Theodore Lauer Rhyne

Intramyocardial variability in integrated backscatter: effects of coronary occlusion and reperfusion.

The present study was undertaken to characterize regional myocardial alterations of reflected ultrasound during the cardiac cycle in normal, ischemic, and postischemic reperfused myocardium. Time-averaged integrated backscatter (IB) and cardiac cycle-dependent amplitude modulation were measured from subepicardial, midmyocardial, and subendocardial regions of the left ventricular apex and the midportion of the right ventricular free wall under normal conditions (n = 5), after 1 hr of 100% acute left anterior descending (LAD) occlusion (n = 8), and after 15 min LAD occlusion plus 120 min reperfusion (n = 5) in anesthetized, ventilated open-chest dogs. A significant increase in time-averaged IB was observed in the subepicardium, the midmyocardium, and the subendocardium during ischemia and reperfusion, but there was no intramyocardial variability. Cardiac cycle-dependent amplitude modulation of IB was significantly higher in the normal subendocardium than in the subepicardium (4.3 +/- 0.6 vs 2.9 +/- 0.8 dB, p less than .01) and midmyocardium (2.8 +/- .05 dB, p less than .01). This transmural gradient in amplitude modulation was abolished during ischemia and reperfusion. We conclude that cardiac cycle-dependent amplitude modulation in IB has a transmural dependence in the normal myocardium and this is abolished during acute myocardial ischemia.

Relation of Ultrasonic Backscatter and Acoustic Propagation Properties to Myofibrillar Length and Myocardial Thickness

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.

Radiation coupling of a disk to a plane and back or a disk to a disk: An exact solution

The radiation coupling or coupling by propagating waves is solved for a disk in an infinite baffle to a plane and back or equivalently a disk to a disk both in infinite baffles. The radiation coupling is defined as a linear filter operating between lumped mechanical components which may be incorporated into transducer models. The impulse response of the radiation‐coupling filter and the Fourier transfer function for the radiation‐coupling filter are solved in closed form. The radiation‐coupling gain (loss) is applicable to the correction of experimental data and to the absolute calibration of circular transducers by self‐reciprocity measurements.

Acoustic Propagation Properties of Normal, Stunned, and Infarcted Myocardium Morphological and Biochemical Determinants

BACKGROUND Identification of viable but stunned myocardium remains a major problem. Since stunned myocardium results in impairment of myocardial function without any structural damage and infarcted myocardium causes major structural disruption, we postulated that acoustic properties could distinguish between the two insults. METHODS AND RESULTS Anesthetized open-chest dogs underwent a total occlusion of the left anterior descending coronary artery for 15 minutes (stunned, n = 7) and 90 minutes (infarcted, n = 8), followed by reperfusion for 3 hours. Circumflex coronary artery perfusion territory (n = 15) served as normal control tissue. Regions of myocardium were quantitatively evaluated with a scanning laser acoustic microscope operating at 100 MHz and a research ultrasound system operating at 4 to 7 MHz. Four ultrasonic parameters were determined: attenuation coefficient (an index of loss per unit distance), speed of propagation, a spatial variation of propagation speed called the heterogeneity index (HI), and ultrasonic backscatter at 5 MHz (IBR5). Myocardial water, lipid, and protein contents of normal, stunned, and infarcted myocardium were also determined. The attenuation coefficient of normal myocardium (179 +/- 20 dB/cm) was significantly greater than that of stunned (136 +/- 7 dB/cm, P < .001) and infarcted (130 +/- 8 dB/cm, P < .001) myocardium. The propagation speed of normal myocardium (1597 +/- 6 m/s) was similar to that of stunned (1600 +/- 6 m/s) and significantly higher than that of infarcted (1575 +/- 7 m/s, P < .001) myocardium. The HI for specimen thicknesses of 75 to 100 microns showed an increase of 33% between normal (5.0 +/- 0.8 m/s) and stunned (7.5 +/- 2.3 m/s, P < .05) myocardium. However, for the infarcted myocardium (5.8 +/- 2.0 m/s), the HI was essentially the same as that of the normal myocardium (5.0 +/- 0.8 m/s). The IBR5 of normal (-47.1 +/- 1.0 dB) was not significantly different from that of stunned myocardium (-46.8 +/- 0.9 dB). The IBR5 of infarcted myocardium (-42.4 +/- 1.0 dB) was significantly greater than that of normal myocardium. Myocardial water and protein contents were similar in the normal and stunned myocardium. Water content in the infarcted myocardium (80.8 +/- 2%) was significantly greater (P < .05) than in the normal (72.7 +/- 1.3%), and protein content of 18.5 +/- 0.7% was significantly lower (P < .05) than the normal (21.4 +/- 0.8%). Lipid content was increased in the stunned (8.5 +/- 0.5%) and virtually absent in the infarcted myocardium (0.8 +/- 0.3%) compared with normal (5.5 +/- 0.6%). CONCLUSIONS We conclude that acoustic propagation properties can identify stunned and infarcted myocardium and may be related to biochemical/morphological differences.

The myocardial signature: Absolute backscatter, cyclical variation, frequency variation, and statistics

This paper studies the absolute myocardial backscatter as a function of the frequency and phase of the cardiac cycle. This was achieved by calibration of the ultrasonic instrumentation and the random diffraction process. We have discovered a first-order model in which the scattering from the myocardium is Rayleigh scattering with a cardiac cycle variation in the scattering cross section. Furthermore, the statistics are approximately those of a radio frequency waveform with two independent Gaussian components (Rayleigh envelope). Deviations from the first-order model suggest measurable fine structure related to myocardial ultrastructure. This model has profound effects on the choice of optimal radiation patterns and signal processing schemes for preparing diagnostic parameters (e.g., integrated backscatter).

Apparatus and method for obtaining ultrasonic backcatter measurement from tissue

Optimal measurement of ultrasonic random backscatter from the myocardium is obtained by band limiting and whitening the received signal, squaring, summing and scaling same. The whitening is carried out for all spectrally altering factors to which the ultrasonic signal has been subjected. This includes whitening for the power law frequency response characterstics of the myocardium itself. Scaling includes a factor accounting for the energy of the effective transmitted ultrasonic signal and a factor providing appropriate units of measurement. The optimal measurement may be time averaged over one or more heartbeats for use in the diagnosis of ischemia or other cardiac conditions. It may be subjected to discrete Fourier transform analysis, to obtain its amplitude modulation and phase characteristics for similar purposes.

Estimation of myocardial infarct size with ultrasonic tissue characterization.

BackgroundUltrasonic tissue characterization (UTC) can distinguish normal from infarcted myocardium. Infarcted myocardium shows an increase in integrated backscatter and loss of cardiac cycle-dependent variation in backscatter. The cyclic variation of backscatter is closely related to regional myocardial contractile function; the latter is a marker of myocardial ischemia. The present study was designed to test the hypothesis that intramural cyclic variation of backscatter can map and estimate infarct size. Methods and ResultsTransmural myocardial infarction was produced in 12 anesthetized, open-chest dogs by total occlusion of the left anterior descending coronary artery for 4 hours. A real-time ultrasonic tissue characterization instrument, which graphically displays integrated backscatter Rayleigh 5, cardiac cycle-dependent variation, and patterns of cyclic variation in backscatter, was used to map infarct size and area at risk of infarction. Staining with 2,3,4-triphenyltetrazolium chloride (TTC) and Patent Blue Dye was used to estimate infarct size and the area at risk, respectively. The ratio of infarct size to area at risk of infarction determined with UTC correlated well with that determined with TTC (r = 0.862, y=23.7±0.792x). Correlation coefficients for infarct size and area at risk were also good (r = 0.736, y=12.3 ± 737x for infarct size and r = 0.714, y = 5.80 ± 1.012x for area at risk). However, UTC underestimated both infarct size and area at risk. ConclusionsUltrasonic tissue characterization may provide a reliable, noninvasive method to estimate myocardial infarct size.

Role of ultrasonic tissue characterization to distinguish reversible from irreversible myocardial injury.

Tissue characterization reflects structural and functional integrity of tissues. Inasmuch as reversible ischemia causes no structural damage and irreversible ischemia results in persistent structural myocardial damage, we postulated that ultrasonic tissue characterization can distinguish the two types of injuries. Anesthetized open chest dogs underwent 15 minutes (group 1, n = 5) and 90 minutes (group 2, n = 8) of acute total occlusion of the left anterior descending coronary artery, followed by 3 hours of reperfusion. Myocardial ischemia-infarction was confirmed with segment shortening, electronmicroscopic examination, and triphenyl tetrazolium chloride staining. Integrated backscatter Rayleigh 5 (IBR5), a measure of ultrasonic backscatter, and Fourier coefficient of amplitude modulation (FAM), an index of cardiac cycle dependent variation in backscatter, were measured at baseline, during ischemia, and after reperfusion. Group 1 (reversible ischemia) showed an increase in IBR5 from -48 +/- 1.2 dB at control to -45 +/- 1.0 dB (p less than 0.01) during ischemia, which returned to baseline after reperfusion (-47 +/- 1.3 dB). FAM was blunted during ischemia (6.2 +/- 1.0 dB during control versus 1.2 +/- 1.0 dB during ischemia, p less than 0.01) and recovered completely during reperfusion. Segment shortening was abolished during ischemia (18% +/- 3% during control versus -12% +/- 5% during ischemia, p less than 0.01) and recovered partially during reperfusion (4% +/- 5%). The group 2 animals with irreversible myocardial injury showed an increase in IBR5, from -49 +/- 1.2 dB during control to -44 +/- 1.0 dB during ischemia (p less than 0.01) and paradoxical bulging of the ischemic region (17% +/- 3% to -7% +/- 3%, p less than 0.01) during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of Peak and Modal Aortic Blood Flow Velocities With Invasive Measures of Left Ventricular Performance

The purpose of this study was to determine the accuracy of Doppler-derived modal and maximum velocity and peak and mean acceleration of ascending aortic blood for the assessment of left ventricular systolic function. Studies were performed in six anesthetized open-chest dogs. Doppler-derived modal velocity, maximum velocity, and peak and mean acceleration were compared with left ventricular dP/dt, maximum aortic blood flow, and rate of blood flow measured with an electromagnetic flow probe under varying inotropic states. Maximum Doppler velocity showed better correlation (r = 0.94, y = 0.34 + 3.95) with maximum aortic blood flow than the modal velocity (r = 0.85, y = 1.49 + 3.85x). Peak acceleration also correlated better with the rate of blood flow (r = 0.92, y = 12.3 + 4.92x) than the mean acceleration (r = 0.83, y = 12.2 + 4.27x). Modal and maximum velocity and mean and peak acceleration correlated well with left ventricular dP/dt. We conclude that peak modal and peak maximum velocity and peak and mean acceleration are accurate measurements of left ventricular function. Maximum velocity and peak acceleration are more accurate than modal velocity and mean acceleration.

IBR5: An Optimal Measurement of Integrated Backscatter and Cyclic Variation of Integrated Backscatter

Various methods have been developed to measure the coefficient of volume backscatter. For these measures, correction has made for signal energy, instrumentation/transducer filtration, diffraction and bulk loss, while using various square law or log magnitude detectors. Also, tissue backscatter has been measured as a function of frequency and the statistics of the backscatter has been examined. This paper unites methods of measuring a properly scaled (unbiased) estimate of the backscatter coefficient with knowledge of the scattering statistics and frequency response using statistical communications techniques. The maximum likelihood, minimum variance, unbiased estimator for wideband measurement of backscatter is developed together with its performance. The measurement technique has strong implications for system design for measuring cyclic myocardial backscatter.