A hypothesis regarding vascular acoustic emission accompanying arterial injury induced by balloon angioplasty

M. J. Vonesh; L. F. Mockros; C. J. Davidson; K. B. Chandran; D. D. McPherson

doi:10.1007/BF02684173

A hypothesis regarding vascular acoustic emission accompanying arterial injury induced by balloon angioplasty

M. J. Vonesh, L. F. Mockros, C. J. Davidson, K. B. Chandran, D. D. McPherson

Medicine, Cardiology Division

Research output: Contribution to journal › Article › peer-review

Abstract

Stress-induced structural damage is often accompanied by sound release. This behavior is known as acoustic emission (AE). We hypothesize that vascular injury such as that produced by balloon angioplasty is associated with AE. Postmortem human peripheral arterial specimens were randomly partitioned into test (n = 10) and control segments (n = 10). Test segments were inserted into a pressurization circuit and subjected to two consecutive hydrostatic pressurizations. Amplitude, frequency, and energy content of the AE signals released during pressurization were quantified. Test and matched control segments subsequently underwent identical histological processing. Pressure-induced tissue trauma was estimated via computerized histomorphometric analysis of the resulting slides (n = 100). Vascular acoustic emission (VAE) signals exhibited an amplitude range of ±5.0 μbars and were observed to occur during periods of increasing intraluminal pressure. The VAE signal power within the monitored bandwidth was concentrated below 350 Hz. More than 25 times as much VAE energy was released during the first pressurization as during the second: 1,855 ± 513.8 mJ vs. 73 ± 44.9 mJ (mean ± SEM, p < 0.006). Estimates of circumferential intimal wall stress at AE onset averaged 170 kPa, slightly below reported values of arterial tissue rupture strength. Histomorphometric estimates of tissue trauma was greater for the test than their matched control segments (p < 0.0001). These preliminary data suggest that detectable acoustic energy is released by vascular tissue subjected to therapeutic stress levels. Histological analysis suggest that the underlying source of sound energy may be related to tissue trauma, independent of histological preparation artifacts. From this preliminary work, we conclude that VAE may be a fundamental property accompanying vascular tissue trauma, which may have applications to improving balloon angioplasty outcomes.

Original language	English (US)
Pages (from-to)	882-895
Number of pages	14
Journal	Annals of Biomedical Engineering
Volume	25
Issue number	5
DOIs	https://doi.org/10.1007/BF02684173
State	Published - 1997

Funding

Acknowledgment--We thank Cynthia Shane for her expert preparation of this manuscript. This study was supported, in part, by the Feinberg Cardiovascular Research Institute and the National Institutes of Health-National Heart, Lung, and Blood Institute Grants HL-46550 and RR-10912. This work was presented in part at the American College of Cardiology Meetings, New Orleans, LA, March 19-22, 1995.

Keywords

Atherosclerosis
Biomechanics
Plaque rupture
Restenosis
Vascular mechanics

ASJC Scopus subject areas

Biomedical Engineering

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10.1007/BF02684173

Cite this

@article{d0aa7bd8303149248177fb651f509b54,

title = "A hypothesis regarding vascular acoustic emission accompanying arterial injury induced by balloon angioplasty",

abstract = "Stress-induced structural damage is often accompanied by sound release. This behavior is known as acoustic emission (AE). We hypothesize that vascular injury such as that produced by balloon angioplasty is associated with AE. Postmortem human peripheral arterial specimens were randomly partitioned into test (n = 10) and control segments (n = 10). Test segments were inserted into a pressurization circuit and subjected to two consecutive hydrostatic pressurizations. Amplitude, frequency, and energy content of the AE signals released during pressurization were quantified. Test and matched control segments subsequently underwent identical histological processing. Pressure-induced tissue trauma was estimated via computerized histomorphometric analysis of the resulting slides (n = 100). Vascular acoustic emission (VAE) signals exhibited an amplitude range of ±5.0 μbars and were observed to occur during periods of increasing intraluminal pressure. The VAE signal power within the monitored bandwidth was concentrated below 350 Hz. More than 25 times as much VAE energy was released during the first pressurization as during the second: 1,855 ± 513.8 mJ vs. 73 ± 44.9 mJ (mean ± SEM, p < 0.006). Estimates of circumferential intimal wall stress at AE onset averaged 170 kPa, slightly below reported values of arterial tissue rupture strength. Histomorphometric estimates of tissue trauma was greater for the test than their matched control segments (p < 0.0001). These preliminary data suggest that detectable acoustic energy is released by vascular tissue subjected to therapeutic stress levels. Histological analysis suggest that the underlying source of sound energy may be related to tissue trauma, independent of histological preparation artifacts. From this preliminary work, we conclude that VAE may be a fundamental property accompanying vascular tissue trauma, which may have applications to improving balloon angioplasty outcomes.",

keywords = "Atherosclerosis, Biomechanics, Plaque rupture, Restenosis, Vascular mechanics",

author = "Vonesh, {M. J.} and Mockros, {L. F.} and Davidson, {C. J.} and Chandran, {K. B.} and McPherson, {D. D.}",

note = "Funding Information: Acknowledgment--We thank Cynthia Shane for her expert preparation of this manuscript. This study was supported, in part, by the Feinberg Cardiovascular Research Institute and the National Institutes of Health-National Heart, Lung, and Blood Institute Grants HL-46550 and RR-10912. This work was presented in part at the American College of Cardiology Meetings, New Orleans, LA, March 19-22, 1995.",

year = "1997",

doi = "10.1007/BF02684173",

language = "English (US)",

volume = "25",

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T1 - A hypothesis regarding vascular acoustic emission accompanying arterial injury induced by balloon angioplasty

AU - Vonesh, M. J.

AU - Mockros, L. F.

AU - Davidson, C. J.

AU - Chandran, K. B.

AU - McPherson, D. D.

N1 - Funding Information: Acknowledgment--We thank Cynthia Shane for her expert preparation of this manuscript. This study was supported, in part, by the Feinberg Cardiovascular Research Institute and the National Institutes of Health-National Heart, Lung, and Blood Institute Grants HL-46550 and RR-10912. This work was presented in part at the American College of Cardiology Meetings, New Orleans, LA, March 19-22, 1995.

PY - 1997

Y1 - 1997

N2 - Stress-induced structural damage is often accompanied by sound release. This behavior is known as acoustic emission (AE). We hypothesize that vascular injury such as that produced by balloon angioplasty is associated with AE. Postmortem human peripheral arterial specimens were randomly partitioned into test (n = 10) and control segments (n = 10). Test segments were inserted into a pressurization circuit and subjected to two consecutive hydrostatic pressurizations. Amplitude, frequency, and energy content of the AE signals released during pressurization were quantified. Test and matched control segments subsequently underwent identical histological processing. Pressure-induced tissue trauma was estimated via computerized histomorphometric analysis of the resulting slides (n = 100). Vascular acoustic emission (VAE) signals exhibited an amplitude range of ±5.0 μbars and were observed to occur during periods of increasing intraluminal pressure. The VAE signal power within the monitored bandwidth was concentrated below 350 Hz. More than 25 times as much VAE energy was released during the first pressurization as during the second: 1,855 ± 513.8 mJ vs. 73 ± 44.9 mJ (mean ± SEM, p < 0.006). Estimates of circumferential intimal wall stress at AE onset averaged 170 kPa, slightly below reported values of arterial tissue rupture strength. Histomorphometric estimates of tissue trauma was greater for the test than their matched control segments (p < 0.0001). These preliminary data suggest that detectable acoustic energy is released by vascular tissue subjected to therapeutic stress levels. Histological analysis suggest that the underlying source of sound energy may be related to tissue trauma, independent of histological preparation artifacts. From this preliminary work, we conclude that VAE may be a fundamental property accompanying vascular tissue trauma, which may have applications to improving balloon angioplasty outcomes.

AB - Stress-induced structural damage is often accompanied by sound release. This behavior is known as acoustic emission (AE). We hypothesize that vascular injury such as that produced by balloon angioplasty is associated with AE. Postmortem human peripheral arterial specimens were randomly partitioned into test (n = 10) and control segments (n = 10). Test segments were inserted into a pressurization circuit and subjected to two consecutive hydrostatic pressurizations. Amplitude, frequency, and energy content of the AE signals released during pressurization were quantified. Test and matched control segments subsequently underwent identical histological processing. Pressure-induced tissue trauma was estimated via computerized histomorphometric analysis of the resulting slides (n = 100). Vascular acoustic emission (VAE) signals exhibited an amplitude range of ±5.0 μbars and were observed to occur during periods of increasing intraluminal pressure. The VAE signal power within the monitored bandwidth was concentrated below 350 Hz. More than 25 times as much VAE energy was released during the first pressurization as during the second: 1,855 ± 513.8 mJ vs. 73 ± 44.9 mJ (mean ± SEM, p < 0.006). Estimates of circumferential intimal wall stress at AE onset averaged 170 kPa, slightly below reported values of arterial tissue rupture strength. Histomorphometric estimates of tissue trauma was greater for the test than their matched control segments (p < 0.0001). These preliminary data suggest that detectable acoustic energy is released by vascular tissue subjected to therapeutic stress levels. Histological analysis suggest that the underlying source of sound energy may be related to tissue trauma, independent of histological preparation artifacts. From this preliminary work, we conclude that VAE may be a fundamental property accompanying vascular tissue trauma, which may have applications to improving balloon angioplasty outcomes.

KW - Atherosclerosis

KW - Biomechanics

KW - Plaque rupture

KW - Restenosis

KW - Vascular mechanics

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A hypothesis regarding vascular acoustic emission accompanying arterial injury induced by balloon angioplasty

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