J
THoRAc CARDIOVASC SURG
86:742·745, 1983
Type I left ventricular rupture after mitral valve replacement Rupture of the left ventricle in the atrioventricular (A V) groove is a rare and usually fatal complication of mitral valve replacement (MVR). The successful repair of a delayed type I left ventricular rupture is described. The technique of repair is described, the literature reviewed, and three further cases from the authors' experience are reported.
R. Devineni, M.D., F.R.C.S.(C), and F. N. McKenzie, M.D., F.R.C.S.(C), London, Ontario, Canada
In
1967, Roberts and Morrow] described the fatal complication of rupture of the posterior left ventricular wall after mitral valve replacement (MVR) in two cases among 64 autopsies performed on patients who had undergone cardiac valve replacement. In the past decade several reports have appeared outlining the possible causes, preventive measures, and techniques of repair of this complication." Treasure and associates' suggested classification of these ruptures into type I, located in the posterior atrioventricular groove, and type II, located in the midportion of the posterior left ventricle. Recently, a type III classification has been proposed for ruptures located midway between type I and II sites.' Each type can be further divided according to time of diagnosis into early (intraoperative diagnosis) and delayed lesions (diagnosis made at some time postoperatively). To our knowledge, successful repair of a delayed type I rupture has not been previously described.
Case report A 55-year-old woman underwent MVR for dominant post-rheumatic mitral stenosis. There was moderate calcification of the mitral cusps but not of the anulus. Cold cardioplegic arrest with systemic hypothermia to 30° C was used. The valve was cleanly excised leaving a 2 mm rim of anulus and replaced with a 27 mm Carpentier-Edwards xenograft attached with interrupted, buttressed, 2-0 Ethibond sutures with the pledgets on the ventricular aspect. The valve was seated easily and no From the Division of Cardiovascular and Thoracic Surgery, University Hospital, London, Ontario, Canada. Received for publication Dec. 29, 1982. Accepted for publication March 8, 1983. Address for reprints: Dr. F. N. McKenzie, University Hospital, P.O. Box 5339, Terminal "A," London, Ontario, Canada N6A 5A5.
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problems were encountered in weaning the patient after 65 minutes of cardiopulmonary bypass. A temporary flexiblevent had been positioned across the mitral xenograft. The heart was gently, manually elevated to de-aerate the left ventricle through the apex. Complete hemostasis was obtained without difficulty. AU vital signs were stable in the intensive care unit (lCU) for 1 hour. She then started bleeding profusely through the mediastinal drains, 1,500 mI of blood draining in 15 minutes and the systolic blood pressure dropping to 50 mm Hg. Rapid replacement of volume maintained the blood pressure around 70 mm Hg while the sternotomy was reopened in the ICU. The source of bleeding was identified on the posterolateral aspect of the left ventricle and some control was obtained by finger pressure while the patient was quickly returned to the operating room. Femoral-femoral bypass was instituted and the left ventricle was decompressed with an apical vent. Examination of the posterior left ventricle revealed a large spurting hematoma in the region of the atrioventricular (AV) groove. The hematoma was partially evacuated in an attempt to localize the tear (Fig. 1), which extended for 3 em along the AV groove. Repair with several interrupted buttressed sutures was attempted but was clearly doomed to failure because of the friability of the left ventricular muscle in the AV groove. Overlying this area was a large left atrial appendage that had been previously ligated from within the left atrium. With the use of several buttressed 3-0 Prolene sutures, the left atrial appendage was sutured into and around the left ventricular defect to cover and tamponade the AV groove hematoma (Fig. 1). The area was packed with Surgicel and Avitene and a length of gauze packing. Only the skin was approximated. In the ICU the patient's condition remained stable and the mean blood pressure was rigidly controlled in the 60 to 70 mm Hg range with a nitroprusside infusion. She was returned to the operating room the next day for removal of the packing and, with hemostasis confirmed, the sternum was closed. Subsequently, the patient did well and was discharged on the tenth day. A two-dimensional echocardiogram before discharge showed a normal mitral prosthesis and left ventricular function. The electrocardiogram and enzyme studies did not show any evidence of an infarct to suggest injury to the circumflex coronary artery. At 6 months the patient remains
Volume 86 Number 5
Left ventricular rupture after MVR
November, 1983
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LEFT ATRIAL APPENlJAG£
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Fig. I. Diagrams showing a tear in the atrioventricular groove following mitral valve replacement, with hematoma and hemorrhage around the coronary sinus and circumflex artery. Technique of repair using the left atrial appendage is illustrated.
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Fig. 2. Diagrams illustrating the various types of left ventricular rupture following mitral valve replacement and a possible etiologic factor in type III rupture. fully active, with normal left ventricular contour and function on echocardiography.
Discussion A review of the 62 cases reported in the literature shows that a type I left ventricular rupture can occur with any type of prosthesis, whereas a type II rupture is more common with a high-profile and strut valve (Starr-Edwards, porcine, or pericardial valve). A type III rupture, occurring between the AV groove and the insertion of the papillary muscle,' is likely to be produced from the strut of a xenograft valve (Fig. 2). The majority of patients with this complication are women with dominant mitral stenosis.
Etiologic factors in type I rupture include extensive excision of a heavily calcified and fibrosed valve, use of too large a prosthesis, and placement of sutures deeply into the posterior left ventricular myocardium. As a precaution, attempts should not be made to remove large chunks of calcium from the anulus, and part of the posterior cusp may be left intact if it is fibrosed and adherent to the underlying left ventricular muscle. Injury to the circumflex coronary artery, either during MVR or during repair of the AV tear, has been reported." Too large a prosthesis may be a factor, especially in reoperations if the left atrium is adherent to the pericardium and excessive tension is applied to appose a small anulus to a large prosthesis.
The Journal of Thoracic and Cardiovascular Surgery
7 4 4 Devineni and McKenzie
Possible etiologic factors in type II and III ruptures include the use of a large high-profile prosthesis or strut valve in a small left ventricle, lifting the heart too abruptly and sharply to de-aerate the left ventricular apex, and traction on a rigid papillary muscle. On the basis of both morbid and operative anatomy of the mitral valve, we consider it unlikely that a type III rupture is related to the posterior chordae tendineae, as has been suggested." A more likely cause would be injury from the strut of a xenograft valve (Fig. 2). If the heart is elevated to expose the apex for de-aeration, a wise precaution would be to elevate both the left atrium and left ventricle with a hand behind the heart so as to avoid tilting only the left ventricle against the valve strut. A rigid-angled or rigid-tipped vent may injure the left ventricular wall and cause a hematoma and rupture. 5 A late complication has been the development of a false aneurysm at the site of rupture. I I, 12 This is a possibility even after successful repair of the primary tear. Left ventricular rupture following MVR has a high mortality, about 65%. Intraoperative type I rupture (55% of total) has a mortality of 45% and type II rupture a mortality of 35%. There has been no report of survival in the delayed rupture group. In 1977, while discussing a paper by Bjork, Henze, and Rodriguez on this subject, Rainer" mentioned a survivor of a delayed type II rupture. The prognosis is best for the early, intraoperative left ventricular ruptures, for early recognition is essential. Type II ruptures can best be dealt with by placing Teflon-buttressed sutures through healthy myocardium. External Dacron patch closure has been used successfully." Ideally, repair should be undertaken on a relaxed, empty left ventricle; thus cardiopulmonary bypass and a left ventricular vent are useful. Type I ruptures are more difficult to repair owing to difficulty in localizing the tear amid the hematoma. In the case reported, it was fortuitous that a large left atrial appendage overhanging the defect could be used to close the rupture. The cause of the rupture in this case is not clear. It is possible that the process started with a deep suture in the posterior anulus tearing through the left ventricular myocardium and anulus. One of us (R. D.) has encountered this complication in three other female patients. All three tears occurred in heavily calcified valves and were discovered intraoperatively during weaning from bypass. All were type I lesions and all were fatal. In the first case, as a fmal resort, the prosthetic valve (3M Starr-Edwards) was removed and repair attempted from within the left
atrium. Ventricular fibrillation and intermittent crossclamping of the aorta had been used. In the second patient, a 29 mm Carpentier-Edwards xenograft was used and the entire posterior AV groove had avulsed. Cold cardioplegic arrest had been used in this patient. A Lillehei-Kaster prosthesis had been used in the third patient, and there was a tear along the medial commissure where a large chunk of calcium had been excised. This procedure had been done on an empty beating heart at normothermia. It has been recommended that type I ruptures are better repaired from within the left atrium, if necessary removing the prosthesis and reimplanting it with large buttressed sutures.i' We used this approach in one case, but it was not successful. Once the left atrium and left ventricle separate at the AV groove, there may not be any strong tissue left to hold valve sutures. A type III injury may be more amenable to successful repair from inside the left ventricle as was reported by Miller, Johnson, and Ivey" in 1979 and by Celemin and associates14 in 1982. Left ventricular rupture following MVR is encountered more often than reported, with an approximate incidence of 0.5% to 2%. The prognosis is ominous, .particularly that of the delayed type. With certain precautions, the risk of this complication can be minimized. Careful excision of the valve, particularly the posterior leaflet, using a properly sized valve, limiting the sutures to the anulus only, avoiding excessive tension on the papillary muscles during excision, and gentle elevation of both the left atrium and left ventricle for de-aeration are some worthwhile precautions.
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REFERENCES Roberts WC, Morrow AG: Causes of early postoperative death following cardiac valve replacement. Clinico-pathologic correlations in 64 patients studied at necropsy. J THORAC CARDIOVASC SURG 54:422-437, 1967 MacVaugh H, Joyner CR, Pierce WS, Johnson J: Repair of subvalvular left ventricular aneurysm occurring as a complication of mitral valve replacement. J THoRAe CARDIOVASC SURG 58:291-295, 1969 MacVaugh H III, Joyner CR, Johnson J: Unusual complications during mitral valve replacement in the presence of calcification of the annulus. Ann Thorac Surg 11:336342, 1971 Treasure RL, Rainer WG, Strevey TE, Sadler TR: Intraoperative left ventricular rupture associated with mitral valve replacement, Chest 66:511-514, 1974 Chi S, Beshore R, Gonzales-Lavin L: Left ventricular wall rupture after mitral valve replacement. Report of successful repair in 2 patients. Ann Thorac Surg 22:380-382, 1976 Bjork VO, Henze A, Rodriguez L: Left ventricular
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rupture as a complication of mitral valve replacement. Surgical experience with eight cases and a review of the literature. J THORAC CARDIOVASC SURG 73:14-22, 1977 Zacharias A, Groves LK, Cheanvechai C, Loop FD, Effler DB: Rupture of the posterior wall of the left ventricle after mitral valve replacement. J THORAC CARDIOVASC SURG 69:259-263, 1975 Nili M, Salomon J, Haleri A, Schuchman E, Levy MJ: Left ventricular rupture after mitral valve replacement. Scand J Thorac Cardiovasc Surg 15:235-238, 1981 Nunez L, Gil-Aguado M, Cerron M, Celemin D: Delayed rupture of the left ventricle after mitral valve replacement with bioprosthesis. Ann Thorac Surg 27:465-467, 1979 Miller DW Jr, Johnson DD, Ivey TD: Does preservation of the posterior chordae tendineae enhance survival during
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mitral valve replacement? Ann Thorac Surg 28:22-27, 1979 Sharratt GP, Ross JK, Monro JL, Johnson AM: Intraoperative left ventricular perforation with false aneurysm formation. Br Heart J 38:1154-1159, 1976 Diethrich EB, Koopot R, Kinard SA: Pseudoaneurysm of atrioventricular groove. A late complication of mitral valve replacement. J THORAC CARDIOVASC SURG 74:47-50, 1977 Rainer WG: Discussion of Bjork et al" Celemin D, Nunez L, Gil-Aguado M, Larrea JL: Intraventricular patch repair of left ventricular rupture following mitral valve replacement. New technique. Ann Thorae Surg 33:638-640, 1982
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