Premature ventricular complexes (PVCs) have been reported for ultrasound with gas body contrast agent for diagnostic B-mode and also for burst mode at substantially lower peak rarefactional pressure amplitudes (PRPAs). For B mode, injured cardiomyocytes have been associated with the PVCs. The objective was to determine if the PVCs induced by burst mode at lower PRPAs are associated with cardiomyocyte injury. Anesthetized hairless rats were exposed to focused 1.5 MHz ultrasound in a water bath. Evans blue dye was injected IP at 100 mg/kg in saline. 2 ms bursts or square envelopes of 1.8 µs pulses with 230 µs spacing (simulated B-mode) were triggered 1:4 at end systole during 300 s exposures. Definity™ contrast agent was diluted in saline and infused IV at 10 µL/kg/min. PVCs were observed on ECG recordings and stained cardiomyocytes were counted in frozen sections from heart samples taken the next day. Results are reported as means ± one standard deviation for 5-rat groups. Pulsed ultrasound at 2.0 MPa PRPA induced 148±50 PVCs and 960±220 stained cardiomyocytes, both statistically significant relative to shams (P<0.01), but neither effect was significant at 1.0 MPa. Ultrasound bursts produced significant (P<0.01) PVCs and stained cardiomyocytes of 222±17 and 370±239, respectively, at 1.0 MPa and 77±43 and 271±74, respectively, at 0.5 MPa, but not at 0.25 MPa. PVCs induced by burst mode ultrasound at substantially lower PRPAs than for pulsed ultrasound were associated with a significant increase in irreversible cardiomyocyte injury.