Modeling the loss of echogenicity from ultrasound contrast agents

Abstract

Acoustically induced loss of echogenicity (LOE) from ultrasound contrast agents (UCAs) has been exploited in imaging techniques to improve delineation of pathology. Determination of the type of cavitation that accompanies LOE can be experimentally difficult to determine due to the complex microbubble activity elicited. A theoretical model has been derived to predict the LOE originating from rupture of the UCA shell, from stable cavitation, or from inertial cavitation. The predictions of the model for each cavitation phenomena will be compared to recent experimental LOE measurements of the lipid-based UCA Definity® and echogenic liposomes insonified by Doppler pulses from a clinical scanner. The backscatter coefficient was calculated for a population of UCAs exposed to 6-MHz pulsed ultrasound of duration 1.67μs—8.33 μs. The change in the total backscatter coefficient was used to predict the LOE. The size distribution of UCAs was adjusted according to the specific type of cavitation triggered by the ultrasound exposure. Comparison of the theoretical predictions and experimental measurements suggest that shell rupture is the dominant mechanism for LOE for both Definity® and echogenic liposomes. These results will be discussed in conjunction with a recently developed cavitation index to predict the LOE of UCAs.