BACKGROUND: Ultrasonic backscatter demonstrates a cardiac cycle-dependent modulation. The exact mechanism of the modulation is under debate. The objective of the present study was to test the hypothesis that a change in size and configuration of myofilaments from systole to diastole alters acoustic propagation properties and backscatter. METHODS AND RESULTS: In vivo measurements were made of integrated backscatter at 5 MHz (IBR5), followed by in vitro measurements of ultrasonic attenuation, speed, and heterogeneity index using a scanning laser acoustic microscope at 100 MHz. Studies were performed in canine hearts (16) arrested in systole (8) with calcium chloride or arrested in diastole (8) with potassium chloride. Sarcomere length was measured with a calibrated eyepiece on a Ziess microscope. Wall thickness was measured with calipers. The attenuation coefficient of 220 +/- 34 dB/cm during systole was significantly higher than the coefficient of 189 +/- 24 dB/cm during diastole (P < .01); the IBR5 of -44.7 +/- 1.2 dB during systole was significantly greater than the IBR5 of -47.0 +/- 1.0 dB during diastole (P < .01); the ultrasonic speed of 1591 +/- 11 m/s during systole was higher than the speed of 1575 +/- 4.2 m/s during diastole (P < .01); and the heterogeneity index of 7.4 +/- 1.8 m/s during systole was significantly lower than the index of 9.0 +/- 2.0 m/s during diastole (P < .02). The sarcomere length of 1.804 +/- 0.142 microns during diastole was significantly higher than the length of 1.075 +/- 0.177 micron during systole (P < .01). Wall thickness was significantly greater during systole than during diastole (20 +/- 3 versus 9 +/- 3 mm, P < .01). CONCLUSIONS: Ultrasonic backscatter and propagation properties are directly related to sarcomere length and myocardial thickness and may be responsible for cardiac cycle-dependent variation in backscatter.
BACKGROUND: Ultrasonic backscatter demonstrates a cardiac cycle-dependent modulation. The exact mechanism of the modulation is under debate. The objective of the present study was to test the hypothesis that a change in size and configuration of myofilaments from systole to diastole alters acoustic propagation properties and backscatter. METHODS AND RESULTS: In vivo measurements were made of integrated backscatter at 5 MHz (IBR5), followed by in vitro measurements of ultrasonic attenuation, speed, and heterogeneity index using a scanning laser acoustic microscope at 100 MHz. Studies were performed in canine hearts (16) arrested in systole (8) with calcium chloride or arrested in diastole (8) with potassium chloride. Sarcomere length was measured with a calibrated eyepiece on a Ziess microscope. Wall thickness was measured with calipers. The attenuation coefficient of 220 +/- 34 dB/cm during systole was significantly higher than the coefficient of 189 +/- 24 dB/cm during diastole (P < .01); the IBR5 of -44.7 +/- 1.2 dB during systole was significantly greater than the IBR5 of -47.0 +/- 1.0 dB during diastole (P < .01); the ultrasonic speed of 1591 +/- 11 m/s during systole was higher than the speed of 1575 +/- 4.2 m/s during diastole (P < .01); and the heterogeneity index of 7.4 +/- 1.8 m/s during systole was significantly lower than the index of 9.0 +/- 2.0 m/s during diastole (P < .02). The sarcomere length of 1.804 +/- 0.142 microns during diastole was significantly higher than the length of 1.075 +/- 0.177 micron during systole (P < .01). Wall thickness was significantly greater during systole than during diastole (20 +/- 3 versus 9 +/- 3 mm, P < .01). CONCLUSIONS: Ultrasonic backscatter and propagation properties are directly related to sarcomere length and myocardial thickness and may be responsible for cardiac cycle-dependent variation in backscatter.
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