OBJECTIVES: This study investigated the influence of imaging method, acoustic power, and dose of contrast agent on the occurrence of premature ventricular contraction during myocardial contrast echocardiography. METHODS: Myocardial contrast echocardiography was performed with a Toshiba POWER VISION 6000 and YM454 (Definity in USA) contrast agent. Myocardial contrast echocardiography in the short-axis view at the mid-papillary muscle level and electrocardiography in lead II were recorded on videotape in nine awake beagles. The imaging method was continuous, using 1:1 and 1:4 intermittent end-systolic triggered mode. Acoustic power was low, middle and high (as mechanical index, 0.4, 0.8 and 1.0 at continuous mode and 0.6, 1.0 and 1.4 at intermittent mode). YM454 was given intravenously at doses of 1, 10, 30, 50 and 100 microliters/kg/min. Premature ventricular contractions were counted on the videotape for each experimental condition. The examination was repeated on a separate day to ascertain the reproducibility. RESULTS: At low and middle acoustic power, no premature ventricular contraction was induced with any combinations of YM454 doses and trigger intervals. The highest incidence of premature ventricular contraction was 5.1% of all ultrasound pulses at the combination of high acoustic power, 1:4 intermittent and 30 microliters/kg/min of YM454. All premature ventricular contractions induced by trigger mode were observed concomitantly to the end-systolic phase. Reproducibility was low at 0.9%. CONCLUSIONS: Although high acoustic power, intermittent myocardial contrast echocardiography with high dose of contrast agent induced premature ventricular contractions, the incidence of premature ventricular contractions was low. Low acoustic power or low dose of contrast agent induced no premature ventricular contractions.
OBJECTIVES: This study investigated the influence of imaging method, acoustic power, and dose of contrast agent on the occurrence of premature ventricular contraction during myocardial contrast echocardiography. METHODS: Myocardial contrast echocardiography was performed with a Toshiba POWER VISION 6000 and YM454 (Definity in USA) contrast agent. Myocardial contrast echocardiography in the short-axis view at the mid-papillary muscle level and electrocardiography in lead II were recorded on videotape in nine awake beagles. The imaging method was continuous, using 1:1 and 1:4 intermittent end-systolic triggered mode. Acoustic power was low, middle and high (as mechanical index, 0.4, 0.8 and 1.0 at continuous mode and 0.6, 1.0 and 1.4 at intermittent mode). YM454 was given intravenously at doses of 1, 10, 30, 50 and 100 microliters/kg/min. Premature ventricular contractions were counted on the videotape for each experimental condition. The examination was repeated on a separate day to ascertain the reproducibility. RESULTS: At low and middle acoustic power, no premature ventricular contraction was induced with any combinations of YM454 doses and trigger intervals. The highest incidence of premature ventricular contraction was 5.1% of all ultrasound pulses at the combination of high acoustic power, 1:4 intermittent and 30 microliters/kg/min of YM454. All premature ventricular contractions induced by trigger mode were observed concomitantly to the end-systolic phase. Reproducibility was low at 0.9%. CONCLUSIONS: Although high acoustic power, intermittent myocardial contrast echocardiography with high dose of contrast agent induced premature ventricular contractions, the incidence of premature ventricular contractions was low. Low acoustic power or low dose of contrast agent induced no premature ventricular contractions.