, Zangrillo A, et al: Management and decision-making strategy for systolic anterior motion after mitral valve repair. J Thorac Cardiovasc Surg 137:320-325, 2009