Tyco-Mallinckrodt, USA
The objective of the study is to use Angiotensin Converting Enzyme (ACE) as a biomarker of non-viability post myocardial infarction (MI) for the potential assessment of residual myocardial viability.
Standard ACE inhibitor (e.g. Lisinopril) is modified to incorporate radioactive 125I and 99mTc and tested for the retention of the inhibitory potency by competitive binding assays. The overexpression of ACE following myocardial infarction (MI) in a rat model, quantified by ex-vivo autoradiography is correlated with the biodistribution of the radiotracer in-vivo.
The ACE expression post MI was quantified by ex-vivo autoradiography of the sections of heart. The radiolabled ACE inhibitor was displaced by functionalized Lisinopril almost quantitatively, thus preserving the inhibitory potency of native Lisinorpil. The results on the in vivo biodistribution of the radiolabeled Lisinopril post MI showed a significant uptake by the heart compared to sham controls in rats. The clinical significance and limitations of ACE mediated scintigraphy will be discussed.
Imaging ACE post MI for the assessment of viability may be feasible with a single injection mapping the non-viable sections precisely compared to the existing inconvenient dual injection (e.g. Tl-201) or dual technique (SPECT and PET) protocols.