Abstract
Positron emission tomography (PET) for in vivo monitoring of phosphatidylserine externalization and glucose metabolism can potentially provide early predictors of outcome of cardioprotective therapies after myocardial infarction. We performed serial [⁶⁸Ga]annexin A5 PET (annexin-PET) and [¹⁸F]fluorodeoxyglucose PET (FDG-PET) after myocardial infarction to determine the time of peak phosphatidylserine externalization in relation to impaired glucose metabolism in infracted tissue. Annexin- and FDG-PET recordings were obtained in female (C57BL6/N) mice on days 1 to 4 after ligation of the left anterior descending (LAD) artery. [⁶⁸Ga]annexin A5 uptake (%ID/g) in the LAD artery territory increased from 1.7 ± 1.1 on day 1 to 5.0 ± 3.3 on day 2 and then declined to 2.0 ± 1.4 on day 3 (p = .047 vs day 2) and 1.6 ± 1.4 on day 4 (p = .014 vs day 2). These results matched apoptosis rates as estimated by autoradiography and fluorescein staining. FDG uptake (%ID/g) declined from 28 ± 14 on day 1 to 14 ± 3.5 on day 4 (p < .0001 vs day 1). Whereas FDG-PET revealed continuous loss of cell viability after permanent LAD artery occlusion, annexin-PET indicated peak phosphatidylserine expression at day 2, which might be the optimal time point for therapy monitoring.
Highlights
Positron emission tomography (PET) for in vivo monitoring of phosphatidylserine externalization and glucose metabolism can potentially provide early predictors of outcome of cardioprotective therapies after myocardial infarction
Single-photon emission computed tomography (SPECT) and PET studies have indicated that uptake of radiolabeled annexin A5 can serve as a marker for measuring levels of phosphatidylserine (PS) externalization in the outer plasma membrane in both animal and human tissues.[9,10,11]
We found that annexin A5 uptake within the infarcted myocardium peaked on the second day after the infarct, as shown by the concordance of PET and ex vivo autoradiography findings
Summary
Positron emission tomography (PET) for in vivo monitoring of phosphatidylserine externalization and glucose metabolism can potentially provide early predictors of outcome of cardioprotective therapies after myocardial infarction. # 2012 Decker Publishing imaging of myocardial survival and viability and lends itself to translation into large-animal models or humans using clinical PET/computed tomography (CT).[8] It is well established that [18F]fluorodeoxyglucose (FDG)-PET gives quantitative information about the viability and function of damaged myocardium in vivo.[8] More recently, single-photon emission computed tomography (SPECT) and PET studies have indicated that uptake of radiolabeled annexin A5 can serve as a marker for measuring levels of phosphatidylserine (PS) externalization in the outer plasma membrane in both animal and human tissues.[9,10,11] This is based on the affinity of annexin A5 for the plasma membrane PS, which is presented during apoptosis and, to some degree, during other forms of cell death.[10,12] Annexin A5 is an anticoagulant protein that binds with high affinity to externalized PS and forms a twodimensional molecule network through protein–protein interactions on the surface of cells at risk.[13]. Glucose metabolism, as an indicator of myocardial viability To address this issue, we performed pairs of PET acquisitions with [68Ga]annexin A5 and FDG in mice for 4 days following an irreversible ligation of the left anterior descending (LAD) artery. We sought to identify the time of peak PS levels in comparison with impaired glucose metabolism as the optimal time point for future application of a PET method for monitoring cardioprotective therapies
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