Journal of Cardiothoracic and Vascular Anesthesia Blog

E-Challenges & Clinical Decisions

2011-12-22T10:32:00.000-08:00

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

A52-YEAR-OLD MAN presented to an outside hospital with a chief complaint ofsevere shortness of breath with severe coughing; the patient had been experiencingweakness, dizziness, chest tightness, and mild shortness of breath at home fora total of four days before his arrival. Upon admission to the outsidehospital, the patient was diagnosed via an electrocardiogram with an acuteinferior wall myocardial infarction, and he immediately underwent cardiaccatheterization, which revealed an occluded right coronary artery. He had asuccessful percutaneous intervention with stenting of the right coronaryartery. On the same day postprocedure, the patient was found to be in heartfailure with clinical evidence of cardiogenic shock. A transthoracicechocardiogram (TTE) revealed a postmyocardial infarction (MI) ventricularseptal defect (VSD). An intra-aortic balloon pump was inserted to optimizeemodynamics, and the patient was placed in the intensive care unit without theneed for intubation. An immediate transfer was arranged, and the patient arrived at the authors' facility later thatevening. The time from admission to the initial hospital followed by coronaryintervention, the identification of the VSD, and the subsequent transfer to theauthors' facility was less than 24 hours. The patient's past medical historywas significant for morbid obesity, non-insulin-dependent diabetes, and Valleyfever. The patient was a nonsmoker without any pertinent family history anddenied any previous surgical procedures. The patient's medications includedaspirin, eptifibatide, and furosemide. A bedside TTE performed at the authors'institution revealed a basal VSD measuring approximately 1 cm in diameter by 1cm in length. Additional findings included preserved left ventricular functionwith a left ventricular ejection fraction of 55% and normal right ventricularfunction; the left ventricle displayed basal inferior hypokinesis. The gradientacross the VSD was 45 mmHg with left-to-right flow and a right ventricularsystolic pressure of 40 mmHg. There were no other associated valvularabnormalities. Fifty hours after the admission to the authors' facility andbased on the echocardiographic findings and clinical scenario, the treatmentmodality was agreed upon by consensus among the medical intensivist, cardiacsurgeon, and interventional cardiologist. It was decided that the patient wouldundergo percutaneous closure of the VSD. The preprocedure laboratory studieswere unremarkable. The patient was taken to the interventional cardiologysuites, and after the placement of standard monitors with the insertion of anarterial catheter, general anesthesia was induced with etomidate androcuronium; the airway was secured without difficulty. Anesthesia wasmaintained with sevoflurane and cisatracurium.

IntraoperativeTransesophageal Echocardiographic Findings

Anintraoperative transesophageal echocardiogram (TEE) was performed using aPhilips iE33 ultrasound system with a x7-2 t transesophageal echocardiographicprobe (Philips Medical Systems, Andover, MA). The noteworthy findings includedthe following: (1) normal ventricular function with a left ventricular ejectionfraction of 55%; (2) no evidence of a VSD was notable in the standardmidesophageal 4-chamber and 2-chamber views; (3) in the transgastric short-axisview at 0-degrees, a VSD was evident measuring approximately 1.1 cm in diameterand 1 cm in length with left-to-right flow and the presence of an inferior leftventricular aneurysm (Fig 1); (4) inserting the TEE probe deeper in thetransgastric short-axis view, displayed a continued VSD 1 cm in length; (5) theright ventricle was moderately dilated with mildly reduced right ventricularfunction; and (6) there was moderate tricuspid regurgitation.

Fig1 Transgastric transesophageal echocardiographic images showing (A) leftventricular aneurysm (arrow) with (B) the VSD (arrow) after MI. RV, rightventricle; LV, left ventricle.

Discussion

Thefollowing challenges were met in this case:

1.Should the VSD closure proceed percutaneously as planned, or should the patientundergo surgical repair? If yes to percutaneous closure, what are thelimitations? If yes to surgical repair, what are the implications and risks inthe operative and postoperative course?

2.How should the percutaneous closure be performed in the context of thedescribed anatomy and the selection of occluder device size(s)?

3.What are the risks and complications associated with deployment of multipleoccluder devices?

Optional

Thefollowing options were considered: (1) percutaneous closure with the use of oneoccluder device with potential residual VSD, (2) percutaneous closure with thedeployment of two occluder devices with possible residual VSD or no residualVSD, and (3) sternotomy with open surgical repair of the VSD withcardiopulmonary bypass.

Strategy

After extensive discussion with the medicalintensivist, interventional cardiologist, cardiac surgeon, echocardiologist, and anesthesiologist, adecision was made to proceed with deployment of at least one and possibly twoAmplatzer (AGA Medical Corp, Plymouth, MN) occluder devices. The final decisionto initiate percutaneous closure was based primarily on the anatomy of the VSD,which appeared to have a sigmoidal or serpiginous structure, as well as theadjacent inferior left ventricular aneurysm. An Amplatzer occluder could bedeployed in either one of two distinct segments of the VSD with anticipatedpartial obliteration of the VSD.

Rationale

Theuse of the Society of Thoracic Surgeons risk scoring/calculator system does notsupport the calculation of risk mortality or morbidity and mortality in thesetting of complex cardiac procedures. Unless the patient undergoes coronaryartery bypass graft surgery and/or valve surgery, the Society of ThoracicSurgeons risk scoring estimation cannot be performed.1 Therefore, for thispatient, it was very difficult to estimate the risk of mortality or the overallmorbidity/mortality of a percutaneous procedure for the repair of the VSDversus open surgical repair of the VSD. However, factors to be consideredincluded a recent MI (<6 days prior) with a VSD coupled with a leftventricular aneurysm. In addition, cardiogenic shock with the use of anintra-aortic balloon pump for hemodynamic stabilization also should beconsidered when performing a risk analysis; the overall risk can be estimatedto be very high. Although the use of occluder devices for the closure of VSDshas been fairly well established as an acceptable method of amelioratingsmaller VSDs, its efficacy in closing larger VSDs still is not established.Evidence indicates that the percutaneous closure of larger VSDs with oneoccluder, even with a residual defect, may allow significant hemodynamicstabilization and myocardial fibrosis to form so that a surgical repair of anyresidual VSD may be performed at a later time. After the deployment of aninitial 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 shuntremained (Fig 3). There is a paucity of literature describing the use of twoAmplatzer occluder devices to close a VSD; therefore, the long-term ramificationsof double-device deployment are relatively unknown. Regardless of theintervention performed, the time from VSD diagnosis to intervention is asignificant predictor of morbidity and mortality, and rapid intervention inthis case was critical.

Fig2 The transgastric view after the first closure device implantation withsignificant residual VSD blood flow (arrow).

Fig3 Three-dimensional transesophageal echocardiographic images displaying doubleAmplatzer occluder devices with a small residual shunt (arrow).

PostoperativeCourse

Thepatient tolerated the procedure well without any evidence of anesthetic orprocedural-related complications. During the procedure and postoperatively, thepatient did not require any inotropic agents or pressors. After the procedure,the patient was transferred to the intensive care unit in stable condition andremained intubated. On postoperative day 2, the patient was extubated, and theintra-aortic balloon pump and the pulmonary artery catheter were removed. Afollow-up TTE on postoperative day 2 revealed evidence of a very small (<0.5cm) residual VSD with no significant gradient. The dual Amplatzer occluderswere well seated with no evidence of a rocking motion.

Conclusions

Thiscase highlights how an acute MI can lead to the formation of a VSD as well asan inferior left ventricular aneurysm. Although the VSD was initially estimatedvia TTE to be fairly small (1 cm x 1 cm), the intraoperative TEE revealed acomplex VSD with aserpiginous anatomic structure. Although larger VSDs traditionallyare corrected with the deployment of one Amplatzer occluder or correctivecardiac surgery with anticipated residual VSD, this defect was able to becorrected with the deployment of two Amplatzer occluder devices. The use of anAmplatzer occluder device for the closure of post-MI VSDs dates back to 1998,and several centers have reported results from small series of Amplatzerinterventions.2-4 In addition, the results from a US registry assessingimmediate and midterm outcomes from the use of Amplatzer devices for post-MIVSDs were released in 2004.5 The use of 2-dimensional TEE coupled with3-dimensional TEE in assessing VSD occluder placement has been shownpreviously, and the authors also determined a 3-dimensional TEE to be veryhelpful in delineating the VSD anatomy in addition to guiding occluder siteplacement and deployment.6 In light of this patient's recent MI and cardiogenicshock, the decision to proceed with a percutaneous procedure was deemed to poseless morbidity and mortality compared with traditional surgical repair, andthis 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 residualpostmyocardial infarction ventricular septal defect with the Amplatzer septaloccluder. Heart 80:522-524, 1998

3.J.A. Goldstein, I.P. Casserly, D.T. Balzer, et al: Transcatheter closure ofrecurrent postmyocardial infarction ventricular septal defects utilizing theAmplatzer postinfarction VSD device: A case series. Catheter Cardiologic Intv59:238-243, 2003

4.J. Ahmed, P.N. Ruygrok, N.J. Wilson, et al: Percutaneous closure ofpost-myocardial infarction ventricular septal defects: A single centreexperience. Heart Lung Circ 17:119-123, 2008

5.R. Holzer, D. Balzer, Z. Amin, et al: Transcatheter closure of postinfarctionventricular 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 apost-myocardial infarction ventricular septal defect guided by real-timethree-dimensional echocardiography. Eur J Echocardiogr 10:569-571, 2009

E-Challenges & Clinical Decisions

2011-10-18T12:41:00.000-07:00

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

2011-04-12T12:37:00.000-07:00

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

2010-10-15T14:04:00.000-07:00

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.

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

E-CHALLENGES & CLINICAL DECISIONS

2010-09-22T15:21:00.000-07:00

Feroze Mahmood, MD
Madhav Swaminathan, MD
Section Editors

Coronary Artery Bypass Graft Surgery and Moderate Aortic Stenosis: When To Leave Well Enough Alone
Andrea Xavier, MD, Jason Erlich, MD, and Adam B. Lerner, MD

AN 84-YEAR-OLD man with a history of coronary artery disease (CAD) presented with unstable angina. The patient had a history of percutaneous transluminal coronary angioplasty of the circumflex artery 12 years prior but now had increasing angina, increasing dyspnea on exertion, and fatigue. The patient underwent cardiac catheterization that showed severe 3-vessel CAD, normal biventricular systolic function with an ejection fraction of 61%, mild aortic stenosis with an aortic valve area (AVA) of 1.6 cm2 with a maximum transvalvular gradient of 32 mmHg, and trace aortic regurgitation.

The patient’s past medical history was notable for hypertension, non–insulin-dependent diabetes mellitus, chronic renal insufficiency (creatinine of 1.6 mg/dL), hypercholesterolemia, and a Schatzki ring for which he had undergone esophageal dilation several years earlier. His medications included simvastatin, lisinopril, atenolol, hydrochlorothiazide, terazosin, glipizide, and aspirin. The patient was scheduled for coronary artery bypass graft surgery.

On arrival to the preoperative unit, the patient was in no distress with a blood pressure of 160/70 mmHg and a heart rate of 68 beats/min. He was 72 inches tall with a weight of 90 kg. His preoperative laboratory workup was unremarkable. His electrocardiogram showed a sinus rhythm with occasional premature atrial beats and a first-degree atrioventricular conduction
delay. He was taken to the operating room and underwent an uneventful placement of appropriate monitoring.

INTRAOPERATIVE TRANSESOPHAGEAL ECHOCARDIOGRAPHIC EXAMINATION

After the induction of anesthesia, a transesophageal echocardiographic probe was passed without difficulty. The transesophageal echocardiographic examination was performed with an IE-33 ultrasound system with an OMNI-III TEE probe(Philips Medical Systems, Andover, MA).

FINDINGS

Findings included the following: (1) a hyperdynamic leftventricle with an ejection fraction estimated at 75%, (2) mildto-moderate thickening and calcification of the 3 aortic valve leaflets (Fig 1), (3) a mild-to-moderate decrease in aortic valve leaflet mobility, (4) an instantaneous peak gradient of 28

Fig 1. (A) A midesophageal short-axis view of the aortic valve from the pre–cardiopulmonary bypass transesophageal echocardiographic examination. The 3 aortic valve leaflets show mild-to-moderate thickening and calcification as well as a mild-to-moderate decrease in leaflet excursion. (B) A midesophageal long-axis view of the aortic valve withcolor Doppler interrogation reveals color aliasing consistent with turbulent flow through a narrowed aortic valve orifice.

Fig 2. The velocity time profile of blood flow through the aortic valve generated with continuous-wave Doppler interrogation from the deep transgastric window. Peak and mean pressure gradients across the aortic valve are shown.

mmHg and a mean gradient of 18 mmHg across the aortic valve at a cardiac output of 4.5 L/min (Fig 2), (5) AVA calculated by the use of the continuity equation of 1.2 cm2, (6) trace aortic
insufficiency, and (7) trace mitral regurgitation (Figs 1 and 2 and Video).

ECHOCARDIOGRAPHIC CHALLENGES

The AVA calculated intraoperatively corresponds to moderate aortic stenosis that had been diagnosed as mild stenosis preoperatively. This potential increase in the grade of severity suggests the consideration of adding an aortic valve replacement to the scheduled coronary artery bypass graft procedure. Why is there a discrepancy in the measurements of AVA? Is the measurement of AVA using continuity correct? What can the authors do to confirm the measurement? Are there other echocardiographic findings that the authors can use to help make a decision on what to do for this patient?

CONFOUNDING VARIABLES

Symptoms are an important trigger in the decision tree for the management of aortic stenosis and valve replacement. Are the patient’s symptoms from CAD or aortic stenosis? Adding an aortic valve replacement adds risk to this procedure. Do the risks outweigh the benefits in this patient? The rate of progression of aortic stenosis varies from patient to patient and can impact the decision-making process. Can the authors get some estimate of this rate in the present patient?

THE AUTHORS’ DECISION

After careful consideration, the authors decided not to perform an aortic valve replacement because they felt that the risk of adding in aortic valve replacement was too high given the patient’s age and comorbidities. They felt that mild-to-moderate thickening and calcification of leaflets portended a slower progression of stenosis, and they felt that the patient’s life expectancy was such that he would likely never become symptomatic from aortic stenosis.

E-CHALLENGES & CLINICAL DECISIONS

2010-08-13T14:51:00.000-07:00

2010-04-13T07:23:00.000-07:00

Rheumatic Mitral and Aortic Stenosis: To Replace or Not To Replace—That Is the Question—Part 2

Melanie Darke, MD, John Pawloski, MD, Kamal R. Khabbaz, MD, and Feroze Mahmood, MD

This is the second part of the E-challenge case presented in the last issue of the Journal. This section includes a narrative of the clinical decisions made in the operating room and the evidence to support them. The readers are referred to the Journal web site for viewing the video presentation of the echo loops and their explanation. In an effort to make the experience/discussion interactive, a web-based discussion forum (blog site) also has been set up on the web site for the readers to comment and share their opinions. To enhance the educational experience and to keep the discussion focused, the online discussion will be moderated/edited by the section editors.

INTRAOPERATIVE CHALLENGE (VIDEOS 1 AND 2)

1. Assessment of the severity of aortic stenosis (AS).
2. The impact of concomitant mitral stenosis (MS) on the echocardiographic assessment of AS is debatable.1-3

3. The AVA was not calculated in the aforementioned studies, and stenosis severity was estimated with gradients during cardiac catheterization.

4. Because of slow progression, it is recommended that “prophylactic aortic valve replacement (AVR)” may not be indicated.

5. However, it is also recommended that rheumatic AS progresses more rapidly than rheumatic aortic regurgitation.5 This is because aortic regurgitation can be caused by only a mild valvular abnormality, whereas AS develops after signiﬁcant valvular abnormality;5 hence, patients with mild AS in rheumatic heart valve disease.

6. The question was as follows: does the increased stroke volume after mitral valve replacement serve to increase the aortic valve area (AVA) or the gradient (ie, improve the stenosis or worsen it)?
7. Furthermore, there is not a cutoff value of the absolute AVA that is an indication for AVR.6 The need for AVR is determined by the presence of symptoms of ventricular decompensation rather than the AVA.6
8. The patient’s body surface area was 1.6 m2, with an aortic annular size of 1.8 cm, raising the possibility of a patient prosthesis mismatch after a size 19 prosthetic valve.7
9. The increased likelihood of a patient prosthesis mismatch in concomitant AVR during surgery for rheumatic stenosis of the mitral valve has been reported. This may be because of the greater preponderance of rheumatic heart disease in females who have a smaller body surface area, ascending aorta, and aortic annulus.8,9

INTRAOPERATIVE COURSE

1. Mitral valve replacement only.
2. Aortic valve was considered mildly stenotic and not calciﬁed with the hope of eventual improvement of AVA with improved stroke volume.
3. Immediate post–cardiopulmonary bypass AVA was measured to be 1.27 cm2 (continuity equation) and a peak gradient of 27 mmHg.
4. The pre–cardiopulmonary bypass AVA was 1.07 cm2 via the continuity equation with a peak gradient of 16 mmHg. There was a marginal improvement in the AVA but a simultaneous increase in the peak gradient with similar hemodynamics.
5. Improvement in the ﬁnal AVA and gradient did not speciﬁcally meet the criteria for the diagnosis of AS or “pseudo-AS.” 10

UNANSWERED QUESTIONS

1. Was it really “pseudo-AS” (ie, did the AVA actually signiﬁcantly improve after the mitral valve replacement)?
2. Was it more signiﬁcant AS than anticipated (ie, the AS in AVA, but a simultaneous improvement in peak was more severe than measured because of low ﬂow, gradient)? and this is manifested as an insigniﬁcant improvement.
3. Should the aortic valve have been replaced?

REFERENCES

1. Honey M: Clinical and haemodynamic observations on combined mitral and aortic stenosis. Br Heart J 23:545-555, 1961

2. Katznelson G, Jreissaty RM, Levinson GE, et al: Combined aortic and mitral stenosis. A clinical and physiological study. Am J Med
29:242-256, 1960

3. Zitnik RS, Piemme TE, Messer RJ, et al: The masking of aortic stenosis by mitral stenosis. Am Heart J 69:22-30, 1965

4. Vaturi M, Porter A, Adler Y, et al: The natural history of aortic valve disease after mitral valve surgery. J Am Coll Cardiol 33:2003-2008, 1999

5. Choudhary SK, Talwar S, Juneja R, et al: Fate of mild aortic valve disease after mitral valve intervention. J Thorac Cardiovasc Surg 122:583-586, 2001

6. ACC/AHA guidelines for the management of patients with valvularheart disease. A report of the American College of Cardiology/American Heart Association. Task Force on Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease). J Am Coll Cardiol 32:1486-1588, 1998

7. Pibarot P, Dumesnil JG: Prosthesis-patient mismatch: Definition,clinical impact, and prevention. Heart 92:1022-1029, 2006

8. Roberts WC, Ko JM: Some observations on mitral and aortic valve disease. Proc (Bayl Univ Med Cent) 21:282-299, 2008

9. Roberts WC, Ko JM, Schumacher JR, et al: Combined mitral and aortic stenosis of rheumatic origin with double-valve replacement in an octogenarian. Int J Cardiol 2008 [Epub ahead of print]

10.Maslow AD, Mahmood F, Poppas A, et al: Intraoperative dobutamine stress echocardiography to assess aortic valve stenosis. J Cardiothorac Vasc Anesth 20:862-866, 2006

2010-02-04T15:50:00.000-08:00

Rheumatic Mitral and Aortic Stenosis: To Replace or Not To Replace

That Is the Question—Part 1

Melanie Darke, MD, John Pawloski, MD, Kamal R. Khabbaz, MD, and Feroze Mahmood, MD

The Patient was a 64-year-old woman who presented to her cardiologist with an episode of shortness of breath. She also gave a history of progressive decline in her functional capacity over the last few months. Her chest radiograph showed bilateral pulmonary congestion. Based on her presentation, she was diagnosed as having congestive heart failure and was admitted to the hospital for diuresis and a workup. A transthoracic echocardiogram was done, which showed normal systolic function, moderate mitral stenosis (MS) with a mitral valve area of 1.41 cm2 with a peak gradient of 22 mmHg, and a mean gradient of 9 mmHg. She also had moderate mitral regurgitation and a question of a bicuspid aortic valve and mild aortic stenosis (AS) with peak and mean gradients of 19 and 13 mmHg, respectively. Her cardiac catheterization did not show any coronary artery disease.
Her past medical history was significant for hiatus hernia, hypertension, asthma, and type-2 diabetes mellitus. She had undergone multiple surgeries under general anesthesia in the past without any problems. She was born and grew up in South America, but she did not have a specific history of rheumatic fever. Based on the clinical examination and results of investigations, a diagnosis of rheumatic MS was made, and she was scheduled to undergo an elective mitral valve replacement. She was taking aspirin, enalapril, furosemide, metformin, metoprolol, and sertraline.
On the day of the surgery, she was found to be in sinus rhythm, conscious and alert, and in no apparent respiratory distress. She was 5 feet 1 inch tall and weighed 144 lb. Her hematology and blood chemistry results were with in normal limits. She was taken to the operating room, and, after placement of appropriate monitors, general anesthesia was induced uneventfully and the airway was secured.

Fig 1. A midesophageal 4-chamber view showing
classic diastolic doming of the mitral valve

An intraoperative transesophageal echocardiographic (TEE) examination was performed with an IE-33 ultrasound system with an OMNI-III TEE probe (Philips Medical Systems, Andover, MA).

Presentation 1 (Video A and B): Mitral Valve (Fig 1)

1. Severely thickened and deformed (typical hockey stick deformity)
2. Diastolic bowing of mitral valve and moderate mitral regurgitation.
3. Subvalvular fibrosis and chordal shortening
4. Moderate MS, peak gradient 16 mmHg, and mean gradient 8 mmHg
5. Mitral valve area � 1.32 cm2

Fig 2. A midesophageal short-axis view of the aortic valve during
systolic opening and a planimetered aortic valve area of 1.2 cm2.

Aortic Valve (Fig 2)
1. Trileaflet valve
2. Mildly thickened and retracted
3. Trace aortic regurgitation
4. Left ventricular outflow tract and aortic annulus diameter � 1.8 cm
5. Aortic valve area (AVA) by planimetry 1.32 cm2,by continuity equation 0.97-1.07 cm2; a peak gradient of 16 mmHg was measured with continuous wave Doppler

ECHO CHALLENGES
The aortic valve is considered protected when there is MS because of reduced stroke volume and flow. Hence, it is possible to have a "low" gradient despite significant aortic valvular stenosis because concomitant MS leads to a low stroke volume.
Is this the case in this patient?
If so, then what is the true AVA?
Are clinicians "UNDERESTIMATING" the AS due to mitral stenosis?1
Low gradient is due to low flow (ie, reduced stroke volume and the actual AS is more than moderate; ie, improved stroke volume may worsen the gradient and the severity of AS).
Are clinicians "OVERESTIMATING" the AS due to MS?
AVA is flow dependent, and the small AVA is because of low flow; hence, improvement in stroke volume after mitral valve replacement (MVR) will improve the AVA.

CONFOUNDING VARIABLES
1. Concomitant aortic valve replacement during MVR for rheumatic disease for mild AS is debatable.
2. Is the rheumatic AS severe enough to warrant surgery?
3. Does the progression of rheumatic AS differ from the calcific AS?2
4. If the aortic valve will eventually require surgery, are the risks of a redo aortic valve replacement more or less than mitral and aortic valves being replaced simultaneously?

REFERENCES
1. Zitnik RS, Piemme TE, Messer RJ, et al: The masking
of aortic stenosis by mitral stenosis. Am Heart J 69:22-30,
1965
2. Choudhary SK, Talwar S, Juneja R, et al: Fate of mild aortic
valve disease after mitral valve intervention. J Thorac Cardiovasc
Surg 122:583-586, 2001