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Comparison of Microsphere-Equivalent Blood Flow (¹⁵O-Water PET) and Relative Perfusion (^99mTc-Tetrofosmin SPECT) in Myocardium Showing Metabolism-Perfusion Mismatch

¹ Department of Nuclear Medicine, University Hospital, Aachen University of Technology, Aachen, Germany
² Department of Internal Medicine I (Cardiology), University Hospital, Aachen University of Technology, Aachen, Germany

Myocardial perfusion imaging with ^99mTc-tetrofosmin is based on the assumption of a linear correlation between myocardial blood flow (MBF) and tracer uptake. However, it is known that ^99mTc-tetrofosmin uptake is directly related to energy-dependent transport processes, such as Na⁺/H⁺ ion channel activity, as well as cellular and mitochondrial membrane potentials. Therefore, cellular alterations that affect these energy-dependent transport processes ought to influence ^99mTc-tetrofosmin uptake independently of blood flow. Because metabolism (¹⁸F-FDG)-perfusion (^99mTc-tetrofosmin) mismatch myocardium (MPMM) reflects impaired but viable myocardium showing cellular alterations, MPMM was chosen to quantify the blood flow-independent effect of cellular alterations on ^99mTc-tetrofosmin uptake. Therefore, we compared microsphere-equivalent MBF (MBF_micr; ¹⁵O-water PET) and ^99mTc-tetrofosmin uptake in MPMM and in "normal" myocardium. Methods: Forty-two patients with severe coronary artery disease, referred for myocardial viability diagnostics, were examined using ¹⁸F-FDG PET and ^99mTc-tetrofosmin perfusion SPECT. Relative ¹⁸F-FDG and ^99mTc-tetrofosmin uptake values were calculated using 18 segments per patient. Normal myocardium and MPMM myocardium were classified using a previously validated ^99mTc-tetrofosmin SPECT/¹⁸F-FDG PET score. In addition, ¹⁵O-water PET was performed to assess kinetic-modeled MBF (MBF_kin), the water-perfusable tissue fraction (PTF), and the resulting MBF_micr (MBF_kin·PTF), which is comparable to tracer uptake values. ^99mTc-tetrofosmin uptake and MBF_micr values were calculated for all normal and MPMM segments and averaged within their respective classifications. Results: Mean relative ^99mTc-tetrofosmin uptake was 86% ± 1% in normal myocardium and 56% ± 1% in MPMM, showing a significant difference (P < 0.001), as was expected from the classification. Contrary to these findings, mean MBF_micr in MPMM myocardium was 0.60 ± 0.03 mL·min^-1·mL^-1, which did not significantly differ from normal myocardium (0.64 ± 0.01 mL·min^-1·mL^-1). All values are given as mean ± SEM. Conclusion: Differences between reduced ^99mTc-tetrofosmin uptake and the unchanged MBF_micr in MPMM myocardium suggest that the pathophysiologic basis of MPMM is not a blood flow reduction but cellular alterations that affect uptake and retention of ^99mTc-tetrofosmin independently of blood flow. Therefore, it seems that perfusion deficits in MPMM myocardium are greatly overestimated by ^99mTc-tetrofosmin and that it tends to give false-positive findings.

Key Words: metabolism-perfusion mismatch • ^99mTc-tetrofosmin • ¹⁸F-FDG • myocardial blood flow • ¹⁵O-water

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