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SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair Lynn M. Charls, BA, RN, Rochester, Minnesota
Systolic anterior motion (SAM) is a postoperative complication experienced by patients undergoing mitral valve repair. The incidence of SAM after mitral valve repair ranges from 5 to 10%. Early recognition of the signs and symptoms of SAM is imperative to the management of these patients. This article presents the pathopysiology of mitral valve dysfunction to give the practitioner a clear understanding of the dynamics of SAM. This article’s main focus is the detection and management of SAM and the most current treatment modalities. A case study is used to illustrate the complex management necessary for the patient with SAM. (Heart Lung® 2003;32:402-6.)
INTRODUCTION Systolic anterior motion (SAM) results when the anterior leaflet of the mitral valve partially obstructs the left ventricular outflow tract (LVOT).1 SAM can occur in patients with Hypertrophic Obstructive Cardiomyopathy, in patients post myocardial infarction, and in those who have undergone mitral valve repair, but it may also be present in the postoperative course of a patient at risk for mitral valve regurgitation/prolapse.2,3 This article focuses on recognizing clinical conditions that may manifest themselves as SAM after mitral valve repair and the clinical manifestations and interventions used to treat the condition and reduce potential associated complications postoperatively.
PATHOPHYSIOLOGY OF THE MITRAL VALVE Knowledge of normal mitral valve anatomy is essential in understanding SAM. The mitral valve has 2 leaflets: the anterior leaflet that consumes 35% of the valve circumference and the posterior leaflet that consumes 65% of the valve circumference. In spite of this inequality, the surface areas of From the Mayo Medical Center, Cardiac Surgery Intensive Care Unit, St. Mary’s Hospital, Rochester, Minnesota. Reprint requests: Lynn M. Charls, BA, RN, Mayo Medical Center, Cardiac Surgery ICU, St. Mary’s Hospital, 1216 2nd Street SW, Rochester, MN 55902. Copyright © 2003 by Mosby, Inc. 0147-9563/2003/$30.00 ⫹ 0 doi:10.1016/j.hrtlng.2003.07.004
402
www.heartandlung.org
the anterior leaflet and posterior leaflet are nearly equal (Fig 1). The posterior mitral annulus is a dynamic structure that shortens during systole. This shortening of the posterior annulus during systole results in a phasic narrowing of the mitral valve opening. This concept is demonstrated in that during diastole the combined area of the anterior and posterior leaflets is about 9.9 square cm. However, during systole, the annulus and leaflets surface area contracts to about half that size (5.2 square cm), somewhat in the same manner of a sphincter. In addition, the mitral valve does not naturally close at the leaflet-free margins. A large area of leaflet tissue overlaps the opposing leaflet and forms a tight seal when the valves close during systole.4 The point at which the 2 leaflets overlap and meet to form this seal is called the coaptation point. In some circumstances, the anterior valve leaflet may not be fully in the closed position during systole, and a portion of it may obstruct the LVOT (Fig 2).
PATHOPYSIOLOGY OF SAM Literature suggests that SAM is caused by the velocity of left ventricular outflow on the ventricular surface of the anterior leaflet of the mitral valve. The position and abnormalities of the mitral valve leaflets contribute to SAM. Studies of the mitral valve after repair report very similar findings.5 First, there is a shortening of the distance between the mitral valve coaptation point and the septum. This shortened distance is caused either by increasing the posterior leaflet size or by elongating the anterior
NOVEMBER/DECEMBER 2003
HEART & LUNG
Charls
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
Fig 1 Anatomy of mitral valve
leaflet during the repair process, causing an increased area of anterior leaflet exposed to the LVOT flow. Second, during surgical repair of the papillary muscles, the mitral valve may be displaced anteriorly, positioning it toward the LVOT and exposing the anterior leaflet more directly into the flow of the LVOT.6-8 Fluid overload in the perioperative and postoperative periods will also cause a left shift of the septum. The leftward bulge in the septum will narrow the LVOT. Hypovolemia postoperatively will cause a decrease in the end-diastolic volume in the left ventricle narrowing the LVOT. All these conditions contribute to the development of SAM in the postoperative mitral valve repair patient. There is some debate as to how and why the anterior leaflet is pulled into the LVOT once the above circumstances occur.9-13 In one theory, the anterior leaflet is pulled into the LVOT by the Venturi mechanism (Giovanni Venturi, 1746-1822) in which there is a pressure drop distal to a restriction. That pressure drop, however, can be restored to prerestriction pressure if there is a dilation of the
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passage immediately distal to the stenosis with an angle of no more than 15 degrees. The drop of pressure immediately beyond the restriction pulls the mitral valve into the LVOT. Studies were conducted measuring the angles of the mitral valve leaflets at coaptation point. A mean of 21 degrees was found thus challenging this theory.14 The other theory by which the leaflet is pulled into the LVOT is flow drag. An example of flow drag is illustrated by an open door in a windy hallway. The airflow, faster down the center of the hallway, pulls the door out into the airstream. As the open door is swung into the hallway, more of its surface area is exposed to the wind so the door picks up speed until it finally slams shut.3 Applying this illustration to the mitral valve, it is possible that the flow drag of blood moving past the anterior leaflet pulls it out into the LVOT, where it then causes obstruction. Some studies hypothesize a combined effect. The Venturi mechanism elevates the valve leaflet toward the septum, and drag lifts the leaflet toward the septum.15,16
www.heartandlung.org
403
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
Charls
Fig 2 Normal mitral valve leaflets. AO–aorta; RA–right atrium; LA–left atrium; RV–right ventricle; LV–left ventricle.
DIAGNOSIS OF SAM Transesophageal echocardiography (TEE) or 2-dimensional and doppler echocardiography are essential in the diagnosis of SAM. In SAM, the mitral valve, which is situated anteriorly in the left ventricular cavity, will have residual portions of the anterior leaflet extending past the coaptation point and thus protruding into the LVOT. The echocardiography will also reveal a small left ventricle and/or a bulging septum (Fig 3). Depending on the type of repair, the coaptation point will be closer to the septum. Patients with previously documented SAM present with symptoms of dyspnea, angina, palpations, congestive heart failure, near syncope, syncope, arrhythmias or a combination of symptoms.17 Since the incidence of SAM is 5 to 10% in patients undergoing mitral valve repair and the postoperative management is complicated, all patients in our institution having a mitral valve repair have a TEE in the OR after coming off cardiopulmonary bypass.
MANAGEMENT OF THE PATIENT POST MITRAL VALVE REPAIR WITH SAM As aforementioned, hypervolemia or hypovolemia may precipitate SAM. Therefore, the patient with a mitral valve repair may initially have a normal TEE. Although all cardiac surgical patients are at
404
www.heartandlung.org
Fig 3 Left side of heart with SAM
risk for postoperative hypovolemia, the patient with SAM presents a more dynamic picture. In all patients, hypovolemia decreases cardiac output resulting in decreased blood pressure, increased heart rate, cool extremities, and decreased urine output. In SAM, the anterior leaflet obstructs the LVOT. When these patients become hypovolemic, the immediate effects of hypovolemia are more pronounced. Even a slight decrease of the end-diastolic volume in the left ventricle narrows the outflow tract even further. This produces an even greater Venturi effect and in turn drag, adding to the likelihood of obstruction, resulting in decreased stroke volume, cardiac output, and ultimately decreased blood pressure. SAM may also become manifest in the setting of hypervolemia. Increased right ventricular volume, as indicated by elevated pulmonary artery pressures will also bulge the ventricular septum leftward thereby narrowing the LVOT. In these circumstances, nitroglycerin should be considered to lower pulmonary artery pressures immediately.18 The immediate postoperative management of a patient with SAM focuses on keeping the left ven-
NOVEMBER/DECEMBER 2003
HEART & LUNG
Charls
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
tricle optimally expanded to keep the LVOT open. Volume replacement and maintenance, with either crystalloid or colloid solutions, are the primary focus for management of a patient with SAM. The left ventricle must be fully expanded to minimize LVOT obstruction. In addition, heart rate should be stabilized to maximize left ventricular filling time. Tachyarrhythmias decrease diastolic filling times and therefore diminish left ventricular end diastolic volume. Beta-blockers are the drug of choice to treat tachyarrhythmias in the setting of SAM.14,17 A continuous intravenous infusion is recommended more than bolus administration because it is easier to titrate the beta blocker to obtain a slower heart rate with only minimal decrease in blood pressure. The use of positive inotropes, such as epinephrine, which increase the heart rate and contractility, must be used with caution in this patient population.1 Their use adversely affects left ventricular filling time and may also cause the ventricle a more hyperdynamic condition, resulting in the narrowing of the LVOT, thereby increasing the severity of SAM. Diminished systemic vascular resistance in the postoperative period hampers management of SAM because it indicates diminished left ventricle filling pressure. The goal in managing SAM is to maintain the left ventricular volume. Therefore, nitroprusside and other commonly used measures to decrease systemic vascular resistance should be avoided. Because SAM may be transient or long term, subsequent treatment is based on the severity of symptoms. The presence of severe or worsening symptoms may make surgical intervention necessary. Surgical intervention would consist of moving the anterior leaflet of the mitral valve out of the LVOT either by shortening the posterior leaflet size or by elongating the anterior leaflet or positioning the mitral valve more posteriorly. The type of correction would depend on the original surgery.19
CASE STUDY A case study is useful in demonstrating the clinical consequence of SAM postoperatively. A 67-year-old man was admitted with a known history of mitral valve regurgitation caused by rheumatic heart disease and scheduled for a mitral valve repair. The pre-operative echocardiogram showed bileaflet prolapse with normal left ventricular function. The intra-operative course was uneventful. The post-cardiopulmonary bypass TEE showed SAM, so the patient was treated with Esmolol 30 mg, Albu-
HEART & LUNG
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min 500 cc, and Normal Saline 500 cc and transferred to the Cardiac Surgical Intensive Care Unit. His cardiac output was 7.87 L per minute; cardiac index was 3.82 L per minute; systemic vascular resistance was 1424 (Dynes); and systemic resistance was 18 Woods units. The patient remained stable and was extubated within several hours. Systolic blood pressure (SBP) was maintained between 90 and 110 mm Hg with nitroprusside, and right atrial pressure was maintained between 8 and 12 mm Hg with Albumin 250 cc boluses. Eighteen hours postoperatively, the patient exhibited hypotension with SBP in the lower 70s and tachycardia. A systolic heart murmur was noted, and the patient was treated with Esmolol 30 mg and an infusion was started at 90 mcg per kg per minute and titrated to keep the heart rate below 100. A TEE was performed and severe SAM was noted, and phenylephrine 80 mcg per kg per minute was added to Esmolol to maintain blood pressure. Esmolol was discontinued after 8 hours because of a seconddegree heart block. Norepinephrine 0.2 mcg per kg per minute and epinephrine 0.05 mcg per kg per minute were added to maintain SBP. The patient was weaned from both phenylephrine and norepinephrine on postoperative day 2. He was also weaned off epinephrine on day 4. The patient was transferred to the Intermediate Care Area on day 5, and metropolol 50 mg every 12 hours and disopyramide phosphate 200 mg every 12 hours were started on day 6. A TEE on day 7 revealed moderate to severe mitral regurgitation secondary to SAM. The patient was discharged home on postoperative day 8. This patient was readmitted to his local hospital with complaints of shortness of breath and chest pain on postoperative day 17 and subsequently transferred to our facility. He then underwent a repeat mitral valve repair to position the anterior leaflet more posteriorly. His postoperative course was unremarkable and no evidence of SAM was seen on his postoperative TEE. The patient was transferred to the Intermediate Care Area on day 2 and discharged home on day 7. Discussion, in retrospect, focused on whether the hypotension that the patient experienced after his first surgery was caused by hypovolemia or caused by a mechanical abnormality and SAM symptomology. This case study demonstrates that recognition and early treatment with volume and beta-blockers stablized the patient’s condition. Ultimately, surgical correction of the position of the anterior leaflet of the mitral valve was necessary to treat SAM.
www.heartandlung.org
405
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
SUMMARY All patients undergoing a mitral valve repair are at risk for developing SAM. Consequently, understanding the anatomical changes that create SAM provides insight to detection and management. Special attention should be paid to the results of the post-cardiopulmonary bypass TEE. The postoperative patient with SAM will exhibit the same clinical picture as a patient that is hypovolemic. The difference is that the patient with SAM will have a rapid decrease in blood pressure, not gradual, as you would see with hypovolemia. The patient will not respond to volume as rapidly and will require a larger amount of volume to raise blood pressure. These patients also respond negatively to inotropes and may have a systolic murmur. Postoperative management focuses on maintenance of optimum left ventricle filling volume in the left ventricle to minimize obstruction of the LVOT by the anterior leaflet of the mitral valve. Prompt recognition and vigilant management of the postoperative patient experiencing SAM minimizes hemodynamic effects and potential complications associated with this condition.
REFERENCES 1. Canniere DD, Jansens JL, Unger P, Le Clerc JL. Left ventricular outflow tract obstruction after mitral valve replacement. Ann Thorac Surg 1997;64:1805-6. 2. Qin JX, Shiota T, Lever HM, Rubin DN, Bauer F, Kim YJ, et al. Impact of left ventricular outflow velocity in hypertrophic cardiomyopathy. J Am Coll Cardiol 2002;39(2):308-14. 3. Hrovatin E, Piazza R, Pavan D, Mimo R, Macor F, Dall’Aglio V, et al. Dynamic left ventricular outflow tract obstruction in the setting of acute anterior myocardial infarction. a serious and potentially fatal complication? Echocardiography 2002;19(6): 449-55. 4. Franco KL, Verrier ED. Advanced therapy in cardiac surgery. BC Decker: St Louis, 1999. p. 220-1. 5. Maslow AD, Regan MM, Haering JM, Johnson RG, Levine RA. 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 1999;34:2096-104.
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Charls
6. He S, Hopmeyer J, Lefebvre XP, Schwammenthal E, Yoganathan AP, Levine RA. Importance of leaflet elongation in causing systolic anterior motion of the mitral valve. J Heart Valve Dis 1997;6(2):149-59. 7. Schwammenthal E, Makatami S, He S, Hopmeyer J, Sagie A, Weyman A, et al. Mechanism of mitral regurgitation in hypertrophic cardiomyopathy. Mismatch of posterior to anterior leaflet length and mobility. Circulation 1998;98(9):85665. 8. Perier P, Hagen T, Stumpf J. Septal myectomy for left ventricular outflow tract obstruction after mitral valve repair. Ann Thorac Surg 1994;57:1328-30. 9. Nakatani S, Marwick T, Lever H, Thomas JD. Resting echocardiographic features of latent left ventricular outflow obstruction in hypertrophic cardiomyopathy. Am J Cardiol 1996; 78(6):662-7. 10. Sherrid MV, Gunsburg DZ, Moldenhauer s, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2000;36(4):1344-54. 11. Nakatani S, Schwammenthal E, Lever HM, Levine RA, Lytle BW, Thomas JD. New insights into the reduction of mitral valve systolic anterior motion after ventricular septal myectomy in hypertrophic obstructive cardiomyopathy. Am Heart J 1996;131:294-300. 12. Sherrid MV. Dynamic left ventricular outflow obstruction in hypertrophic cardiomyopathy revisited. Cardiol Rev 1998;6: 135-45. 13. Yoganathan AP, Lemmon JD, Kim YH, Peter GW, Levine RA, Vesier CC. A three-dimensional computational investigation Of intraventricular fluid dynamics. examination into the initiation of systolic anterior motion of the mitral valve leaflets. J Biomechanical Eng 1995;116:307-14. 14. Sherrid MV, Chu CK, Delia E, Mogtader A, Dwyer EM Jr. An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. J Am Coll Cardiol 1993; 22:816-25. 15. Bruce CJ, Nishimura RA, Tajik AJ, Schaff HV, Danielson GK. Fixed left ventricular outflow tract obstruction in presumed hypertrophic obstructive cardiomyopathy. implications for therapy. Ann Thorac Surg 1999;68:100-4. 16. Ommen SR, Nishimura RA. A physician’s guide to the treatment of hypertrophic cardiomyopathy. Treatment of patients with hypertrophic cardiomyopathy. a clinician’s guide-2001. Heart Views 2000;1(10):394-401. 17. Kurotobi S, Naito H, Sano T, Arisawa J, Matsushita T, Takeuchi M, et al. Left ventricular regional systolic motion in patients with right ventricular pressure overload. Int J Cardiol 1998;67(1):55-63. 18. Sherrid MV, Pearle G, Gunsburg D. The mechanism of benefit of negative inotropes in obstructive hypertrophic cardiomyopathy. Circulation 1998;97:41-7. 19. Sherrid MV, Chaudhry FA, Swistel DG. Obstructive hypertrophic cardiomyopathy. echocardiography, pathophysiology, and the continuing evolution of surgery for obstruction. Ann Thorac Surg 2003;75(2):620-32.
NOVEMBER/DECEMBER 2003
HEART & LUNG
Systolic anterior motion (SAM) is a postoperative complication experienced by patients undergoing mitral valve repair. The incidence of SAM after mitral valve repair ranges from 5 to 10%. Early recognition of the signs and symptoms of SAM is imperative to the management of these patients. This article presents the pathopysiology of mitral valve dysfunction to give the practitioner a clear understanding of the dynamics of SAM. This article’s main focus is the detection and management of SAM and the most current treatment modalities. A case study is used to illustrate the complex management necessary for the patient with SAM. (Heart Lung® 2003;32:402-6.)
INTRODUCTION Systolic anterior motion (SAM) results when the anterior leaflet of the mitral valve partially obstructs the left ventricular outflow tract (LVOT).1 SAM can occur in patients with Hypertrophic Obstructive Cardiomyopathy, in patients post myocardial infarction, and in those who have undergone mitral valve repair, but it may also be present in the postoperative course of a patient at risk for mitral valve regurgitation/prolapse.2,3 This article focuses on recognizing clinical conditions that may manifest themselves as SAM after mitral valve repair and the clinical manifestations and interventions used to treat the condition and reduce potential associated complications postoperatively.
PATHOPHYSIOLOGY OF THE MITRAL VALVE Knowledge of normal mitral valve anatomy is essential in understanding SAM. The mitral valve has 2 leaflets: the anterior leaflet that consumes 35% of the valve circumference and the posterior leaflet that consumes 65% of the valve circumference. In spite of this inequality, the surface areas of From the Mayo Medical Center, Cardiac Surgery Intensive Care Unit, St. Mary’s Hospital, Rochester, Minnesota. Reprint requests: Lynn M. Charls, BA, RN, Mayo Medical Center, Cardiac Surgery ICU, St. Mary’s Hospital, 1216 2nd Street SW, Rochester, MN 55902. Copyright © 2003 by Mosby, Inc. 0147-9563/2003/$30.00 ⫹ 0 doi:10.1016/j.hrtlng.2003.07.004
402
www.heartandlung.org
the anterior leaflet and posterior leaflet are nearly equal (Fig 1). The posterior mitral annulus is a dynamic structure that shortens during systole. This shortening of the posterior annulus during systole results in a phasic narrowing of the mitral valve opening. This concept is demonstrated in that during diastole the combined area of the anterior and posterior leaflets is about 9.9 square cm. However, during systole, the annulus and leaflets surface area contracts to about half that size (5.2 square cm), somewhat in the same manner of a sphincter. In addition, the mitral valve does not naturally close at the leaflet-free margins. A large area of leaflet tissue overlaps the opposing leaflet and forms a tight seal when the valves close during systole.4 The point at which the 2 leaflets overlap and meet to form this seal is called the coaptation point. In some circumstances, the anterior valve leaflet may not be fully in the closed position during systole, and a portion of it may obstruct the LVOT (Fig 2).
PATHOPYSIOLOGY OF SAM Literature suggests that SAM is caused by the velocity of left ventricular outflow on the ventricular surface of the anterior leaflet of the mitral valve. The position and abnormalities of the mitral valve leaflets contribute to SAM. Studies of the mitral valve after repair report very similar findings.5 First, there is a shortening of the distance between the mitral valve coaptation point and the septum. This shortened distance is caused either by increasing the posterior leaflet size or by elongating the anterior
NOVEMBER/DECEMBER 2003
HEART & LUNG
Charls
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
Fig 1 Anatomy of mitral valve
leaflet during the repair process, causing an increased area of anterior leaflet exposed to the LVOT flow. Second, during surgical repair of the papillary muscles, the mitral valve may be displaced anteriorly, positioning it toward the LVOT and exposing the anterior leaflet more directly into the flow of the LVOT.6-8 Fluid overload in the perioperative and postoperative periods will also cause a left shift of the septum. The leftward bulge in the septum will narrow the LVOT. Hypovolemia postoperatively will cause a decrease in the end-diastolic volume in the left ventricle narrowing the LVOT. All these conditions contribute to the development of SAM in the postoperative mitral valve repair patient. There is some debate as to how and why the anterior leaflet is pulled into the LVOT once the above circumstances occur.9-13 In one theory, the anterior leaflet is pulled into the LVOT by the Venturi mechanism (Giovanni Venturi, 1746-1822) in which there is a pressure drop distal to a restriction. That pressure drop, however, can be restored to prerestriction pressure if there is a dilation of the
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passage immediately distal to the stenosis with an angle of no more than 15 degrees. The drop of pressure immediately beyond the restriction pulls the mitral valve into the LVOT. Studies were conducted measuring the angles of the mitral valve leaflets at coaptation point. A mean of 21 degrees was found thus challenging this theory.14 The other theory by which the leaflet is pulled into the LVOT is flow drag. An example of flow drag is illustrated by an open door in a windy hallway. The airflow, faster down the center of the hallway, pulls the door out into the airstream. As the open door is swung into the hallway, more of its surface area is exposed to the wind so the door picks up speed until it finally slams shut.3 Applying this illustration to the mitral valve, it is possible that the flow drag of blood moving past the anterior leaflet pulls it out into the LVOT, where it then causes obstruction. Some studies hypothesize a combined effect. The Venturi mechanism elevates the valve leaflet toward the septum, and drag lifts the leaflet toward the septum.15,16
www.heartandlung.org
403
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
Charls
Fig 2 Normal mitral valve leaflets. AO–aorta; RA–right atrium; LA–left atrium; RV–right ventricle; LV–left ventricle.
DIAGNOSIS OF SAM Transesophageal echocardiography (TEE) or 2-dimensional and doppler echocardiography are essential in the diagnosis of SAM. In SAM, the mitral valve, which is situated anteriorly in the left ventricular cavity, will have residual portions of the anterior leaflet extending past the coaptation point and thus protruding into the LVOT. The echocardiography will also reveal a small left ventricle and/or a bulging septum (Fig 3). Depending on the type of repair, the coaptation point will be closer to the septum. Patients with previously documented SAM present with symptoms of dyspnea, angina, palpations, congestive heart failure, near syncope, syncope, arrhythmias or a combination of symptoms.17 Since the incidence of SAM is 5 to 10% in patients undergoing mitral valve repair and the postoperative management is complicated, all patients in our institution having a mitral valve repair have a TEE in the OR after coming off cardiopulmonary bypass.
MANAGEMENT OF THE PATIENT POST MITRAL VALVE REPAIR WITH SAM As aforementioned, hypervolemia or hypovolemia may precipitate SAM. Therefore, the patient with a mitral valve repair may initially have a normal TEE. Although all cardiac surgical patients are at
404
www.heartandlung.org
Fig 3 Left side of heart with SAM
risk for postoperative hypovolemia, the patient with SAM presents a more dynamic picture. In all patients, hypovolemia decreases cardiac output resulting in decreased blood pressure, increased heart rate, cool extremities, and decreased urine output. In SAM, the anterior leaflet obstructs the LVOT. When these patients become hypovolemic, the immediate effects of hypovolemia are more pronounced. Even a slight decrease of the end-diastolic volume in the left ventricle narrows the outflow tract even further. This produces an even greater Venturi effect and in turn drag, adding to the likelihood of obstruction, resulting in decreased stroke volume, cardiac output, and ultimately decreased blood pressure. SAM may also become manifest in the setting of hypervolemia. Increased right ventricular volume, as indicated by elevated pulmonary artery pressures will also bulge the ventricular septum leftward thereby narrowing the LVOT. In these circumstances, nitroglycerin should be considered to lower pulmonary artery pressures immediately.18 The immediate postoperative management of a patient with SAM focuses on keeping the left ven-
NOVEMBER/DECEMBER 2003
HEART & LUNG
Charls
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
tricle optimally expanded to keep the LVOT open. Volume replacement and maintenance, with either crystalloid or colloid solutions, are the primary focus for management of a patient with SAM. The left ventricle must be fully expanded to minimize LVOT obstruction. In addition, heart rate should be stabilized to maximize left ventricular filling time. Tachyarrhythmias decrease diastolic filling times and therefore diminish left ventricular end diastolic volume. Beta-blockers are the drug of choice to treat tachyarrhythmias in the setting of SAM.14,17 A continuous intravenous infusion is recommended more than bolus administration because it is easier to titrate the beta blocker to obtain a slower heart rate with only minimal decrease in blood pressure. The use of positive inotropes, such as epinephrine, which increase the heart rate and contractility, must be used with caution in this patient population.1 Their use adversely affects left ventricular filling time and may also cause the ventricle a more hyperdynamic condition, resulting in the narrowing of the LVOT, thereby increasing the severity of SAM. Diminished systemic vascular resistance in the postoperative period hampers management of SAM because it indicates diminished left ventricle filling pressure. The goal in managing SAM is to maintain the left ventricular volume. Therefore, nitroprusside and other commonly used measures to decrease systemic vascular resistance should be avoided. Because SAM may be transient or long term, subsequent treatment is based on the severity of symptoms. The presence of severe or worsening symptoms may make surgical intervention necessary. Surgical intervention would consist of moving the anterior leaflet of the mitral valve out of the LVOT either by shortening the posterior leaflet size or by elongating the anterior leaflet or positioning the mitral valve more posteriorly. The type of correction would depend on the original surgery.19
CASE STUDY A case study is useful in demonstrating the clinical consequence of SAM postoperatively. A 67-year-old man was admitted with a known history of mitral valve regurgitation caused by rheumatic heart disease and scheduled for a mitral valve repair. The pre-operative echocardiogram showed bileaflet prolapse with normal left ventricular function. The intra-operative course was uneventful. The post-cardiopulmonary bypass TEE showed SAM, so the patient was treated with Esmolol 30 mg, Albu-
HEART & LUNG
VOL. 32, NO. 6
min 500 cc, and Normal Saline 500 cc and transferred to the Cardiac Surgical Intensive Care Unit. His cardiac output was 7.87 L per minute; cardiac index was 3.82 L per minute; systemic vascular resistance was 1424 (Dynes); and systemic resistance was 18 Woods units. The patient remained stable and was extubated within several hours. Systolic blood pressure (SBP) was maintained between 90 and 110 mm Hg with nitroprusside, and right atrial pressure was maintained between 8 and 12 mm Hg with Albumin 250 cc boluses. Eighteen hours postoperatively, the patient exhibited hypotension with SBP in the lower 70s and tachycardia. A systolic heart murmur was noted, and the patient was treated with Esmolol 30 mg and an infusion was started at 90 mcg per kg per minute and titrated to keep the heart rate below 100. A TEE was performed and severe SAM was noted, and phenylephrine 80 mcg per kg per minute was added to Esmolol to maintain blood pressure. Esmolol was discontinued after 8 hours because of a seconddegree heart block. Norepinephrine 0.2 mcg per kg per minute and epinephrine 0.05 mcg per kg per minute were added to maintain SBP. The patient was weaned from both phenylephrine and norepinephrine on postoperative day 2. He was also weaned off epinephrine on day 4. The patient was transferred to the Intermediate Care Area on day 5, and metropolol 50 mg every 12 hours and disopyramide phosphate 200 mg every 12 hours were started on day 6. A TEE on day 7 revealed moderate to severe mitral regurgitation secondary to SAM. The patient was discharged home on postoperative day 8. This patient was readmitted to his local hospital with complaints of shortness of breath and chest pain on postoperative day 17 and subsequently transferred to our facility. He then underwent a repeat mitral valve repair to position the anterior leaflet more posteriorly. His postoperative course was unremarkable and no evidence of SAM was seen on his postoperative TEE. The patient was transferred to the Intermediate Care Area on day 2 and discharged home on day 7. Discussion, in retrospect, focused on whether the hypotension that the patient experienced after his first surgery was caused by hypovolemia or caused by a mechanical abnormality and SAM symptomology. This case study demonstrates that recognition and early treatment with volume and beta-blockers stablized the patient’s condition. Ultimately, surgical correction of the position of the anterior leaflet of the mitral valve was necessary to treat SAM.
www.heartandlung.org
405
SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair
SUMMARY All patients undergoing a mitral valve repair are at risk for developing SAM. Consequently, understanding the anatomical changes that create SAM provides insight to detection and management. Special attention should be paid to the results of the post-cardiopulmonary bypass TEE. The postoperative patient with SAM will exhibit the same clinical picture as a patient that is hypovolemic. The difference is that the patient with SAM will have a rapid decrease in blood pressure, not gradual, as you would see with hypovolemia. The patient will not respond to volume as rapidly and will require a larger amount of volume to raise blood pressure. These patients also respond negatively to inotropes and may have a systolic murmur. Postoperative management focuses on maintenance of optimum left ventricle filling volume in the left ventricle to minimize obstruction of the LVOT by the anterior leaflet of the mitral valve. Prompt recognition and vigilant management of the postoperative patient experiencing SAM minimizes hemodynamic effects and potential complications associated with this condition.
REFERENCES 1. Canniere DD, Jansens JL, Unger P, Le Clerc JL. Left ventricular outflow tract obstruction after mitral valve replacement. Ann Thorac Surg 1997;64:1805-6. 2. Qin JX, Shiota T, Lever HM, Rubin DN, Bauer F, Kim YJ, et al. Impact of left ventricular outflow velocity in hypertrophic cardiomyopathy. J Am Coll Cardiol 2002;39(2):308-14. 3. Hrovatin E, Piazza R, Pavan D, Mimo R, Macor F, Dall’Aglio V, et al. Dynamic left ventricular outflow tract obstruction in the setting of acute anterior myocardial infarction. a serious and potentially fatal complication? Echocardiography 2002;19(6): 449-55. 4. Franco KL, Verrier ED. Advanced therapy in cardiac surgery. BC Decker: St Louis, 1999. p. 220-1. 5. Maslow AD, Regan MM, Haering JM, Johnson RG, Levine RA. 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 1999;34:2096-104.
406
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