Ann Thorac Surg 2008;86:1994-1996. doi:10.1016/j.athoracsur.2008.05.005
© 2008 The Society of Thoracic Surgeons
Case Reports
Successful Surgical Management for Severe Mitral Regurgitation Unmasked After Pericardiectomy for Chronic Constrictive Pericarditis
Teruya Nakamura, MDa,*,
Takafumi Masai, MDa,
Takashi Yamauchi, MDa,
Takahiro Higuchi, MDa,
Hiroshi Ito, MDb,
Yuko Toyoshima, MDb,
Yoshiki Sawa, MDc
a Division of Cardiovascular Surgery, Sakurabashi-Watanabe Hospital, Osaka, Japan
b Division of Cardiology, Sakurabashi-Watanabe Hospital, Osaka, Japan
c Department of Surgery, Osaka University Graduate School of Medicine, Suita, Japan
Accepted for publication May 5, 2008.
* Address correspondence to Dr Nakamura, Division of Cardiovascular Surgery, Sakurabashi-Watanabe Hospital, 2-4-32 Umeda, Kita-Ward, Osaka, 530-0001, Japan (Email: teruyan{at}kure-nh.go.jp).
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Abstract
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A 78-year-old cachectic woman who previously had repair of atrial septal defect was admitted to the hospital for congestive heart failure. Cardiac workup revealed chronic constrictive pericarditis; no evidence of coronary or valvular disease was found. She underwent corrective surgery for pericardiectomy. Intraoperative transesophageal echocardiography after pericardiectomy demonstrated acute development of severe mitral regurgitation, which was not preoperatively observed. She eventually required mitral valve replacement and tricuspid valve repair after conservative management failed. She recovered from the operation and was discharged. We believe that this is the first report of successful surgical management of mitral regurgitation that developed acutely after pericardiectomy.
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Introduction
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Constrictive pericarditis is a chronic inflammatory process that leads to pericardial thickening and compression of the heart. The cause is idiopathic in the majority of cases, and in some cases, it includes acute pericarditis, infection, malignancy, radiation, rheumatoid disease, trauma, and previous cardiotomy [1]. Total pericardiectomy is the treatment of choice, which usually results in immediate relief of constriction and subsequently in improved hemodynamics without adverse sequelae [1, 2]. Here we report an unusual case of severe mitral regurgitation (MR) and cardiogenic shock, which was manifested acutely after pericardiectomy.
A 78-year-old woman was admitted to our hospital for history of malaise, shortness of breath, and leg edema that had been ongoing for a few months. Past medical and surgical history was significant for repair of atrial septal defect 7 years prior to the presentation, chronic obstructive pulmonary disease, and chronic renal insufficiency. Physical examination demonstrated a slender, markedly cachectic woman who appeared chronically ill. She had signs of right heart failure, including jugular venous distension, hepatomegaly, and pretibial edema. Chest auscultation revealed a coarse sound on breathing and no cardiac murmur. Electrocardiogram showed sinus rhythm and no evidence of myocardial ischemia. A chest roentgenogram showed cardiomegaly, pleural effusion, and pulmonary edema. Echocardiogram showed preserved left ventricular systolic function and pericardial thickening associated with diastolic ventricular dysfunction. There was only mild MR and tricuspid regurgitation (Fig 1A). Cardiac catheterization showed an elevated end-diastolic pressure (20 mm Hg) with a typical "square root sign," which strongly suggested constrictive pericarditis. There was no evidence of coronary artery disease.
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Fig 1. Transthoracic Doppler echocardiogram (A) before and (B) after pericardiectomy. Note that mitral regurgitation is mild preoperatively but is severe after pericardiectomy.
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She underwent "phrenic-to-phrenic" pericardiectomy with an inferoposterior pericardial release using cardiopulmonary bypass. A thickened pericardium was found all around the heart, especially around the left ventricle. Intraoperative transesophageal echocardiogram demonstrated acute development of MR. She was hemodynamically unstable, which necessitated inotropic support and insertion of an intra-aortic balloon pump. There was no dyssynergy on the left ventricular wall motion or ST-T change on electrocardiogram between pericardiectomy, suggesting that no ischemic event was involved. We elected not to operate on the mitral valve at that point, as the patient was so ill that she did not seem to be able to tolerate a further procedure.
Postoperatively intra-aortic balloon pump was removed, but she remained critically ill. Her condition progressively deteriorated, despite the optimal medical management. Serial echocardiograms showed worsening MR and tricuspid regurgitation with time (Fig 1B). A decision was made to proceed for another operation 3 weeks after the pericardiectomy. When the mitral valve was exposed we found that both leaflets as well as the subvalvular apparatus were calcified, and there were also commissural fusion and A2 prolapse. The mitral valve was replaced using a tissue valve and the tricuspid valve was repaired using an annuloplasty ring. Postoperatively, she remained in the intensive care unit for a long period of time, requiring prolonged inotropic support and ventilation. She slowly recovered and was transferred to a rehabilitation facility 3 months after the operation. Postoperative echocardiogram showed preserved left ventricular function and normal prosthetic valve function.
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Comment
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We believe that this is the first report of successful surgical management of severe MR and cardiogenic shock, which was manifested acutely after pericardiectomy. There are two previous literature reports describing MR after pericardiectomy in which the valve incompetence subsided in time and did not require operations [3, 4]. This case, however, was unique because the "rescue" operation was inevitable as optimal medical management failed to alleviate MR, and the patient's condition progressively deteriorated with cardiogenic shock and multiple organ dysfunction. At the time of the mitral valve operation, we carefully considered 2 options (ie, to repair or to replace the mitral valve). It is generally accepted that mitral repair is superior to valve replacement in terms of better early and long-term outcomes and lowering risk of thromboembolism [5]. Nevertheless, we elected to replace the mitral valve for the following reasons: first, the valve leaflets as well as the chords were severely calcified and there was some commissural fusion, and because the possibility of rheumatic disease could not be excluded in the operating room. Histologically, the valve demonstrated "severe degenerative change with severe calcification and hyalinization." Thus, it seemed that the valve disease would be best treated by valve replacement. Second, the patient would not have tolerated any further procedure if repair was not durable and MR recurred in a short period of time.
It is not clear why MR developed acutely after pericardiectomy. Although ischemic MR due to injury to the coronary arteries was a possibility, it was unlikely in this case based on electrocardiographic and echocardiographic findings. Buckingham and colleagues [3] suggested two hypotheses, in which change in the left ventricular geometry and shift of the papillary muscles caused insufficient coaptation of the mitral leaflets. Terada and colleagues [4] reported a serial assessment of the left ventricular wall motion by cardiac catheterization, and they suggested that increased mobility of the lateral wall, in conjunction with an increase in the left ventricular volume, might be one of the causes of the perioperative mitral valve dysfunction. These hypotheses explain why MR subsided once compensation for the altered ventricular wall motion occurred. In this case, however, the valve findings were consistent with a primary disease. MR can persist or even occur de novo after repair of atrial septal defect, possibly due to increase of preload to the left heart [6]. Moreover, the presence of constriction and resultant tamponade physiology potentially obscures the clinical manifestation of MR [7]. Based on the hypotheses previously noted, it is unlikely that conservative management would have controlled MR and led to a better outcome.
In conclusion, we report our experience of successful surgical management of acute MR after pericardiectomy. Although previous reports suggested that spontaneous remission can occur, surgery is a viable option, and the decision is made depending on clinical course. Surgery is also indicated if ehocardiographic findings suggest the primary valve disease.
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References
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- Bertog SC, Thambidorai SK, Parakh K, et al. Constrictive pericarditis: etiology and cause-specific survival after pericardiectomy Am Coll Cardiol 2004;43:1445-1452.[Abstract/Free Full Text]
- Chowdhury UK, Subramaniam GK, Kumar AS, et al. Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques Ann Thorac Surg 2006;81:522-529.[Abstract/Free Full Text]
- Buckingham Jr RE, Furnary AP, Weaver MT, Floten HS, Davis RF. Mitral insufficiency after pericardiectomy for constrictive pericarditis Ann Thorac Surg 1994;58:1171-1174.[Abstract]
- Terada Y, Mitsui T, Yamada S. Mitral regurgitation after pericardiectomy for constrictive pericarditis Jpn J Thorac Cardiovasc Surg 1999;47:27-30.[Medline]
- Shuhaiber J, Anderson RJ. Meta-analysis of clinical outcomes following surgical mitral valve repair or replacement Eur J Cardiothorac Surg 2007;31:267-275.[Abstract/Free Full Text]
- Speechly-Dick ME, John R, Pugsley WB, Sturridge MF, Swanton RH. Secundum atrial septal defect repair: long-term surgical outcome and the problem of late mitral regurgitation Postgrad Med J 1993;69:912-915.[Abstract/Free Full Text]
- Srichai MB, Casserly IP, Lever HM. Cardiac tamponade masking clinical presentation and hemodynamic effects of papillary muscle rupture after acute myocardial infarction J Am Soc Echocardiogr 2002;15:1000-1003.[Medline]
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Abstract
Introduction
