Are ECG Premature Complexes Induced by Ultrasonic Cavitation Electrophysiological Responses to Irreversible Cardiomyocyte Injury?

Abstract The objective of this study was to explore the relationship between premature complexes (PCs) in the electrocardiogram (ECG) and lethal injury of cardiomyocytes induced by ultrasound exposure of the heart with contrast-agent gas bodies in the circulation. Anesthetized rats were exposed in a heated water bath to 1.55 MHz focused ultrasound with bursts triggered at end systole during contrast agent infusion. PCs were detected in ECG recordings and cardiomyocyte necrosis was scored by identifying Evans blue–stained cells in multiple frozen sections. With 0.1 μL/kg/min infusion of contrast agent for 5 min, both effects increased strongly for 2-ms bursts with increasing peak rarefactional pressure amplitude >1 MPa. At 8 MPa, statistically significant effects were found even for no agent infusion relative to sham tests. For 2-ms bursts at 2 MPa, the highly significant bioeffects seen for 10-, 1- and 0.1-μL/kg/min infusion became marginally significant for 0.01 μL/kg/min, which indicated a lower probability of cavitation nucleation. Burst duration variation from 0.2–20 ms produced no substantial trends in the results. Overall, the two effects were well correlated ( r2 = 0.88). The PCs occurring during contrast-enhanced ultrasound therefore appear to be electrophysiological responses to irreversible cardiomyocyte injury induced by ultrasonic cavitation. (E-mail: douglm@umich.edu )