Correlation of ultrasound-induced premature beats and cavitation in vivo

Abstract

Exposure of the heart to pulsed ultrasound can produce arrhythmias such as premature ventricular contractions (PVCs). Recently, studies indicate that microbubble ultrasound contrast agents can further increase the sensitivity of the heart to ultrasound by lowering the pressure threshold for PVCs. It was hypothesized that the physical mechanisms for ultrasound-induced PVCs involve acoustic cavitation. To test this hypothesis, a passive cavitation detector (PCD) was used to directly measure cavitation in vivo and to correlate the detected output with the occurrence of a premature beat. Experiments were performed with adult anesthetized mice. Boluses of either a contrast agent (Optison) or saline were delivered via tail vein injections. Pulsed ultrasound exposures were performed at 200 kHz with pulse durations of 1 ms and peak negative pressures ranging between 0.1 and 0.25 MPa. A 5-MHz focused transducer was used as a passive listening device of acoustic signals. For the acoustic conditions above, premature beats were found in all mice injected with Optison and the effect correlated with PCD signal amplitude. Neither premature beats nor cavitation activity were observed among animals injected with saline and exposed to ultrasound. These results are consistent with cavitation as a mechanism for this bioeffect.