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Myocardial Distribution of Indium-111-Antimyosin Fab and Technetium-99m-Sestamibi in Experimental Nontransmural Infarction

Departments of Cardiology and Pulmonology, Nuclear Medicine and Experimental Animal Research, Georg August University, Göttingen, Germany

Correspondence: For reprints contact: Andreas J. Morguet, MD, Dept. of Cardiology and Pulmonology, Center of Internal Medicine, Georg August University, Robert-Koch-Str. 40, D-3400 Göttingen, Germany.

ABSTRACT

Early revascularization in acute myocardial infarction results in normal, necrotic and partially damaged and partially salvaged ("intermediate") myocardium. By combining a perfusion tracer and a marker for myocardial injury, we attempted to differentiate between these three types of cardiac tissue. The LAD was occluded in nine pigs for 45 min and then reperfused. After 48 and 72 hr, 74 MBq ¹¹¹In-antimyosin Fab and 740 MBq ^99mTc-sestamibi, respectively, were injected intravenously. Normally perfused myocardium was labeled with fluorescein and the heart excised. Three to four slices were cut from the apex. Tetrazolium staining revealed the zone of necrosis. Tracer distribution on double-nuclide scintigrams of the slices also reflected the three different myocardial zones. Guided by fluorescence and macrohistochemistry, tissue samples were excised from each zone. In relation to normal myocardium, mean activity in the intermediate zone was 0.82 ± 0.20 for ^99mTc-sestamibi and 2.84 ± 1.31 for ¹¹¹In-antimyosin Fab. Activity in necrotic myocardium was 0.30 ± 0.19 and 3.95 ± 2.47, respectively. These results show that ¹¹¹In-antimyosin Fab fragments not only accumulate in necrotic but also in intermediate myocardium. Therefore, an overestimation of infarct size may occur if ¹¹¹In-antimyosin Fab fragments are used alone without a perfusion tracer.