RT Journal Article
SR Electronic
T1 Quantification of 99mTc-duramycin uptake kinetics in the area-at-risk after myocardial ischemia and reperfusion using a compartment model
JF Journal of Nuclear Medicine
JO J Nucl Med
FD Society of Nuclear Medicine
SP 1446
OP 1446
VO 50
IS supplement 2
A1 Said Audi
A1 Joseph Capacete
A1 Zhixin Li
A1 Ming Zhao
YR 2009
UL http://jnm.snmjournals.org/content/50/supplement_2/1446.abstract
AB 1446 Objectives 99mTc-duramycin is a novel radiopharmaceutical that detects apoptosis and necrosis by recognizing phosphatidylethanolamine (PE). Prior studies demonstrated that 99mTc-duramycin is particularly suitable for cardiac applications, due to its low molecular weight, fast blood clearance, avid infarct binding and minimal hepatic background. The aim of this study was to quantitatively characterize the in vivo kinetics of 99mTc-duramycin in the area-at-risk using compartmental analysis. Methods Myocardial infarction was induced in rats. 99mTc-Duramycin was injected iv. At 3, 10, 20, 60 and 180 min, the radioactivity in infarcted and normal myocardium was measured (%ID/g). A compartment model was developed consisting of vascular and tissue regions representing the vascular and tissue regions of the myocardium, with blood activity as input. For infarct myocardium, the model allows for tracer diffusionbetween vascular and tissue regions, and sequestration within the tissue region via specific binding. Results Model results show that the sequestration of 99mTc-Duramycin within tissue region of infarct myocardium follows linear kinetics. The rate of tracer diffusion (0.22 ml/min/g) between vascular and tissue region of infarct myocardium is larger than the rate of sequestration (0.05 ml/min/g) within the tissue region. Conclusions Model results suggest that the rate of diffusion of 99mTc-Duramycin is not a limiting factor for the binding within the tissue region of infarct myocardium. The model provides a means for quantitative interpretation of the 99mTc-Duramycin kinetic data in terms of the dominant factors that determines its disposition in infarct tissue.