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Systolic anterior motion of the mitral valve after mitral valve repair without a ring
Systolic Anterior Motion of the Mitral Valve After Mitral Valve Repair Without a Ring Kiyoyuki Eishi, MD, Kouhei Kawazoe, MD, and Yasunaru Kawashima, MD Division of Cardiovascular Surgery, National Cardiovascular Center of Japan, Osaka, Japan
We report a case of systolic anterior motion of the mitral valve after mitral reconstruction without a semirigid mitral annular ring. A 56-year-old man with mitral regurgitation due to ruptured chordae tendineae underwent mitral valve reconstruction by replacement of chordae tendineae, leaflet excision, and suture annuloplasty
without an annular ring. Postoperatively, left ventricular outflow tract obstruction developed and echocardiography revealed systolic anterior motion of the mitral valve. These findings disappeared after medication with a fiblocking drug. (Ann Thorac Surg 2993;55:2023-5)
L
3/4 mitral regurgitation and no pressure gradient between the left ventricle and aorta. The patient was referred for a mitral valve operation in 1991. At the time of operation, mitral exploration revealed ruptured chordae in the midportion of the posterior mitral leaflet and remarkable prolapse of the whole posterior leaflet. All the chordae of the anterior mitral leaflet were elongated significantly, resulting in a mild prolapse. Six artificial chordae (4-0 expanded polytetrafluoroethylene suture) [5] were implanted on the anterior leaflet (four on the posterior papillary muscle and two on the anterior papillary muscle), and another six chordae on the posterior mitral leaflet (two on the posterior papillary muscle and four on the anterior papillary muscle). A part of both scallops around the anterolateral commissure, which showed severe myxomatous degeneration, was excised and the cleft was repaired. Annuloplasties were then employed on both commissural sides to reduce the annular size by means of suture plications. After the patient was weaned from cardiopulmonary bypass, no evidence of mitral insufficiency was noted by transesophageal echocardiograms. However, he complained of general fatigue and palpi-
eft ventricular outflow tract (LVOT) obstruction caused by systolic anterior motion (SAM) of the mitral valve has been described as a complication of mitral valve reconstruction with a Carpentier ring [14]. It was suggested that the semirigid ring prevents the normal systolic decrease in the anteroposterior size of the mitral annulus and its subsequent posterior movement. We report a case of SAM after mitral valve reconstruction without an annuloplasty ring. A 56-year-old man was referred in 1989 because of palpitation and edema of the lower extremities. He had complained of increasing palpitation for 3 years. There was no history of rheumatic fever, recent fever, or infection. Physical examination revealed a regular pulse rate of 86/min with deficits, a blood pressure of 136/60 mm Hg supine, a respiratory rate of 12/min, and a temperature of 36.8"C. Chest examination revealed the lateral displacement of the cardiac apex and the presence of s,. A grade 4/6 holosystolic murmur was best heard at the apex, but no diastolic murmur was present. An electrocardiogram revealed normal sinus rhythm, left ventricular hypertrophy, and no ischemic ST-T wave changes. Chest roentgenogram showed a cardiothoracic ratio of 0.47 and no pulmonary congestion. Echocardiography revealed dilatation of both the left atrium (48 mm) and the left ventricle (end-diastolic dimension of 56 mm) (Table 1).The left ventricular outflow tract width, measured from the coaptation point of mitral closure to the left side of the septum, was normal (19 mm in systole). There was a thickening of both anterior and posterior mitral leaflets and remarkable systolic prolapse of the mid and medial portions of the posterior mitral leaflet, suggesting tom chordae around the midportion. Also, mild systolic prolapse of the anterior mitral leaflet was observed. Doppler echocardiography showed grade Accepted for publication June 17, 1992. Address reprint requests to Dr Eishi, Division of Cardiovascular Surgery, National Cardiovascular Center of Japan,5-7-1 Fujishirc-dai, Suita, Osaka 565, Japan. 0 1993 by The
Society of Thoracic Surgeons
Table 1 . Summary of Echographic Findings
Postoperative Without
Blocker
Postoperative With Blocker
0
47
5
LVOT DdlDs (mm) IVS Thdnhs (mm)
56/28 24/19 12/20
FS
0.50
Mitroaortic angle (degrees)
118
47/28 1510 13/22 0.40 111
43/29 1818 11/17 0.33 118
Variable Pressure gradient at LVOT (mm Hg) LV DdDs (mm)
Preoperative
Ds = dimension in systole; Dd = dimension in diastole; FS = fraction shortening; IVS = interventricular septum; LV = left ventricular; LVOT = left ventricular outflow tract; Thd = thickness in diastole; Ths = thickness in systole.
0003-4975/93/$6.00
1014
CASE REPORT EISHI ET AL MITRAL VALVE SYSTOLIC ANTERIOR MOTION
Ann Thorac Surg 1993;55.101>5
.
Fig 1. M-mode echocardiograms: (A) Marked systolic prolapse of posterior leaflet I S seen before valvuloplasty. (B) The left ventricular outflow tract is smaller and systolic anterior motion ( S A M ) of the mitral valve is present after valvuloplasty. (0The outflow tract becomes larger and systolic anterior motion disappears after treatment with propranolol hydrochloride.
-
tation 2 weeks after operation. Postoperative echocardiography revealed LVOT obstruction (pressure gradient of 47 mm Hg),SAM of the mitral valve, a grade 2/4 mitral regurgitation, and a small amount of pericardial effusion. The anterior mitral leaflet almost contacted the ventricular septum during systole, and the severity of SAM was graded as moderate [4] (Fig 1). The end-diastolic dimension of the left ventricle decreased to 47 mm, and LVOT width in diastole narrowed to 15 mm. After treatment with propranolol hydrochloride, a Pblocking drug at a dose of 45 mg a day, the general fatigue decreased and repeated echocardiography revealed the complete disappearance of LVOT obstruction, S A M of the mitral valve, and mitral regurgitation. Although the end-diastolic dimension of the left ventricle decreased to 43 mm, the end-systolic dimension increased to 29 mm.
The mitral valve reconstruction in our patient did not include a ring annuloplasty technique, and the replacement of chordae tendineae on both mitral leaflets was performed using expanded polytetrafluoroethylene sutures. This procedure may have drawn the anterior leaflet into the outflow tract in the systolic phase. Postoperatively, in this patient, end-diastolic left ventricular dimension decreased, but end-systolic dimension did not decrease. The Pblocking drug, then, increased the endsystolic left ventricular outflow tract dimension, resulting in the disappearance of SAM of the mitral valve. Therefore, the excessive surface of leaflets drawn by the implanted chordae was thought to be a cause of S A M of the mitral valve, and this complication responded well to the Pblocking drug.
Comment
References
Left ventricular outflow tract obstruction caused by S A M of the mitral valve has been described as a complication of mitral valve reconstruction with a semirigid annular ring [14]. This complication was reported in 4.5% to 10% of patients undergoing Carpentier valvuloplasty for degenerative mitral regurgitation [14]. The phenomenon of SAM after mitral valvuloplasty has not been described in patients with rheumatic valvulitis or other causes of mitral regurgitation except myxomatous degeneration [I, 41. Therefore, enhanced mobility and the excessive surface of the mitral leaflet may partially block the left ventricular outflow during systole. In addition to patients with annuloplasty rings, patients with mitral annular calcification have also been reported to have LVOT narrowing and SAM [6, 71. It was suggested that the Carpentier ring or calcified annulus produces the narrowing of the mitroaortic angle [l] and prevents the normal systolic decrease in the anteroposterior size of the mitral annulus and its subsequent posterior movement [MI.Postoperatively, left ventricular dimension as well as outflow tract dimension decreased and the thickness of the interventricular septum increased, but no asymmetric septa1 hypertrophy was present [4]. Abrupt reduction of left ventricular volume might indicate SAM of the mitral valve as well as LVOT narrowing.
1. Mihaileanu S, Marino JP, Chauvaud S, et al. Left ventricular outflow obstruction after mitral valve repair (Carpentier's 2.
3.
4.
5. 6.
7. 8.
technique): proposed mechanisms of disease. Circulation 1988;78(Suppl1):78-84. Kronzon I, Cohen ML, Winer HE, Colvin SB. Left ventricular outflow obstruction: a complication of mitral valvuloplasty. J Am Coll Cardiol 1984;4825-8. Galler M, Kronzon I, Slater J, et al. Long-term follow-up after mitral valve reconstruction: incidence of postoperative left ventricular outflow obstruction. Circulation 1986;74(Suppl1): 99-103. Schiavone WA, Cosgrove DM, Lever HM, Stewart WJ,Salcedo F.E. Long-term follow-up of patients with left ventricular outflow tract obstruction after Carpentier ring mitral valvuloplasty. Circulation 1988;78(Suppl1):6&5. Kawame K, Ichikawa H, Kosakai Y, Ohara K,Kitoh Y, Fujita T. Replacement of chordae tendineae with FIFE suture for mitral valve prolapse. Jpn J Cardiovasc Surg 1990;1963W. Lindvall K, Herrlin B. Mitral annulus calcification, systolic anterior motion of the anterior mitral leaflet and outflow obstruction in two patients without hypertrophic cardiomyopathy. Acta Med %and 1981;209:513-8. Slater J, Kronzon I, Cohen ML. Left ventricular outflow tract anatomy in patients with mitral annular calcification [Abstract]. Chest 1984;86:315.
Waggoner AD, Perez JE,Barzilai B, Rosenbloom M, Eaton MH, Cox JL. Left ventricular obstruction resulting from insertion of mitral prostheses leaving the native leaflets intact: adverse clinical outcome in seven patients. Am Heart J 1991; 122:48%7.
We report a case of systolic anterior motion of the mitral valve after mitral reconstruction without a semirigid mitral annular ring. A 56-year-old man with mitral regurgitation due to ruptured chordae tendineae underwent mitral valve reconstruction by replacement of chordae tendineae, leaflet excision, and suture annuloplasty
without an annular ring. Postoperatively, left ventricular outflow tract obstruction developed and echocardiography revealed systolic anterior motion of the mitral valve. These findings disappeared after medication with a fiblocking drug. (Ann Thorac Surg 2993;55:2023-5)
L
3/4 mitral regurgitation and no pressure gradient between the left ventricle and aorta. The patient was referred for a mitral valve operation in 1991. At the time of operation, mitral exploration revealed ruptured chordae in the midportion of the posterior mitral leaflet and remarkable prolapse of the whole posterior leaflet. All the chordae of the anterior mitral leaflet were elongated significantly, resulting in a mild prolapse. Six artificial chordae (4-0 expanded polytetrafluoroethylene suture) [5] were implanted on the anterior leaflet (four on the posterior papillary muscle and two on the anterior papillary muscle), and another six chordae on the posterior mitral leaflet (two on the posterior papillary muscle and four on the anterior papillary muscle). A part of both scallops around the anterolateral commissure, which showed severe myxomatous degeneration, was excised and the cleft was repaired. Annuloplasties were then employed on both commissural sides to reduce the annular size by means of suture plications. After the patient was weaned from cardiopulmonary bypass, no evidence of mitral insufficiency was noted by transesophageal echocardiograms. However, he complained of general fatigue and palpi-
eft ventricular outflow tract (LVOT) obstruction caused by systolic anterior motion (SAM) of the mitral valve has been described as a complication of mitral valve reconstruction with a Carpentier ring [14]. It was suggested that the semirigid ring prevents the normal systolic decrease in the anteroposterior size of the mitral annulus and its subsequent posterior movement. We report a case of SAM after mitral valve reconstruction without an annuloplasty ring. A 56-year-old man was referred in 1989 because of palpitation and edema of the lower extremities. He had complained of increasing palpitation for 3 years. There was no history of rheumatic fever, recent fever, or infection. Physical examination revealed a regular pulse rate of 86/min with deficits, a blood pressure of 136/60 mm Hg supine, a respiratory rate of 12/min, and a temperature of 36.8"C. Chest examination revealed the lateral displacement of the cardiac apex and the presence of s,. A grade 4/6 holosystolic murmur was best heard at the apex, but no diastolic murmur was present. An electrocardiogram revealed normal sinus rhythm, left ventricular hypertrophy, and no ischemic ST-T wave changes. Chest roentgenogram showed a cardiothoracic ratio of 0.47 and no pulmonary congestion. Echocardiography revealed dilatation of both the left atrium (48 mm) and the left ventricle (end-diastolic dimension of 56 mm) (Table 1).The left ventricular outflow tract width, measured from the coaptation point of mitral closure to the left side of the septum, was normal (19 mm in systole). There was a thickening of both anterior and posterior mitral leaflets and remarkable systolic prolapse of the mid and medial portions of the posterior mitral leaflet, suggesting tom chordae around the midportion. Also, mild systolic prolapse of the anterior mitral leaflet was observed. Doppler echocardiography showed grade Accepted for publication June 17, 1992. Address reprint requests to Dr Eishi, Division of Cardiovascular Surgery, National Cardiovascular Center of Japan,5-7-1 Fujishirc-dai, Suita, Osaka 565, Japan. 0 1993 by The
Society of Thoracic Surgeons
Table 1 . Summary of Echographic Findings
Postoperative Without
Blocker
Postoperative With Blocker
0
47
5
LVOT DdlDs (mm) IVS Thdnhs (mm)
56/28 24/19 12/20
FS
0.50
Mitroaortic angle (degrees)
118
47/28 1510 13/22 0.40 111
43/29 1818 11/17 0.33 118
Variable Pressure gradient at LVOT (mm Hg) LV DdDs (mm)
Preoperative
Ds = dimension in systole; Dd = dimension in diastole; FS = fraction shortening; IVS = interventricular septum; LV = left ventricular; LVOT = left ventricular outflow tract; Thd = thickness in diastole; Ths = thickness in systole.
0003-4975/93/$6.00
1014
CASE REPORT EISHI ET AL MITRAL VALVE SYSTOLIC ANTERIOR MOTION
Ann Thorac Surg 1993;55.101>5
.
Fig 1. M-mode echocardiograms: (A) Marked systolic prolapse of posterior leaflet I S seen before valvuloplasty. (B) The left ventricular outflow tract is smaller and systolic anterior motion ( S A M ) of the mitral valve is present after valvuloplasty. (0The outflow tract becomes larger and systolic anterior motion disappears after treatment with propranolol hydrochloride.
-
tation 2 weeks after operation. Postoperative echocardiography revealed LVOT obstruction (pressure gradient of 47 mm Hg),SAM of the mitral valve, a grade 2/4 mitral regurgitation, and a small amount of pericardial effusion. The anterior mitral leaflet almost contacted the ventricular septum during systole, and the severity of SAM was graded as moderate [4] (Fig 1). The end-diastolic dimension of the left ventricle decreased to 47 mm, and LVOT width in diastole narrowed to 15 mm. After treatment with propranolol hydrochloride, a Pblocking drug at a dose of 45 mg a day, the general fatigue decreased and repeated echocardiography revealed the complete disappearance of LVOT obstruction, S A M of the mitral valve, and mitral regurgitation. Although the end-diastolic dimension of the left ventricle decreased to 43 mm, the end-systolic dimension increased to 29 mm.
The mitral valve reconstruction in our patient did not include a ring annuloplasty technique, and the replacement of chordae tendineae on both mitral leaflets was performed using expanded polytetrafluoroethylene sutures. This procedure may have drawn the anterior leaflet into the outflow tract in the systolic phase. Postoperatively, in this patient, end-diastolic left ventricular dimension decreased, but end-systolic dimension did not decrease. The Pblocking drug, then, increased the endsystolic left ventricular outflow tract dimension, resulting in the disappearance of SAM of the mitral valve. Therefore, the excessive surface of leaflets drawn by the implanted chordae was thought to be a cause of S A M of the mitral valve, and this complication responded well to the Pblocking drug.
Comment
References
Left ventricular outflow tract obstruction caused by S A M of the mitral valve has been described as a complication of mitral valve reconstruction with a semirigid annular ring [14]. This complication was reported in 4.5% to 10% of patients undergoing Carpentier valvuloplasty for degenerative mitral regurgitation [14]. The phenomenon of SAM after mitral valvuloplasty has not been described in patients with rheumatic valvulitis or other causes of mitral regurgitation except myxomatous degeneration [I, 41. Therefore, enhanced mobility and the excessive surface of the mitral leaflet may partially block the left ventricular outflow during systole. In addition to patients with annuloplasty rings, patients with mitral annular calcification have also been reported to have LVOT narrowing and SAM [6, 71. It was suggested that the Carpentier ring or calcified annulus produces the narrowing of the mitroaortic angle [l] and prevents the normal systolic decrease in the anteroposterior size of the mitral annulus and its subsequent posterior movement [MI.Postoperatively, left ventricular dimension as well as outflow tract dimension decreased and the thickness of the interventricular septum increased, but no asymmetric septa1 hypertrophy was present [4]. Abrupt reduction of left ventricular volume might indicate SAM of the mitral valve as well as LVOT narrowing.
1. Mihaileanu S, Marino JP, Chauvaud S, et al. Left ventricular outflow obstruction after mitral valve repair (Carpentier's 2.
3.
4.
5. 6.
7. 8.
technique): proposed mechanisms of disease. Circulation 1988;78(Suppl1):78-84. Kronzon I, Cohen ML, Winer HE, Colvin SB. Left ventricular outflow obstruction: a complication of mitral valvuloplasty. J Am Coll Cardiol 1984;4825-8. Galler M, Kronzon I, Slater J, et al. Long-term follow-up after mitral valve reconstruction: incidence of postoperative left ventricular outflow obstruction. Circulation 1986;74(Suppl1): 99-103. Schiavone WA, Cosgrove DM, Lever HM, Stewart WJ,Salcedo F.E. Long-term follow-up of patients with left ventricular outflow tract obstruction after Carpentier ring mitral valvuloplasty. Circulation 1988;78(Suppl1):6&5. Kawame K, Ichikawa H, Kosakai Y, Ohara K,Kitoh Y, Fujita T. Replacement of chordae tendineae with FIFE suture for mitral valve prolapse. Jpn J Cardiovasc Surg 1990;1963W. Lindvall K, Herrlin B. Mitral annulus calcification, systolic anterior motion of the anterior mitral leaflet and outflow obstruction in two patients without hypertrophic cardiomyopathy. Acta Med %and 1981;209:513-8. Slater J, Kronzon I, Cohen ML. Left ventricular outflow tract anatomy in patients with mitral annular calcification [Abstract]. Chest 1984;86:315.
Waggoner AD, Perez JE,Barzilai B, Rosenbloom M, Eaton MH, Cox JL. Left ventricular obstruction resulting from insertion of mitral prostheses leaving the native leaflets intact: adverse clinical outcome in seven patients. Am Heart J 1991; 122:48%7.