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Journal of Nuclear Medicine Vol. 48 No. 4 562-567
© 2007 by Society of Nuclear Medicine

doi: 10.2967/jnumed.106.039453

Clinical Investigation

Noninvasive Detection of Programmed Cell Loss with 99mTc-Labeled Annexin A5 in Heart Failure

Bas L.J.H. Kietselaer1, Chris P.M. Reutelingsperger2, Hendrikus H. Boersma3,4, Guido A.K. Heidendal4, Ing Han Liem5, Harry J.G.M. Crijns1, Jagat Narula6 and Leo Hofstra1

1 Department of Cardiology, University Hospital of Maastricht, Maastricht, The Netherlands; 2 Department of Biochemistry, University of Maastricht, Maastricht, The Netherlands; 3 Department of Clinical Pharmacy, University Hospital of Maastricht, Maastricht, The Netherlands; 4 Department of Nuclear Medicine, University Hospital of Maastricht, Maastricht, The Netherlands; 5 Department of Nuclear Medicine, Maxima Medical Center, Veldhoven, The Netherlands; and 6 Division of Cardiology, University of California, Irvine College of Medicine, Irvine, California

Correspondence: For correspondence or reprints contact: Leo Hofstra, University Hospital of Maastricht, Department of Cardiology, P.O. Box 5800, 6202 AZ, Maastricht, The Netherlands. E-mail: L.Hofstra{at}cardio.unimaas.nl

Apoptosis, or programmed cell death (PCD), contributes to the decline in ventricular function in heart failure. Because apoptosis comprises a programmed cascade of events, it is potentially reversible, and timely intervention should delay the development of cardiomyopathy. 99mTc-Labeled annexin A5 has successfully been used for the noninvasive detection of PCD in myocardial infarction and heart transplant rejection. The present study evaluated the role of annexin A5 imaging for detection of PCD in heart failure patients. Methods: Annexin A5 imaging was performed on 9 consecutive heart failure patients with advanced nonischemic cardiomyopathy (dilated, n = 8; hypertrophic, n = 1) and in 2 relatives having the same genetic background as the hypertrophic cardiomyopathy patient but no heart failure. Results: Four of the patients with dilated cardiomyopathy and the 1 with hypertrophic cardiomyopathy and heart failure showed focal, multifocal, or global left ventricular uptake of annexin A5. No uptake was visualized in the remaining 4 patients or in the 2 controls. All cases showing annexin A5 uptake within the left ventricle experienced significant reduction in left ventricular function or functional class. In cases with no annexin A5 uptake, left ventricular function and clinical status remained stable. Conclusion: These data indicate the feasibility of noninvasive PCD detection with annexin imaging in heart failure patients. Annexin A5 uptake is associated with deterioration in left ventricular function, and this association may lend itself to the development of novel management strategies.

Key Words: apoptosis • heart failure • annexin A5

COPYRIGHT © 2007 by the Society of Nuclear Medicine, Inc.




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