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(Circulation. 1997;95:1022-1029.)
© 1997 American Heart Association, Inc.
Articles |
In Vitro Identification of Angioplasty-Induced Injury by Use of Vascular Acoustic Emissions
the Department of Medicine, Section of Cardiology (M.J.V., C.J.D., D.D.M.), and the Department of Biomedical Engineering (M.J.V., L.F.M.), Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, Ill, and the College of Engineering, Department of Biomedical Engineering (K.B.C.), University of Iowa, Iowa City.
Correspondence to David D. McPherson, MD, Section of Cardiology, Northwestern University, 250 E Superior St, Wesley Pavilion, Suite 582, Chicago, IL 60611.
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Abstract |
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Background We have developed a novel method of diagnosing stress-induced vascular injury. This approach uses the sound energy released from atherosclerotic arterial tissue during in vitro balloon angioplasty to characterize type and severity of induced trauma.
Methods and Results Thirty-two postmortem human peripheral arterial specimens 1.0 cm long were subjected to in vitro balloon angioplasty with simultaneous acoustic emission monitoring. Specimens were examined before and after angioplasty to ascertain the extent of angioplasty-induced injury. Gross observation was used to identify dissection. A three-dimensional intravascular ultrasound reconstruction technique was used to estimate the luminal surface area of the specimen. Change in luminal surface area (postangioplasty minus preangioplasty) was used to quantify induced injury. The energy content and spectral distribution of the digitally acquired vascular acoustic emission (VAE) signals were computed. Comparisons of angioplasty-induced trauma with VAE signal characteristics were made. Dissection (mural laceration of variable depth) was observed in 15 of 32 specimens. Eleven showed no evidence of induced dissection, and 6 had preexisting intimal disruptions. The energy content of the VAE signals collected from specimens with dissection was greater than that obtained from those in which dissection was absent: 845±89.4 mJ (mean±SEM; n=15) versus 128±40.8 mJ (n=11; P<.001). Comparison of induced trauma and VAE signal energy demonstrated a proportional relationship (r=.87, P<.001, n=32).
Conclusions VAE signals contain information characterizing type and severity of angioplasty-induced arterial injury. Because vascular injury is related to adverse procedural outcome, development of VAE technology as an adjunct to conventional diagnostic modalities may facilitate optimal balloon angioplasty delivery and postprocedural care.
Key Words: angioplasty • atherosclerosis • coronary disease • balloon
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Introduction |
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The mechanisms of BA are fundamentally traumatic to arterial tissue. Accumulated research demonstrates that BA involves superficial disruption of the intima, fracture of atheromatous plaque, crack propagation, and copious stretching of arterial tissue.1 2 3 4 Dissection secondary to crack propagation is a particularly insidious form of BA-induced arterial trauma involving laceration and/or cleavage of the arterial wall. Dissection has been implicated as a contributing factor to both acute procedural complications (abrupt reclosure,5 6 7 8 ischemia,9 10 myocardial infarction,5 11 12 emergency surgery,5 11 12 13 and coronary microembolization14 15 ) and chronic restenosis of the treatment site.16 17 18 19 20 21 22 Although the presence of dissection has been shown to be an important predictor of clinical outcome after BA intervention, dissection severity may be a better correlate to outcome.9 18 20
Identification of BA-induced dissection may allow prediction of patients at risk for developing complications. Clinically, however, this objective is hindered by the ability of conventional diagnostic techniques, including angiography and IVUS, to accurately identify dissection or soft tissue trauma. Angiographic "evidence" of dissection, for example, involves identification of intraluminal filling defects, extraluminal extravasation of contrast material, linear luminal densities, or luminal staining. These interpretations are subjective, are not amenable to conventional quantitative angiographic analysis, and cover a wide range of potential injury types.19 22 23 24 IVUS imaging techniques, by comparison, also suffer inherent limitations (calcific shadowing, near-field distortion, catheter-to-vessel alignment artifact) that may preclude consistent characterization of vascular trauma.25 26
We have previously described the phenomenon of VAE accompanying stress-induced injury of atherosclerotic arterial tissue.27 AE involves the transient release of strain energy, in the form of sound waves, from a material as it experiences stress-induced structural damage such as fracture. AE has been used in various engineering applications to provide an "acoustic signature" characterizing the type and/or extent of material failure.28 Because angioplasty-induced arterial injury is the result of stress-mediated material damage, we hypothesize that characteristics of the VAE may be used to discriminate the type and severity of induced injury. The objective of this study was to investigate VAE during BA of postmortem human arterial tissue.
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Methods |
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Specimens: Preparation and Imaging
Nineteen human peripheral arterial specimens (iliac and femoral; mean age of donors, >50 years) exhibiting various degrees of atherosclerosis were collected at autopsy. Specimens were washed in isotonic saline and flash-frozen (-80°C) within 6 hours of death. Before we conducted the angioplasty protocol described below, the specimens were warmed to body temperature (37°C) and sectioned into 32 segments 10 mm long.
The arterial segments were subjected to gross examination before and after angioplasty to assess the extent of tissue trauma. Before angioplasty, the arterial segments were examined under a dissecting microscope for evidence of existing intimal disruption. After angioplasty, the segments were again examined for gross signs of BA-induced trauma and visual evidence of mural calcification. Dissection, defined as an intimal laceration propagating into the arterial wall to a variable extent, was nominally classified as either "absent" or "present." Calcification of the wall was also graded as "absent" or "present."
Three-dimensional IVUS imaging of the arterial segments was also performed to provide an objective estimate of tissue trauma within the arterial wall.4 29 30 31 Specimens were placed into an imaging fixture that ensured that the vascular segment retained the same orientation during preangioplasty and postangioplasty IVUS imaging. A 5F, 30-MHz rotating-mirror IVUS catheter (Boston Scientific Inc) was passed over a 0.014-in guidewire coaxial to the tissue. The proximal end of the IVUS catheter was incorporated into a motorized pullback device, allowing precise catheter withdrawal at a constant rate of 0.5 mm/s. Imaging was conducted in a normal saline water bath maintained at 37°C. After all air was flushed from the tissue and catheter tip, IVUS data were recorded on 1/2-in S-VHS videotape during catheter withdrawal for off-line morphometric analysis. Instrumentation settings were optimized for each specimen during preangioplasty imaging and held constant during postangioplasty IVUS imaging.
To objectively quantify BA-induced trauma, off-line IVUS image analysis was performed. Image data were digitized at 1.0-mm intervals, resulting in 10 images per specimen. Digital images were acquired at 256x240-pixel spatial resolution (
0.075 mm/pixel) and 8-bit amplitude resolution with commercial software (ImageComm Systems CardiAcq). Digital IVUS images were subjected to a preprocessing sequence to prepare the data for semiautomated luminal contour extraction. Luminal contours were extracted from the processed images collected from each segment with an interactive computer-automated edge-detection algorithm. The computer algorithm identified the best fit to the luminal contour on the basis of a brightness-gradient method. Fig 1A
shows an original, digital IVUS image. Fig 1B illustrates the superimposed computer-identified contour extracted from the original IVUS image. Manual editing of the identified contours was available to ensure accuracy. All image processing was performed with commercial software (Image-Pro Plus, version 1.0, Media Cybernetics, Inc).
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Variability of the edge-detection algorithm was assessed by two blinded reviewers who repeatedly (two times) used this method to measure luminal contours from 13 randomly selected IVUS images.
Morphometric descriptors of the "luminal" contours were computed for each image before and after angioplasty. Here, "luminal" refers to that portion of the vessel cross section that would function as the blood/tissue interface in vivo. This definition encompasses what is conventionally thought of as the lumen, as well as cracks and/or fissures into the arterial wall. The LP, average lumen area, and minimal lumen diameter were quantified. The LSA (in mm2) of each segment was computed as the sum of the product of the LP (in mm) and a 1.0-mm slice separation distance for the 10 images composing each vascular segment: LSA=
LPx1.0. Segment LSA was estimated before and after angioplasty, referred to as LSApre and LSApost, respectively. 
LSA (in mm2) was used as a measure of BA-induced tissue trauma: LSA=LSApost-LSApre.
Experimental Apparatus
Balloon angioplasty of the arterial segments was performed with a custom-designed experimental device consisting of a circularly cylindrical 8.0-mm-diameter, 3.0-cm-long compliant balloon. This device was custom-designed for integration to a hydraulic pressurization circuit and facilitated collection of VAE data. Arterial segments were placed onto the middle third of the balloon to avoid the effects of nonuniform balloon inflation that potentially occur near the ends during dilatation. The ratio of balloon diameter to vessel minimum lumen diameter was 1.1:1. This ratio was intended to cause dissection and was within the range reported in similar experimental protocols.32 33 A rudimentary AE sensor was constructed from a commercial back-electret condenser microphone (Realistic model 33-1063). The microphone, which has a flat (-3 dB) frequency response between 50 and 15 000 Hz and a sensitivity of 0.00025 V/µbar (1 µbar=0.1 N/m2), was incorporated into one end of a fluid-filled plastic housing behind a protective latex membrane (25 µm). A portion of the sound energy released from the arterial tissue during BA was coupled through the balloon membrane into the fluid continuum of the pressurization circuit for detection.
The balloon device and AE sensor were inserted in series into a hydraulic circuit that allowed controlled, reproducible dilatation of the arterial segment (Fig 2A). Balloon dilatation involved injection of normal saline into the circuit from the end opposite the AE sensor with a Harvard infusion pump (model 600-000). All entrapped air bubbles were purged from the circuit before dilatation, ensuring a continuous fluid pathway between the balloon and AE sensor. Balloon dilatation of the arterial segments was conducted in a normal saline bath maintained at 37°C and enclosed within a sound-attenuating chamber to minimize detection of ambient-source acoustic noise. Simultaneous VAE and balloon pressure signals were recorded in analog and digital formats during angioplasty. As depicted in Fig 2B, real-time VAE signals detected by the AE transducer were entered into the audio channel of a VCR (Panasonic model AG-7300) for preamplification (x400) and high-fidelity analog audio recording. AE signals were then routed to a Gould Universal instrumentation amplifier (model 13-4615-58), which provided additional amplification (x10) and bandpass filtering (10 to 3000 Hz). Intraluminal pressure, measured by a fluid-coupled pressure transducer attached to the pressurization circuit, was entered into a separate Gould Universal instrumentation amplifier calibrated in atmospheres (1 atm=760 mm Hg). Analog hard copy of simultaneous VAE and pressure waveforms was recorded (Gould model TA4000). Digital acquisition of these data was done with a computer-based analog-to-digital recording system (Codas, version 5.50, DATAQ, Inc) sampling at 1000 Hz.
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Balloon Angioplasty Protocol
The 32 arterial segments were subjected to balloon angioplasty by controlled infusion of saline into the pressurization circuit at a flow rate of 0.2 mL/s. To avoid sound artifacts generated during unfurling of the balloon material, the hydraulic circuit was initially pressurized to 0.5 atm (380 mm Hg). This bias pressure ensured complete balloon inflation and uniform contact of the balloon material with the arterial tissue (to establish an efficient acoustic couple) but was below reported levels associated with arterial traumatization.34 35 Maximum balloon pressure was 4.5 atm.
To characterize the ambient noise conditions and sound artifacts arising from balloon inflation alone, pressure and VAE data were also collected during balloon inflation without any arterial tissue. Ten "balloon-alone" trials were randomly conducted under conditions identical to those used for the arterial tissue.
AE Signal Analysis
Digitized waveforms were analyzed off-line with software developed specifically for this application (Matlab Version 4.0, Mathworks, Inc). The objective of the AE signal analysis was to characterize the frequency spectra and energy content of vascular AE accompanying BA-induced dissection. The methodology used in this experiment was adapted from a method that we have previously used to describe the VAE phenomenon.27
A threshold level was established via analysis of the acoustic data collected from the 10 trials in which the balloon was inflated without overlying tissue. Thresholding determination began with computation of the spectrogram of the acoustic data for each of the 10 balloon-only trials. This resulted in an estimate of the frequency distribution of acoustic signal magnitude at 0.064-second intervals. Maximum signal magnitude (over the 1- to 500-Hz bandwidth) was extracted from the magnitude spectrum for each 0.064-second time interval, resulting in the time distribution of maximum FFT magnitude of the acoustic signal. The mean and SD of the maximum FFT magnitude versus time distribution were computed from the 10 independent balloon-only trials. The threshold level was arbitrarily defined as 1 SD greater than the mean maximum FFT magnitude function. The average FFT magnitude threshold level of these 10 experimental runs (5.3 V2) was used to discriminate VAE signals from background noise.
The frequency distribution and energy content of the VAE signals were computed. This analysis was restricted to that portion of the AE data corresponding to sustained, positive dP/dt during balloon inflation between 0.5 and 4.5 atm. The spectrogram of these data was computed, and the previously determined threshold level was used to differentiate the data into signals probably associated with vascular AE or acoustic energy present in the recorded data but having a low probability of being vascular AE (background/ambient noise or balloon artifact). Only superthreshold regions of data were deemed to be "vascular AE" and used in further analyses.
Two characteristics of the VAE signal were extracted from the AE data. VAEEt was computed in the time domain by integrating the squared magnitude of the digitized VAE signal (|v(t)|2, with v(t) in volts) over the period of positive dP/dt for a given balloon inflation by the following equation: VAEEt =
|v(t)|2 dt. Additionally, an estimate of the magnitude spectrum of the VAE signals released during a given balloon inflation was obtained by averaging the spectra of each 0.064-second time interval of the spectrogram function that exceeded the predefined threshold level. The magnitude spectrum is proportional to the distribution of AE signal power as a function of frequency.
Statistical Analysis
Statistical analyses were performed with SPSS for Windows software (release 6.0). Student's t test was used to compare VAE signal characteristics of tissue segments without preexisting intimal trauma grouped by postangioplasty evidence of gross dissection (absent versus present). Two-way ANOVA was used to determine the effects of gross dissection and intramural calcification on the dependent AE signal characteristics (VAEEt). 
2 testing was performed to evaluate the association between calcification and gross dissection. Linear regression analysis was used to determine the relationship between LSA and the AE signal characteristics. Univariate curve fitting of the LSA versus VAEEt data was performed. Significance was defined at a value of P<.05 level unless otherwise indicated. Data are expressed as mean±SEM.
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Results |
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Preangioplasty examination of the 32 specimens revealed no gross evidence of preexisting intimal disruption in 26 of 32 segments. In the 6 specimens in which preexisting intimal disruptions were identified, trauma was presumed to be caused during specimen collection, because no signs of intraluminal thrombosis were observed. On postangioplasty examination, BA-induced dissection was observed in 15 of 26 segments. Eleven of 26 segments without preexisting intimal disruptions showed no gross signs of BA-induced arterial dissection.
The experimental BA device, with a ratio of balloon to lumen diameter of 1.1:1, produced a modest increase in the diameter of the segments (8.3±2.09%). Post-BA lumen area and minimum lumen diameter were greater than their pre-BA counterparts: 48.6±2.26 versus 55.3±2.14 mm2 (pre-BA versus post-BA) and 7.6±0.19 versus 8.2±0.17 mm (pre-BA versus post-BA), respectively (P<.001, n=32).
Fig 3 is a composite figure depicting the gross appearance of representative postintervention tissue segments in which dissection was absent (A) and two segments exhibiting progressively more traumatic dissection (B,C), along with the simultaneous VAE and pressure signals recorded during dilatation of these specimens. Typical VAE and pressure signals recorded from inflation of the balloon alone (D) are also included. Qualitative interpretation of these figures suggests that VAE activity is more pronounced in specimens with BA-induced injury (dissection) than in specimens with less traumatic dilatation (stretching). Acoustic activity from inflation of the balloon alone, although present, was consistently less than that associated with dilatation of arterial tissue.
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Fig 4 depicts a 3D lumenogram constructed from IVUS images collected before and after BA of a vascular segment with dissection. The difference in lumenogram surface area (pre-BA versus post-BA) embodies a measure of BA-induced trauma (LSA). In general, LSA increases after balloon dilatation due to both stretching and fracture mechanisms. Interobserver variability of the computer-automated image analysis algorithm used to calculate LSA was 6.2%. Intraobserver variability of this approach was <1%.
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The average VAE magnitude spectra computed for tissue specimens in which grossly observed dissection was present (n=15), preexisting (n=6), and absent (n=11), along with the average magnitude spectrum computed from the balloon-alone trials (n=10), are demonstrated in Fig 5. Specimens exhibiting signs of dissection, on average, had higher AE magnitudes, particularly in the bandwidth between 100 and 200 Hz. The mean AE magnitude in the 100- to 200-Hz bandwidth was observed to increase, in general, with the presence of BA-induced dissection. The average magnitude spectrum of the balloon-alone trials was lower than that associated with tissue dilatation for all frequencies examined.
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In the 32 segments composing the entire sample population, results of the two-way ANOVA indicated that the presence of dissection was the only factor that had an effect on VAEEt (P<.001) (Table 1). 2 testing revealed that the incidence of intramural calcification and angioplasty-induced dissection were independent variables (P<.25, Table 2).
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In specimens without preexisting intimal disruptions, grouped-means comparison of specimens categorized by presence of BA-induced dissection (absent versus present) demonstrated that VAEEt was different in the two groups: 128±40.8 mJ (n=11) versus 845±89.4 mJ (n=15;P<.001) (mean±SEM, Fig 6). These data suggest that VAE energy content may characterize the type of BA-induced injury (dissecting versus nondissecting). No differences in lumen area or minimum diameter change were noted between the dissecting and nondissecting categories.
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The scatterplot of LSA versus VAEEt is presented in Fig 7. A proportional relationship between LSA and VAEEt was observed for the 32 cases, suggesting a correlation between the amount of acoustic energy released by atherosclerotic arterial tissue during BA and the severity of stress-induced trauma (LSA [mm2]=0.13xVAEEt [mJ]+8.54 [mm2]; r=.87, P<.001, SEE=31.6 mm2, n=32). Curve fitting to a cubic equation provided the best univariate data fit but provided only marginal improvement (r=.88).
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Discussion |
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With BA-induced VAE signals used to characterize the type and severity of BA-induced arterial trauma in postmortem atherosclerotic tissue, our preliminary data suggest that VAE energy content differentiates dissecting from nondissecting dilatations and is proportional to the severity of induced trauma. The following discussion focuses on previous work, the suitability of our experimental model, the method of estimating BA-induced trauma severity, reported results, limitations, and potential implications of this research.
Although the relationship between BA-induced vascular injury and adverse procedural outcome is fairly well understood,5 9 16 17 18 20 a reliable means of diagnosing induced arterial trauma has proved elusive. As a result, procedural efficacy has arguably suffered. Huber et al,11 for example, showed that clinical success rates of patients exhibiting type B dissections (NHLBI classification system) were no different from those of patients without angiographic evidence of dissection. Patients with more traumatic type C through F dissections, in contrast, had a higher incidence of acute complications and an overall success rate of only 38%.11 Black et al,9 in a cohort of 96 patients, identified the length of BA-induced dissection as the strongest independent predictor of acute ischemic complications. Tenaglia et al20 showed, via an IVUS imaging study with 90% 6-month follow-up, that dissection severity was strongly correlated to chronic restenosis.33 Work by Schwartz et al36 in a porcine model of atherosclerosis demonstrated that the neointimal hyperplastic response to injury is proportional to trauma severity. Similar findings were reported in chronic restenosis patients by Nobuyoshi et al,18 who found that intimal hyperplasia was greater in arteries with dissections having medial or adventitial involvement than in arteries with only intimal tears. On the basis of these and other findings, procedural strategies designed to identify and minimize BA-induced trauma have been advocated as potential methods of lowering procedural complication rates.37 38 39 40 The VAE technique, by characterizing BA-induced arterial injury, may facilitate prediction of adverse outcome.
Our experimental model used to investigate the relationship between VAE signal characteristics and BA-induced trauma provides a reasonable approximation to clinical BA. Although BA was conducted in vitro, with an experimental device, the observed mechanisms of action (stretching, plaque cracking, dissection) concurred with those reported in previous postmortem2 41 and IVUS4 23 24 42 43 studies. Gross dissection was observed in 58% (15/26) of our dilated arterial specimens without preexisting intimal disruptions. This dissection rate is somewhat less than that reported in postmortem studies14 but is comparable to that reported for clinical studies that used IVUS imaging techniques.20 A potential factor influencing these results was that the 1.1:1 balloon-to-artery ratio implemented in this study was based on the luminal diameter of the test specimen, not a reference segment. Contrary to the findings reported by Hoyne et al,43 the incidence of dissection in this in vitro study was not related to the presence of intramural calcification.
Computation of the LSA is a novel means of characterizing BA-induced vascular injury. This method is based on quantitative analysis of 3D IVUS reconstructions of arterial segment geometry, which, despite acknowledged limitations,31 have been shown to be accurate in characterizing morphological features of arterial trauma.30 An improvement on the conventional 3D IVUS methodology was our development of an objective, computer-automated luminal contour–detection algorithm instead of brightness-thresholding segmentation. The LSA variable embodies any balloon-mediated alteration resulting in the change of the luminal topography (including tissue cracking, fissuring, and stretching) and physically represents the creation of new surface area within the arterial wall. Most BA remodeling mechanisms will alter LSA and be reflected in this measure. An advantage of using LSA to characterize vascular trauma is that it allows treatment of induced trauma as a continuous variable as opposed to a dichotomous variable (absent/present). As a relative measure, LSA allowed inclusion of the six specimens in which preexisting trauma was observed. Interestingly, three cases were observed in which LSA was negative, implying that LSA decreased as a consequence of BA. Although these are probably attributable to passive elastic recoil mechanisms, they may also be interpreted as BA-mediated "smoothing" of irregular luminal surface topography.
Characteristics of the VAE signals collected during in vitro BA retrospectively identified specimens exhibiting gross dissection from those without. The most marked differences between these groups were exhibited by VAEEt (cumulative, time-limited energy). The distribution of VAEEt for specimens in which gross dissection was present (n=15; range, 523 to 1738 mJ) did not overlap the distribution for specimens in which dissection was absent (n=11; range, 4 to 425 mJ). These findings suggest that a threshold level of AE energy may exist below which dissection is unlikely and above which dissection is probable. The energy content of the VAE signal within the bandwidth between 100 and 200 Hz was greater for dissecting specimens than nondissecting specimens. The importance of the 100- to 200-Hz bandwidth relative to the VAE phenomenon is unknown. Similarly, the reason for trauma differentiation within this bandwidth is unclear.
Our data suggest that the amount of AE energy released by vascular tissue during angioplasty is proportional to the severity of BA-induced tissue trauma. These findings are evident on examination of LSA versus VAEEt. Energy considerations suggest that the total amount of energy released from a material as it experiences mechanical failure is proportional to the surface energy of the material, a loss function incorporating energy losses (including those attributable to acoustic dissipation), and the area of new surfaces formed.44 Because BA-induced tissue injury often involves creation of new surface area within the arterial wall, it is not altogether surprising that characteristics of the VAE signal (particularly energy content) are related to measures of trauma severity.
Several factors may have influenced our findings. The LSA approach used to estimate BA-induced trauma is predicated on high-quality IVUS image data and the accuracy of semiautomated luminal contour identification. Because the arterial tissue was imaged in saline from a coaxial location that ensured a perpendicular angle of vessel wall insonation, IVUS images were nearly optimal. Nevertheless, since dissection may occur within the arterial wall without appreciable separation of the newly created surfaces, it is likely that IVUS was not able to detect the total extent of BA-induced trauma in all image planes. Calcific shadowing and other image artifacts may have also affected our ability to identify the "luminal" contour. Use of 3D IVUS imaging techniques to compute estimates of trauma severity (LSA) may have compounded these problems and, together with edge-detection errors, introduced variability into the data. The complex morphology of the diseased arterial wall along with the heterogeneous composition of the advanced atherosclerotic lesion precludes theoretical elucidation of the exact relationship between VAE energy and BA-mediated surface area creation. Validation of these preliminary findings requires additional work using fresh postmortem specimens, and in vivo utility requires consideration of a number of factors not included in this study (cardiac, respiratory, blood flow, and other acoustic artifacts). In addition to the determination of major tissue disruption, AE analysis may allow the characterization of atheroma morphology at angioplasty. The purpose of this study was to determine whether VAE occurs with tissue disruption, irrespective of atheroma morphology. Studies are under way to determine VAE characteristics that may be associated with specific atheroma morphology.
Sound emission accompanying stress-induced injury of atherosclerotic arterial tissue has been demonstrated. VAE may have the potential to provide the basis for new diagnostic technology. The initial in vitro success of VAE signals to differentiate the type (nondissecting versus dissecting) and severity (LSA magnitude) of stress-induced vascular trauma suggests that this approach may provide unique diagnostic information and therefore be a useful adjunct to angiography and IVUS. Given the prominent role of vascular injury in the pathogenesis of BA procedural complications, further development of diagnostic VAE technology may have profound basic and clinical ramifications.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by the Feinberg Cardiovascular Research Institute and National Institutes of Health, NHLBI, grants HL-46550 and RR-10912. We wish to thank Cynthia Shane for her expert preparation of the manuscript.
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Footnotes |
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Presented in part at the 68th Scientific Sessions of the American Heart Association, Anaheim, Calif, November 13-16, 1995.
Received May 29, 1996; revision received October 7, 1996; accepted October 14, 1996.
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