Effect of Mitral Valve Repair for Mitral of Left Ventricular Mass
Valve Prolapse on Regression
Marc D. Tischler, MD, Kyle A. Cooper, MD, Robert W. Battle, MD, and Bruce J. Leavitt, MD itral regurgitation (MR) representsa condition of M chronic volume overload in which the left ventricle developseccentric hypertrophy to accommodatea significantly increased end-diastolic left ventricular (LV) volume without significant increasesin filling pressuresor diastolic sarcomere length. I** LV mass is significantly greater in patients with MR than in normal subjects.*In patients with chronic MR and moderate LV dilatation, there is regression of LV hypertrophy when the mitral valve is replaced.’ Interpretation of changesin LV volumesand massafter valve replacementmay be confounded by alterations in wall stressspecifically related to disruption of the mitral apparatusand becauseall prosthetic valvesare at least minimally obstructive. Comparedwith replacement,mitral valve repair may result in better preservation of LV function by retaining the tethering effect of the chordal apparatus and moderating the increasein systolic wall stressthat occurs after relief of MR.3,4The present quantitative echocardiographic investigation examines the effect of mitral valve repair on LV massand volume in patients with severe,isolated MR. BetweenMarch 1989 and September1991,8patients underwent mitral valve repair for isolated MR secondary to mitral valve prolapse. No patient had mitral stenosis, or aortic valvular or coronary artery disease. All repairs were performed by median sternotomy and included a combination of Carpentier techniques deemednecessaryat the time of operation, as well as a rigid Carpentier annuloplasty ring. Echocardiographic examinations wereperformed 2.0 f 1.2 months (range I to 3) before surgery. Follow-up examinations wereperformed 10.0 f 3.4 months (range 4 to 14) after surgery. Echocardiographic examinations were performed in the left lateral decubitus position using an Acuson phased-array ultrasonoscope device (Acuson XP-5) with a 2.5 MHz transducer. Parasternal short- and long-axis, and apical 2- and I-chamber images were recorded. All echocardiograms were analyzed in random sequenceby I investigator unawareof the severity of postoperative MR and all other clinical information, using a Microsonics Image- Vue Workstation (Nova Microsonits Inc., Mahwah, New Jersey). Three to 5 cardiac cycles were digitized at end-systole (time of smallest cavity area) and end-diastole (R-wave peak). LV mass, endsystolic, end-diastolic and stroke volumes, and ejection fraction were calculated as previously described.5-7 From the Cardiology Unit, Division of Thoracic and Cardiac Surgery, Medical Center Hospital of Vermont, Burlington, Vermont 05401,and University of Vermont Schoolof Medicine, Burlington, Vermont. Manuscript weived April 9.1992; revisedmanuscriptreceivedand accepted June 10, 1992.
1216
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 70
All data arepresentedas mean f 1 SD. Comparisons betweenpatients before and after mitral valve repair were performed with the paired Student’s t test (2tailed). Differences were considered significant if the null hypothesis could be rejected at the 0.05probability level. All 8patients (4 womenand 4 men,meanage55 f 18 years, range 31 to 78) had severeMR. Three patients werein New York Heart Associationfunctional classZV, 4 in class III, and 1 in class I at the time of surgery. Before surgery, all 8 patients had Doppler and color Doppler evidenceof severe(4+/4+) MR. At the time of thefollow-up tramthoracic examination, 2 patients had no detectableMR, 5 had trace (1+/4+) MR, and 1 had mild to moderate (2+/4+) MR. Individual responsesto mitral valve repair are presentedin Table I. For the entire cohort, LVend-diastolic volume index decreasedfrom 92 f 17 to 71 f 11 ml/m2 (p = O.Ol), whereasend-systolic volume index was not changed (33 f 15 us 32 f 13 ml/m2; p = 0.90). LV ejectionfraction decreased,but not significantly (64 f 15% to 55 f 16%;p = 0.28). LV mass index decreased from 161 f 30 to 132 f 21 drn2 (p = 0.04). In this study, 8 patients were examined before and after mitral valve repair for isolated MR to test the hypothesisthat relief of significant volume overload would lead to a reduction in LV massand that this reduction would occur despite removal of the low-impedanceejection pathway to the left atrium. The results indicate that successfulmitral valve repair is followed by a significant reduction in LV mass,which is accompaniedby reductions in both LV end-diastolic and stroke volumes. It was recently demonstratedthat LV massincreases in association with small increasesin LV volume after balloon mitral valvuloplasty.8Thus, it appearsreasonable that correction of volume overloadwould lead to a reducTABLE I Left Ventricular (LV) Volume and Mass Indexes Before and After Mitral Valve Repair LV End-Diastolic Volume Index
l-v End-Systolic Volume
(ml/m?
Index
LV Mass
Index
(g/m21
(ml/m2)
Pt.
Before
After
Before
After
Before
After
1 2 3 4 5 6 7 8
112 64 109 81 82 102 81 102
67 44 77 71 77 78 74 76
38 15 53 24 28 22 55 28
42 12 49 29 17 27 44 36
149 146 142 156 150 199 215 132
115 134 113
NOVEMBER 1, 1992
139 127 147 173 110
tion in LV mass.In MR, however,the increaseddiastolic for removal of the low-pressureejection pathway into the load is at least partially offset by reduced systolic load as left atrium as a determinant of LV mass. the ventricle ejectsinto the low-pressureleft atrium, enabling LV systolic pressureto decreasemore rapidly for any given preload.3 Elimination of this low-resistance outlet by either mitral valve repair or replacementwould 1. Schuler G, PetersonKL, JohnsonA. FrancisG, DennishG, Utley J, Daily PO, be expectedto lead to increasesin afterload, which may in Ashburn W, RossJ. Temporal responseof left ventricular performanceto mitral surgery. Circulation 1979;59:1218-1231. turn lead to increasesin LV end-systolicvolume and wall valve 2. WisenbaughT. Does normal pump function belie muscledysfunction in pastress.9JoIn valve replacement,this complexity is further tients with chronic severemitral regurgitation? Circu/arion 1988;77:515-525. 3. Bonchek LI, Olinger GN, Siegal R, Tresch D, Keelan M. Left ventricular compoundedby disruption of the mitral valve apparatus performance after mitral reconstructionfor mitral regurgitation. J Thoroc Carand the obstructive properties of prosthetic valves.Other diovasc Surg 1984;88:122-127. investigators using multigated blood pool imaging’ 1 and 4. LessanaA, Herreman F, Bofferty C, CosmaH, Guerin F, Kara M, Degeorges M. Hemodynamic and cineangiographicstudy before and after mitral valvulo M-mode echocardiographic techniques’ found that end- plasty (Carpentier’s Technique). Circularion 1981;64:II-195-11-202. systolic volume did not change appreciably after mitral 5. Reichek N, Helak J, Plappert T, St. John Sutton M, Weher KT. Anatomic valve replacement for MR. This absenceof change in validation of left ventricular massestimatesfrom clinical two-dimensionalechoinitial results. Circulation 1983;67:348-352. end-systolicvolume may result from removal of the low- cardiography: 6. St. John Sutton M, Plappert T, SpiegelA, Raichlen J, Douglas P, Reichek N, resistancepathway being balanced by a reduction in af- EdmundsL. Early postoperativechangesin left ventricular chambersize,archiand function in aortic stenosisand aortic regurgitation and their relation terload due to reduced chamber size.‘* Lessana et al4 tecture, to intraoperative changesin afterload: a prospectivetwodimensional echocardiostudied 26 patients angiographically (14 with isolated graphic study. Circulation 1987;76:77-89. MR, and 12 with mixed stenosisand regurgitation) be- 7. Schiller NB, Acquetella H, Ports TA, Drew D, Goerke J, Ringhertz H, NH, BrundageB, Botvinick EH, Boswell R, CarlssonE, Parmley WH. fore and after mitral valve repair for MR and found Silverman Left ventricular volume from paired biplane two-dimensionalechocardiography. significant reductions in LV end-systolic volume index Circulation 1979;60:547-555. after surgery. Similar results have beenreported by Bon- 8. Tischler MD, St. John Sutton M, Bitt1 JA, Parker JD. Effects of percutaneous valvuloplasty on left ventricular mass and volume, Am J Cardiol chek et a1.3Thus, mitral valve repair may result in lower mitral 1991;68:94C-944. end-systolicwall stressthan doesvalve replacement,per- 9. Wong CYH, Spotnitz HM. Systolic and diastolic propertiesof the humanleft during valve replacementfor chronic mitral regurgitation. Am J Cardiol haps becauseof better preservation of LV function.3J2 ventricle 1981;47:40-50. In the present investigation, mitral valve reconstruc- 10. Rankin JS, Nicholas LM, KouchoukosNT. Experimental mitral regurgitation for MR led to a significant reduction in LV end- tion. Effects on left ventricular function before and after elimination of chronic in the dog. J Thorac Cardiouosc Surg 1975;70:478-488, diastolic volume accompaniedby a significant reduction regurgitation il. BoucherCA, Bingham JB, GsbakkenMD, Okada RD, StraussHW. Block in LV mass. The data indicate that correction of MR PC, Levine FH, Phillips HR. Pohost GM. Early changesin left ventricular size leads to important regressionof hypertrophy in patients and function after correction of left ventricular volume overload. Am J Cardioi 1981;47:991-1004. undergoing mitral valve repair and suggestthat the re- 12. BonchekL. Correction of mitral valve diseasewithout valve replacement.Am duction in end-diastolic volume more than compensates Heart J 1982;104:865-868.
Activation of the Coagulation and Sinus Rhythm
System in Women with Mitral
Stenosis
Syed M. Jafri, MD, Luis Caceres, MD, Howard S. Rosman, MD, Tsunenori Ozawa, MD, Eberhard Mammen, MD, Micheal Lesch, MD, and Sidney Goldstein, MD ystemic embolism is a frequent complication in miS tral stenosis(MS).’ Its incidence increaseswith age and the presence of atria1 fibrillation.2,3 Although pa-
risk. Recently developedassaysare capable of detecting peptides released during activation of the coagulation cascadeand thrombogenesis.5*6 Measurement of these tients with MS and sinusrhythm can alsodevelopsystem- markers may be used to identify patients at risk for ic emboli, the frequency of this event is lower in these thromboembolism.This study was performed to test the patients than in those with atria1 fibrillation.1 Patients hypothesisthat there is activation of coagulation in pawith MS and atria1 fibrillation are consideredat high risk tients with MS and sinus rhythm. Fibrinolytic activity of systemic embolism and require anticoagulant thera- was assayedby measuring D-dimers that are generated p~.~ Because patients with MS and sinus rhythm are from plasmic degradation of cross-linkedfibrin.5 Thromconsideredat low risk for systemicembolism, anticoagu- bin activation was assayed by measuring thrombinlant therapy is not routinely recommended.4It is desir- antithrombin III complexes6 able to identify patients with MS in sinusrhythm who are Patients with MS included 9 women (mean age 52 f at high risk for systemicembolism. There are no reliable 9 years). Clinical diagnoses of MS was confirmed by 2clinical or laboratory parametersavailable to stratify this dimensional echocardiographic and Doppler studies. From the Division of Cardiovascular Medicine, Henry Ford Hospital, Heart and Vascular Institute, 2799 West Grand Boulevard, Detroit, Michigan 48202. Manuscript received March 4, 1992; revised manuscript received and accepted June 2.1992.
The mean mitral valve area for the study group was reduced to I .9 f 0.6 cm2 (Table I). These patients did not have a history of systemic emboli. No patient was receiving antiplatelet or anticoagulant agents. Criteria for exclusion from the study were mild mitral regurgita-
BRIEF REPORTS
1217
Valve Prolapse on Regression
Marc D. Tischler, MD, Kyle A. Cooper, MD, Robert W. Battle, MD, and Bruce J. Leavitt, MD itral regurgitation (MR) representsa condition of M chronic volume overload in which the left ventricle developseccentric hypertrophy to accommodatea significantly increased end-diastolic left ventricular (LV) volume without significant increasesin filling pressuresor diastolic sarcomere length. I** LV mass is significantly greater in patients with MR than in normal subjects.*In patients with chronic MR and moderate LV dilatation, there is regression of LV hypertrophy when the mitral valve is replaced.’ Interpretation of changesin LV volumesand massafter valve replacementmay be confounded by alterations in wall stressspecifically related to disruption of the mitral apparatusand becauseall prosthetic valvesare at least minimally obstructive. Comparedwith replacement,mitral valve repair may result in better preservation of LV function by retaining the tethering effect of the chordal apparatus and moderating the increasein systolic wall stressthat occurs after relief of MR.3,4The present quantitative echocardiographic investigation examines the effect of mitral valve repair on LV massand volume in patients with severe,isolated MR. BetweenMarch 1989 and September1991,8patients underwent mitral valve repair for isolated MR secondary to mitral valve prolapse. No patient had mitral stenosis, or aortic valvular or coronary artery disease. All repairs were performed by median sternotomy and included a combination of Carpentier techniques deemednecessaryat the time of operation, as well as a rigid Carpentier annuloplasty ring. Echocardiographic examinations wereperformed 2.0 f 1.2 months (range I to 3) before surgery. Follow-up examinations wereperformed 10.0 f 3.4 months (range 4 to 14) after surgery. Echocardiographic examinations were performed in the left lateral decubitus position using an Acuson phased-array ultrasonoscope device (Acuson XP-5) with a 2.5 MHz transducer. Parasternal short- and long-axis, and apical 2- and I-chamber images were recorded. All echocardiograms were analyzed in random sequenceby I investigator unawareof the severity of postoperative MR and all other clinical information, using a Microsonics Image- Vue Workstation (Nova Microsonits Inc., Mahwah, New Jersey). Three to 5 cardiac cycles were digitized at end-systole (time of smallest cavity area) and end-diastole (R-wave peak). LV mass, endsystolic, end-diastolic and stroke volumes, and ejection fraction were calculated as previously described.5-7 From the Cardiology Unit, Division of Thoracic and Cardiac Surgery, Medical Center Hospital of Vermont, Burlington, Vermont 05401,and University of Vermont Schoolof Medicine, Burlington, Vermont. Manuscript weived April 9.1992; revisedmanuscriptreceivedand accepted June 10, 1992.
1216
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 70
All data arepresentedas mean f 1 SD. Comparisons betweenpatients before and after mitral valve repair were performed with the paired Student’s t test (2tailed). Differences were considered significant if the null hypothesis could be rejected at the 0.05probability level. All 8patients (4 womenand 4 men,meanage55 f 18 years, range 31 to 78) had severeMR. Three patients werein New York Heart Associationfunctional classZV, 4 in class III, and 1 in class I at the time of surgery. Before surgery, all 8 patients had Doppler and color Doppler evidenceof severe(4+/4+) MR. At the time of thefollow-up tramthoracic examination, 2 patients had no detectableMR, 5 had trace (1+/4+) MR, and 1 had mild to moderate (2+/4+) MR. Individual responsesto mitral valve repair are presentedin Table I. For the entire cohort, LVend-diastolic volume index decreasedfrom 92 f 17 to 71 f 11 ml/m2 (p = O.Ol), whereasend-systolic volume index was not changed (33 f 15 us 32 f 13 ml/m2; p = 0.90). LV ejectionfraction decreased,but not significantly (64 f 15% to 55 f 16%;p = 0.28). LV mass index decreased from 161 f 30 to 132 f 21 drn2 (p = 0.04). In this study, 8 patients were examined before and after mitral valve repair for isolated MR to test the hypothesisthat relief of significant volume overload would lead to a reduction in LV massand that this reduction would occur despite removal of the low-impedanceejection pathway to the left atrium. The results indicate that successfulmitral valve repair is followed by a significant reduction in LV mass,which is accompaniedby reductions in both LV end-diastolic and stroke volumes. It was recently demonstratedthat LV massincreases in association with small increasesin LV volume after balloon mitral valvuloplasty.8Thus, it appearsreasonable that correction of volume overloadwould lead to a reducTABLE I Left Ventricular (LV) Volume and Mass Indexes Before and After Mitral Valve Repair LV End-Diastolic Volume Index
l-v End-Systolic Volume
(ml/m?
Index
LV Mass
Index
(g/m21
(ml/m2)
Pt.
Before
After
Before
After
Before
After
1 2 3 4 5 6 7 8
112 64 109 81 82 102 81 102
67 44 77 71 77 78 74 76
38 15 53 24 28 22 55 28
42 12 49 29 17 27 44 36
149 146 142 156 150 199 215 132
115 134 113
NOVEMBER 1, 1992
139 127 147 173 110
tion in LV mass.In MR, however,the increaseddiastolic for removal of the low-pressureejection pathway into the load is at least partially offset by reduced systolic load as left atrium as a determinant of LV mass. the ventricle ejectsinto the low-pressureleft atrium, enabling LV systolic pressureto decreasemore rapidly for any given preload.3 Elimination of this low-resistance outlet by either mitral valve repair or replacementwould 1. Schuler G, PetersonKL, JohnsonA. FrancisG, DennishG, Utley J, Daily PO, be expectedto lead to increasesin afterload, which may in Ashburn W, RossJ. Temporal responseof left ventricular performanceto mitral surgery. Circulation 1979;59:1218-1231. turn lead to increasesin LV end-systolicvolume and wall valve 2. WisenbaughT. Does normal pump function belie muscledysfunction in pastress.9JoIn valve replacement,this complexity is further tients with chronic severemitral regurgitation? Circu/arion 1988;77:515-525. 3. Bonchek LI, Olinger GN, Siegal R, Tresch D, Keelan M. Left ventricular compoundedby disruption of the mitral valve apparatus performance after mitral reconstructionfor mitral regurgitation. J Thoroc Carand the obstructive properties of prosthetic valves.Other diovasc Surg 1984;88:122-127. investigators using multigated blood pool imaging’ 1 and 4. LessanaA, Herreman F, Bofferty C, CosmaH, Guerin F, Kara M, Degeorges M. Hemodynamic and cineangiographicstudy before and after mitral valvulo M-mode echocardiographic techniques’ found that end- plasty (Carpentier’s Technique). Circularion 1981;64:II-195-11-202. systolic volume did not change appreciably after mitral 5. Reichek N, Helak J, Plappert T, St. John Sutton M, Weher KT. Anatomic valve replacement for MR. This absenceof change in validation of left ventricular massestimatesfrom clinical two-dimensionalechoinitial results. Circulation 1983;67:348-352. end-systolicvolume may result from removal of the low- cardiography: 6. St. John Sutton M, Plappert T, SpiegelA, Raichlen J, Douglas P, Reichek N, resistancepathway being balanced by a reduction in af- EdmundsL. Early postoperativechangesin left ventricular chambersize,archiand function in aortic stenosisand aortic regurgitation and their relation terload due to reduced chamber size.‘* Lessana et al4 tecture, to intraoperative changesin afterload: a prospectivetwodimensional echocardiostudied 26 patients angiographically (14 with isolated graphic study. Circulation 1987;76:77-89. MR, and 12 with mixed stenosisand regurgitation) be- 7. Schiller NB, Acquetella H, Ports TA, Drew D, Goerke J, Ringhertz H, NH, BrundageB, Botvinick EH, Boswell R, CarlssonE, Parmley WH. fore and after mitral valve repair for MR and found Silverman Left ventricular volume from paired biplane two-dimensionalechocardiography. significant reductions in LV end-systolic volume index Circulation 1979;60:547-555. after surgery. Similar results have beenreported by Bon- 8. Tischler MD, St. John Sutton M, Bitt1 JA, Parker JD. Effects of percutaneous valvuloplasty on left ventricular mass and volume, Am J Cardiol chek et a1.3Thus, mitral valve repair may result in lower mitral 1991;68:94C-944. end-systolicwall stressthan doesvalve replacement,per- 9. Wong CYH, Spotnitz HM. Systolic and diastolic propertiesof the humanleft during valve replacementfor chronic mitral regurgitation. Am J Cardiol haps becauseof better preservation of LV function.3J2 ventricle 1981;47:40-50. In the present investigation, mitral valve reconstruc- 10. Rankin JS, Nicholas LM, KouchoukosNT. Experimental mitral regurgitation for MR led to a significant reduction in LV end- tion. Effects on left ventricular function before and after elimination of chronic in the dog. J Thorac Cardiouosc Surg 1975;70:478-488, diastolic volume accompaniedby a significant reduction regurgitation il. BoucherCA, Bingham JB, GsbakkenMD, Okada RD, StraussHW. Block in LV mass. The data indicate that correction of MR PC, Levine FH, Phillips HR. Pohost GM. Early changesin left ventricular size leads to important regressionof hypertrophy in patients and function after correction of left ventricular volume overload. Am J Cardioi 1981;47:991-1004. undergoing mitral valve repair and suggestthat the re- 12. BonchekL. Correction of mitral valve diseasewithout valve replacement.Am duction in end-diastolic volume more than compensates Heart J 1982;104:865-868.
Activation of the Coagulation and Sinus Rhythm
System in Women with Mitral
Stenosis
Syed M. Jafri, MD, Luis Caceres, MD, Howard S. Rosman, MD, Tsunenori Ozawa, MD, Eberhard Mammen, MD, Micheal Lesch, MD, and Sidney Goldstein, MD ystemic embolism is a frequent complication in miS tral stenosis(MS).’ Its incidence increaseswith age and the presence of atria1 fibrillation.2,3 Although pa-
risk. Recently developedassaysare capable of detecting peptides released during activation of the coagulation cascadeand thrombogenesis.5*6 Measurement of these tients with MS and sinusrhythm can alsodevelopsystem- markers may be used to identify patients at risk for ic emboli, the frequency of this event is lower in these thromboembolism.This study was performed to test the patients than in those with atria1 fibrillation.1 Patients hypothesisthat there is activation of coagulation in pawith MS and atria1 fibrillation are consideredat high risk tients with MS and sinus rhythm. Fibrinolytic activity of systemic embolism and require anticoagulant thera- was assayedby measuring D-dimers that are generated p~.~ Because patients with MS and sinus rhythm are from plasmic degradation of cross-linkedfibrin.5 Thromconsideredat low risk for systemicembolism, anticoagu- bin activation was assayed by measuring thrombinlant therapy is not routinely recommended.4It is desir- antithrombin III complexes6 able to identify patients with MS in sinusrhythm who are Patients with MS included 9 women (mean age 52 f at high risk for systemicembolism. There are no reliable 9 years). Clinical diagnoses of MS was confirmed by 2clinical or laboratory parametersavailable to stratify this dimensional echocardiographic and Doppler studies. From the Division of Cardiovascular Medicine, Henry Ford Hospital, Heart and Vascular Institute, 2799 West Grand Boulevard, Detroit, Michigan 48202. Manuscript received March 4, 1992; revised manuscript received and accepted June 2.1992.
The mean mitral valve area for the study group was reduced to I .9 f 0.6 cm2 (Table I). These patients did not have a history of systemic emboli. No patient was receiving antiplatelet or anticoagulant agents. Criteria for exclusion from the study were mild mitral regurgita-
BRIEF REPORTS
1217
