(Circulation. 2000;101:695.)
© 2000 American Heart Association, Inc.
Images in Cardiovascular Medicine |
From the University of Chicago Medical Center, Department of Medicine, Section of Cardiology, Chicago, Ill.
Correspondence to Roberto M. Lang, MD, University of Chicago Medical Center, 5841 S Maryland Ave, MC5084, Chicago, IL 60637. E-mail rlang{at}medicine.bsd.uchicago.edu
A54-year-old woman,
status postmitral valve repair for severe mitral
regurgitation secondary to mitral valve prolapse, was
admitted 7 weeks after surgery with shortness of breath and fatigue.
Hematological studies revealed a Coombs-negative hemolytic anemia
with a hematocrit of 17.1%, haptoglobin of <7.9 mg/dL (normal 51 to
192 mg/dL), LDH of 3165 U/L, total bilirubin of 6.8 mg/dL (indirect of
6.1 mg/dL), and a peripheral blood smear demonstrating
mechanical hemolysis with schistocytosis and red cell fragmentation
(arrows, Figure
, A). A
transesophageal echocardiogram revealed partial
dehiscence of the mitral valve annuloplasty ring (No. 28 Baxter Physio
ring) from the native mitral valve annulus (arrow, B). Color
Doppler images demonstrate severe regurgitation
with fragmentation of the mitral regurgitation (arrow,
C) into a valvular jet and a high-velocity para-ring
regurgitant jet. 3D echocardiographic images reveal a
paravalvular communication (white arrow, D) created by the
dehiscence of the annuloplasty ring from the native mitral valve
annulus. 3D color Doppler images (with color suppression of the
lower-velocity valvular regurgitation)
demonstrates the high-velocity para-ring regurgitant jet (white arrow,
E).
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Hemolytic anemia is a reported, although uncommon, complication of mitral valve repair. Mechanisms of hemolysis that have been suggested include collision of the regurgitant jet into the prosthetic ring, fragmentation of the regurgitant jet by a dehisced annuloplasty ring, and rapid acceleration of a jet through a small para-ring channel.1 2 The probable mechanism in the present case is fragmentation of the regurgitant jet, with rapid acceleration through the para-ring dehiscence. The patient returned to the operating room for mitral valve replacement, after which the hemolytic anemia resolved.
Footnotes
The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Lukes Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Lukes Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.
References
1.
Yeo TC, Freeman WK, Schaff HV, Orsulak TA.
Mechanisms of hemolysis after mitral valve repair: assessment by serial
echocardiography. J Am Coll
Cardiol. 1998;32:717723.
2. Garcia MJ, Vandervoort P, Stewart WJ, Lytle BW, Cosgrove DM III, Thomas JD, Griffin BP. Mechanisms of hemolysis with mitral prosthetic regurgitation: study using transesophageal echocardiography and fluid dynamic simulation. J Am Coll Cardiol. 1996;27:399406.[Abstract]
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