A 48-year-old man was admitted to the hospital because of acute myocardial infarction. Percutaneous coronary intervention (PCI) was involved in the proximal obstruction of the left anterior descending coronary artery ( Fig. 1 A and B). Thallium-201/technetium-99m pyrophosphate dual isotope SPECT (Prizm 2000XP, Picker, Philadelphia, PA, USA) imaging was performed after 48 h following PCI, and the reperfused anteroseptal wall with both high thallium-201 uptake ( Fig. 1 C) and high pyrophosphate uptake ( Fig. 1 D) presented the reperfusion injury as a phenomenon of intracellular calcium overload caused by a change in calcium ion permeability ( Fig. 1 D) despite the salvage of myocardial perfusion immediately after myocardial infarction . Thallium-201 (E)/I-123 beta-methyl iodophenyl-pentadecanoic acid dual isotope SPECT imaging was performed after 1 month, and the oxidative metabolism remained defective ( Fig. 1 F) despite the preserved perfusion ( Fig. 1 E) in the reperfused anteroseptal wall, suggesting a histologic mixture of myocardium and fibrous tissue . After 6 months, no restenosis of the coronary artery was confirmed, but the reperfused anteroseptal wall motion remained reduced. Early reperfusion with PCI limits the infarct size, but the reperfusion itself results in irreversible myocardial reperfusion injury owing to excessive intracellular calcium ion overload . Technetium-99m pyrophosphate has been known to be trapped in intracellular calcium in severely injured myocardium . The visualization of excessive intracellular calcium ion overload caused by irreversible reperfusion injury was shown in this case.
