Erratum

Abstract

A 57-yr-old woman presented to the hospital for further evaluation of recently diagnosed severe primary pulmonary hypertension. Her medical and surgical histories were significant for aortic valvuloplasty in 1961, a St. Jude aortic valve replacement in July 1998, and a subsequent reoperation for the placement of a bioprosthetic aortic valve in September 1998. A permanent pacemaker was placed in 1998 secondary to complete heart block. She experienced increasing shortness of breath, requiring home oxygen for exertion. She had no history of smoking or significant pulmonary history before this diagnosis. Ventilation/perfusion imaging and spiral computed tomography excluded pulmonary embolism. Cardiac catheterization revealed normal coronary arteries, pulmonary artery pressures of 109/42 mm Hg, and a pulmonary capillary wedge pressure of 40 mm Hg. Both transthoracic and transesophageal echocardiography examinations were performed after admission to the hospital. Based on these findings, she underwent a reoperation for placement of a Carpentier-Edwards pericardial mitral valve. The following preoperative and intraoperative transesophageal echocardiography images display the patient's pathology (Figs. 1 and 2) (video clip available at www.anesthesia-analgesia.org).Figure 1.: From this mid-esophageal 4-chamber view the mitral valve appears to be opening adequately at the annular level; however, the mitral valve assumes a “pear-shaped” configuration.Figure 2.: This still-frame image displays a continuous wave Doppler spectral profile representing severe mitral stenosis.The finding of a parachute mitral valve in an adult patient is extremely rare. Most patients are diagnosed in childhood with the pathologic complex known as Shone's Anomaly, which includes a parachute mitral valve and aortic coarctation (68% of patients), atrial septal defect (54% of patients), ventricular septal defect (46% of patients), aortic valve stenosis (32% of patients), subaortic stenosis (20% of patients), and left ventricular hypoplasia (19% of patients) (1). Based on analysis of embryonic specimens, Oosthoek et al. (2) concluded that the development of the anterolateral and posteromedial papillary muscles is disrupted between the 5th and 19th weeks of gestation, thereby forcing the embryonic predecessors of the papillary muscles to condense into a single muscle. This case effectively illustrates how a detailed transesophageal echocardiography examination can aid the physician in clinical decision-making process when presented with a diagnostic dilemma.