Anesth Analg 2007;104:498-499
© 2007 International Anesthesia Research Society
doi: 10.1213/01.ane.0000255072.01863.34
CARDIOVASCULAR ANESTHESIA
A Rare Cause for Severe Mitral Regurgitation After Mitral Valve Replacement
Daniel Bolliger, MD*,
Franziska Bernet, MD
,
Miodrag Filipovic, MD*, and
Manfred D. Seeberger, MD*
From the *Department of Anesthesia and Division of Cardio-Thoracic Surgery, University of Basel Hospital, Basel, Switzerland.
Address correspondence and reprint requests to Daniel Bolliger, MD, Department of Anesthesia, University of Basel Hospital, CH 4031 Basel, Switzerland. Address e-mail to dabolliger{at}uhbs.ch.
A 39-yr-old man with a history of biventricular heart failure presented for mitral and aortic valve replacement surgery. Mediastinal Hodgkin’s disease in his youth had been successfully treated by radiotherapy, but it resulted in a cardiomyopathy with calcification of the pericardium, myocardium, mitral valve, and aortic valve. Preoperative transesophageal echocardiography (TEE) revealed the following: severe mitral and aortic stenoses with mean gradients of 9 mm Hg and 50 mm Hg, respectively; mitral valve area 1.0 cm2; aortic valve area 1.1 cm2; moderate- severe mitral and aortic insufficiency, an estimated systolic pulmonary artery pressure of 55 mm Hg. Both left and right ventricular functions were visually estimated to be normal. Coronary angiography showed no relevant coronary artery disease.
The patient underwent aortic and mitral valve replacements with bileaflet mechanical prostheses. After separation from cardiopulmonary bypass (CPB), the patient’s hemodynamics could not be stabilized, despite the administration of milrinone, epinephrine, and norepinephrine. TEE showed moderately impaired right ventricular function, whereas segmental and global left ventricular systolic functions were estimated as normal in the transgastric short-axis view. In the midesophageal views, the aortic valve prosthesis function was normal. In contrast, TEE analysis of the mitral valve prosthesis revealed severe regurgitation caused by immobilization of a valve leaflet in the open position [Figs. 1 and 2 (Please see video loops available at www.anesthesia-analgesia.org)]. The mitral valve prosthesis was initially inserted in an antianatomical position (the hinge line of the prosthetic valve was perpendicular to the medial-lateral orientation of the native commissural line). After reestablishing CPB and cardioplegic arrest, normal valve prosthesis function was achieved by a 90-degree rotation of the prosthesis. A structure responsible for obstructing leaflet motion could not be identified. The patient was successfully weaned from CPB using vasopressor and inotropic drug support, along with inhaled nitric oxide, to treat pulmonary arterial hypertension. Both left and right ventricular functions were now moderately-to-severely impaired. The postoperative course was complicated by persisting pulmonary hypertension, severe right ventricular failure, and renal failure leading to death days after surgery.
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Figure 1. Failure of prosthesis closure caused by a prosthesis leaflet immobilized in the open position. Midesophageal long-axis view. LA = Left atrium; LV = left ventricle.
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Figure 2. Color-flow imaging showed a severe mitral prosthetic regurgitation caused by failure of prosthesis closure. Midesophageal 2-chamber view. LA = Left atrium; LV = left ventricle.
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Immobilization of prosthetic valve leaflets is a rare complication of mitral valve replacement surgery (1,2). The most frequent cause for this complication is interference of valve closure because of remnants of the subvalvular apparatus, but in many instances the etiology of this abnormality cannot be identified (2,3). Normal valve function is restored by further tissue resection, by a 90-degree rotation of the valve prosthesis, or by both (1–3). More common, failure of prosthetic closure is a late complication after mitral valve replacement caused by thrombus or pannus formation. Although determination of mitral regurgitation can be impaired by prosthetic shadowing or tachycardia, previous reports, and the presented case, illustrate the value of intraoperative TEE to immediately identify the abnormality as a cause for hemodynamic instability after valve replacement surgery.
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Footnotes
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Accepted for publication November 9, 2006.
This article has supplementary material on the Web site: www.anesthesia-analgesia.org.
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REFERENCES
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- Fujii H, Suehiro S, Shibata T, et al. Value of intraoperative transesophageal echocardiography in preventing serious complications during valvular surgery. A report of four cases. J Heart Valve Dis 2002;11:135–8.[Web of Science][Medline]
- Shapira Y, Vaturi M, Weisenberg DE, et al. Impact of intraoperative transesophageal echocardiography in patients undergoing valve replacement. Ann Thorac Surg 2004;78:579–83.[Abstract/Free Full Text]
- Jaggers J, Chetham PM, Kinnard TL, Fullerton DA. Intraoperative prosthetic valve dysfunction: detection by transesophageal echocardiography. Ann Thorac Surg 1995;59:755–7.[Abstract/Free Full Text]
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