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DEPENDENCE OF BOILING HISTOTRIPSY TREATMENT EFFICIENCY ON HIFU FREQUENCY AND FOCAL PRESSURE LEVELS
DEPENDENCE OF BOILING HISTOTRIPSY TREATMENT EFFICIENCY ON HIFU FREQUENCY AND FOCAL PRESSURE LEVELS
DEPENDENCE OF BOILING HISTOTRIPSY TREATMENT EFFICIENCY ON HIFU FREQUENCY AND FOCAL PRESSURE LEVELS
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Figure 7 shows the bisected BH lesions in bovine liver that were produced at 1.5 MHz using pulse durations of 10 ms, 5 ms, 2 ms and 1 ms, with corresponding driving voltages of 110 V, 120 V, 150 Vand 190 V. The rightmost photograph shows a ghost lesion that formed at 200 V with pulse duration of 1 ms. Note that the derated in situ pressures at 110 V correspond to the low output level (i.e., the condition of fully developed shocks) and those at 200 V correspond to high output (i.e., saturated shocks). Table 4 summarizes the peak in situ pressures across different frequencies and different amplitudes derated for propagation in ex vivo bovine liver, as well as the predicted times to reach boiling. For all frequencies, the lowest output level corresponded to the regime of developed shocks in situ, and the highest at 1MHz was close to the regime of saturated shocks in situ. Each exposure was repeated at least 4 times in a given tissue sample for at least 2 different samples. Considering uncertainties associated with tissue structure variability and bisection-related inaccuracies, no difference was found in the size of the BH lesions produced at different pulse durations for a given ultrasound frequency. However, the probability of ghost lesion formation increased for shorter pulse durations. For example, at 1.5 MHz all exposures formed liquefied lesions except for the ones with 1-ms pulses, which produced ghost lesions in 25% of cases. This effect may be attributed to the prefocal shielding by cavitation bubbles, similar to that observed in the PA gels. The corresponding derated peak negative pressure was 14.5 MPa, which corresponded to substantial shielding in the gel phantom (as seen in Tables 2 and 4). Similar dependencies were observed in myocardium (data not provided), but the incidence of ghost lesions was 100% for 2-ms pulses and shorter. Another important observation of exposures at the highest output levels (corresponding to 1-ms and 2-ms pulses) is that the theoretically estimated times to reach boiling temperature exceeded the corresponding pulse durations for all frequencies. That is, the tissue temperature at the focus was not expected to reach 100C within a single pulse, according to weak shock theory predictions, yet experimentally the hyperechoes were observed, and the liquefied BH lesions formed in some (at 1 MHz) or most (at 1.5 MHz) cases.
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1 Figure 7 shows the bisected BH lesions in bovine liver that were produced at 1.5 MHz using pulse durations of 10 ms, 5 ms, 2 ms and 1 ms, with corresponding driving voltages of 110 V, 120 V, 150 Vand 190 V. 2 The rightmost photograph shows a ghost lesion that formed at 200 V with pulse duration of 1 ms. 3 Note that the derated in situ pressures at 110 V correspond to the low output level (i.e., the condition of fully developed shocks) and those at 200 V correspond to high output (i.e., saturated shocks). 4 Table 4 summarizes the peak in situ pressures across different frequencies and different amplitudes derated for propagation in ex vivo bovine liver, as well as the predicted times to reach boiling. 5 For all frequencies, the lowest output level corresponded to the regime of developed shocks in situ, and the highest at 1MHz was close to the regime of saturated shocks in situ. 6 Each exposure was repeated at least 4 times in a given tissue sample for at least 2 different samples. 7 Considering uncertainties associated with tissue structure variability and bisection-related inaccuracies, no difference was found in the size of the BH lesions produced at different pulse durations for a given ultrasound frequency. 8 However, the probability of ghost lesion formation increased for shorter pulse durations. 9 For example, at 1.5 MHz all exposures formed liquefied lesions except for the ones with 1-ms pulses, which produced ghost lesions in 25% of cases. 10 This effect may be attributed to the prefocal shielding by cavitation bubbles, similar to that observed in the PA gels. 11 The corresponding derated peak negative pressure was 14.5 MPa, which corresponded to substantial shielding in the gel phantom (as seen in Tables 2 and 4). 12 Similar dependencies were observed in myocardium (data not provided), but the incidence of ghost lesions was 100% for 2-ms pulses and shorter. 13 Another important observation of exposures at the highest output levels (corresponding to 1-ms and 2-ms pulses) is that the theoretically estimated times to reach boiling temperature exceeded the corresponding pulse durations for all frequencies. 14 That is, the tissue temperature at the focus was not expected to reach 100C within a single pulse, according to weak shock theory predictions, yet experimentally the hyperechoes were observed, and the liquefied BH lesions formed in some (at 1 MHz) or most (at 1.5 MHz) cases.