This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Beller, G. A. Articles by Watson, D. D. Search for Related Content PubMed PubMed Citation Articles by Beller, G. A. Articles by Watson, D. D.

Circulation, Vol 87, 2033-2042, Copyright © 1993 by American Heart Association

ARTICLES

99mTc-sestamibi uptake and retention during myocardial ischemia and reperfusion

GA Beller, DK Glover, NC Edwards, M Ruiz, JP Simanis and DD Watson
Department of Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.

BACKGROUND. 99mTc-methoxyisobutyl isonitrile (Sestamibi) is a new perfusion agent that has shown promise for the noninvasive detection of myocardial salvage after coronary reperfusion in acute myocardial infarction. The objective of this study was to further validate that myocardial uptake and retention of Sestamibi after reperfusion in a canine myocardial infarction model are markers of tissue viability. The hypotheses tested were that if Sestamibi is given early after reperfusion and myocardial uptake is quantitated soon afterward, the degree of ultimate myocardial salvage will be overestimated, and that there will be continued loss of myocardial Sestamibi from ischemic tissue during 3 hours of reperfusion due to accelerated release of Sestamibi from cells already irreversibly injured during the phase of coronary occlusion, reperfusion injury to myocytes still viable early after reflow, or a combination of both mechanisms. METHODS AND RESULTS. In protocol 1, 8.0 mCi Sestamibi was injected intravenously in anesthetized dogs 2-5 minutes after reperfusion preceded by 3 hours of left anterior descending coronary artery (LAD) occlusion. Animals were killed either 5 minutes (n = 7) or 3 hours (n = 9) after Sestamibi administration. Mean endocardial Sestamibi activity was 74 +/- 3% of nonischemic activity in dogs killed early and 31 +/- 2% of nonischemic activity in dogs killed late after Sestamibi administration, indicating myocardial loss of Sestamibi during 3 hours of reflow. Regional flow (percent nonischemic) at the time of Sestamibi administration (2-5 minutes after reperfusion) was comparable in dogs killed early (144 +/- 23%) and dogs killed late (118 +/- 4%, p = NS). In protocol 2, Sestamibi was given intravenously at baseline under normal conditions followed by 3 hours of LAD occlusion and either 4 (n = 6), 30 (n = 9), or 180 minutes (n = 10) of reperfusion. At postmortem, myocardial slices were imaged for quantification of defect magnitude and regional flow (radiolabeled microspheres), and tissue Sestamibi activities were determined by gamma well counting. Coronary sinus Sestamibi activity was serially measured. In these dogs, which were preloaded with Sestamibi at baseline, 3 hours of LAD occlusion followed by 3 hours of reperfusion resulted in a loss of Sestamibi in the endocardial zone of the ischemic region to 40 +/- 6% of nonischemic levels (p < 0.0001). This loss corresponded to a sustained elevation of coronary sinus activity throughout the reflow period. The loss of myocardial Sestamibi was significantly greater than that observed in dogs killed 4 or 30 minutes after reflow. Defect magnitude also worsened over 3 hours of reperfusion as assessed by gamma camera imaging of slices of the excised hearts. CONCLUSIONS. These experimental data suggest that Sestamibi uptake and retention are dependent on myocardial viability as well as regional flow. If Sestamibi is administered early after reperfusion and imaging is performed soon afterward, the degree of myocardial salvage could be significantly overestimated.

This article has been cited by other articles:

				A. Radaelli, C. Loardi, M. Cazzaniga, G. Balestri, C. DeCarlini, M. G. Cerrito, E. N. Cusa, L. Guerra, S. Garducci, D. Santo, et al. Inflammatory Activation During Coronary Artery Surgery and Its Dose-Dependent Modulation by Statin/ACE-Inhibitor Combination Arterioscler. Thromb. Vasc. Biol., December 1, 2007; 27(12): 2750 - 2755. [Abstract] [Full Text] [PDF]

				M. Faraggi The Continuing Story of 201Tl Reverse Redistribution: Reverse Redistribution Is Still Alive, but Is the Myocardium Still Viable? J. Nucl. Med., May 1, 2002; 43(5): 628 - 631. [Full Text] [PDF]

				A. Ayalew, P.-Y. Marie, P. Menu, P.-M. Mertes, S. Audonnet, V. Jouan, P. Olivier, G. Karcher, D. Ungureanu-Longrois, and A. Bertrand 201Tl and 99mTc-MIBI Retention in an Isolated Heart Model of Low-Flow Ischemia and Stunning: Evidence of Negligible Impact of Myocyte Metabolism on Tracer Kinetics J. Nucl. Med., April 1, 2002; 43(4): 566 - 574. [Abstract] [Full Text] [PDF]

				N. Takahashi, C. P. Reinhardt, R. Marcel, and J. A. Leppo Myocardial Uptake of 99mTc-Tetrofosmin, Sestamibi, and 201Tl in a Model of Acute Coronary Reperfusion Circulation, November 15, 1996; 94(10): 2605 - 2613. [Abstract] [Full Text]

				V. Sansoy, D. K. Glover, D. D. Watson, M. Ruiz, W. H. Smith, J. P. Simanis, and G. A. Beller Comparison of Thallium-201 Resting Redistribution With Technetium-99m–Sestamibi Uptake and Functional Response to Dobutamine for Assessment of Myocardial Viability Circulation, August 15, 1995; 92(4): 994 - 1004. [Abstract] [Full Text]