Acoustic emissions associated with ultrasound-induced rupture of ex vivo blood vessels

Abstract

Occlusion of blood vessels using high-intensity focused ultrasound (HIFU) is a potential treatment for arteriovenous malformations and other neurovascular disorders. However, HIFU-induced vessel occlusion can cause vessel rupture resulting in hemorrhage. Possible rupture mechanisms include mechanical effects of acoustic cavitation and hyperthermia of the vessel wall. To investigate the mechanism of vessel rupture and assess the possibility of rupture prediction from acoustic emissions, HIFU exposures were performed on 18 ex vivo porcine femoral arteries with simultaneous passive cavitation detection. Vessels were insonified by a 3.3 MHz focused source with spatial-peak, temporal-peak focal intensity 1728-2791 W/cm2 and a 50% duty cycle for durations up to 5 minutes. Time-dependent acoustic emissions were recorded by an unfocused passive cavitation detector and quantified within low-frequency (10-30 kHz), broadband (0.3-1.1 MHz), and subharmonic (1.65 MHz) bands. Vessel rupture was detected by inline metering of saline flow, recorded throughout each treatment. Rupture prediction tests, using receiver operating characteristic curve analysis, found subharmonic emissions to be most predictive. These results suggest that acoustic cavitation plays an important role in HIFU-induced vessel rupture. In HIFU treatments for vessel occlusion, passive monitoring of acoustic emissions may be useful in avoiding hemorrhage.