Background: Bis (N-ethoxy, N-ethyl dithiocarbamato) nitrido technetium-99m (V) (TcN-NOET) is a neutral lipophilic myocardial perfusion agent. The effect of ischemic injury on the cardiac transport of TcN-NOET and thallium-201 was determined in isolated rabbit hearts.
Methods and results: The multiple indicator dilution method was used to determine the maximum (Emax) and net extraction (Enet, at 5 minutes) of TcN-NOET and TI-201 at control and after 10 minutes (n = 4) or 45 minutes (n = 4) of no-flow ischemia. After 10 minutes of ischemia the mean Emax for T1-201 was unchanged, 0.86 +/- 0.03 vs 0.85 +/- 0.02, whereas TI-201 Enet showed a small decrease from 0.46 +/- 0.03 to 0.40 +/- 0.03, P < .001. Forty-five minutes of ischemia mildly reduced Emax for TI-201 (0.87 +/- 0.04 to 0.74 +/- 0.04, P < .001) and severely reduced Enet (0.46 +/-0.03 vs 0.16 +/- 0.04, P < .001). Neither Emax nor Enet for TcN-NOET was significantly affected by 10 minutes of ischemia (0.54 +/- 0.04 vs 0.58 +/- 0.03 and 0.24 +/- 0.04 vs 0.26 +/- 0.04, respectively). However, severe ischemic injury caused significant reductions versus control in both Emax (0.59 +/- 0.06 vs 0.42 +/- 0.05, P < .001) and Enet (0.27 +/- 0.03 vs 0.18 +/- 0.05, P < .01).
Conclusions: TcN-NOET is a new myocardial perfusion agent with moderate myocardial extraction. Although less sensitive than TI-201 to mild ischemic injury, TcN-NOET extraction and retention are decreased by severe ischemic injury, making uptake of TcN-NOET a possible marker of myocardial viability.