Tc-glucarate kinetics differentiate normal, stunned, hibernating, and nonviable myocardium in a perfused rat heart model.

Autor: Okada, David R., Zhonglin Liu, Johnson, Gerald, Beju, Delia, Khaw, Ban An, Okada, Robert D.
Předmět:
Zdroj: European Journal of Nuclear Medicine & Molecular Imaging; Oct2010, Vol. 37 Issue 10, p1909-1917, 9p, 1 Black and White Photograph, 1 Diagram, 2 Charts, 4 Graphs
Abstrakt: Purpose: Tc-glucarate is an infarct-avid imaging agent. However, patients may have mixtures of normal, irreversibly injured, stunned, and hibernating myocardium. The purposes were to determine Tc-glucarate uptake and clearance kinetics in these four conditions, and its ability to determine the extent of injury. Methods: Twenty-two perfused rat hearts were studied: controls ( n = 5), stunned ( n = 5; 20-min no-flow followed by 5-min reflow), hibernating ( n = 6; 120-min low flow at 4 ml/min), and ischemic-reperfused ( n = 6; 120-min no-flow followed by reflow). Tc-glucarate was then infused. Tracer activity was monitored using a NaI scintillation detector and a multichannel analyzer. Creatine kinase, electron microscopy, and triphenyltetrazolium chloride determined viability. Results: Tc-glucarate 10-min myocardial uptake was significantly greater in ischemic-reperfused (2.50 ± 0.09) (cpm, SEM) than in control (1.74 ± 0.07), stunned (1.68 ± 0.11), and hibernating (1.59 ± 0.11) ( p < 0.05). Tracer retention curves for ischemic-reperfused were elevated at all time points as compared with the other groups. Tc-glucarate 60-min myocardial uptake was significantly greater in ischemic-reperfused (7.60 ± 0.63) than in control (1.98 ± 0.15), stunned (1.79 ± 0.08), and hibernating (2.33 ± 0.15) ( p < 0.05). The 60-min well-counted tracer activity ratio of ischemic-reperfused to control was 9:1 and corroborated the NaI detector results. Creatine kinase, triphenyltetrazolium chloride, and electron microscopy all demonstrated significantly greater injury in ischemic-reperfused compared to the other groups. An excellent correlation was observed between viability markers and tracer activity ( r = 0.99 triphenyltetrazolium chloride; r = 0.90 creatine kinase). Conclusion: Tc-glucarate activity continually and progressively increased in irreversibly injured myocardium. Tc-glucarate uptake was strongly correlated with myocardial necrosis as determined by three independent assessments of viability. There were minimal and similar Tc-glucarate uptakes in control, stunned, and hibernating myocardium. [ABSTRACT FROM AUTHOR]
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