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

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

View larger version (123K): [in this window] [in a new window]   FIGURE 1.  Dual-isotope imaging using 201Tl for left ventricular contour detection and, simultaneously, radiolabeled annexin A5 in patients with dilated cardiomyopathy. (A) Dilated cardiomyopathy patient with rapid deterioration of left ventricular function. Note focal uptake in apex and lateral wall, and slight septal uptake. (B) Dilated cardiomyopathy patient in acute heart failure. Note global uptake of radiolabeled annexin A5. (C) Dilated cardiomyopathy patient in stable clinical condition. Uptake is absent even when image is enhanced to the extent that background radioactivity can be observed. (D) Family member of patient in panel B. No clinical evidence is seen of dilated cardiomyopathy. Note absence of uptake of radiolabeled annexin A5. ANT = anterior; INF = inferior; LAT = lateral; SEPT = septal.

View larger version (41K): [in this window] [in a new window]   FIGURE 2.  Change in LVEF 1 y after annexin imaging. Green bar shows patients with negative scan findings (mean LVEF increase, 7%); red bar shows patients with positive scan findings (mean LVEF decrease, 10%). P = 0.038.

View larger version (15K): [in this window] [in a new window]   FIGURE 3.  Cytokine and oxidative stress (reactive oxygen species) in heart failure lead to caspase 3 activation by release of cytochrome c from mitochondria into cytoplasmic compartment. Activation of caspase 3 results in cytoplasmic proteolysis and DNA fragmentation and, hence, apoptosis. Endogenous upregulation of BCl2- and XIAP-like proteins and loss of DNA fragmentation factors prevent completion of apoptotic process (apoptosis interruptus). Amount of activated caspase 3 is determined by balance of antiapoptotic and proapoptotic factors. The fewer the endogenous antiapoptotic factors, the greater is the residual caspase, the PS externalization, the likelihood of an annexin-positive scan, and the necessity for apoptosis inhibition therapy and the poorer is the prognosis.