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

E-CHALLENGES & CLINICAL DECISIONS

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

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

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