A HYPOTHESIS REGARDING VASCULAR ACOUSTIC-EMISSION ACCOMPANYING ARTERIAL INJURY-INDUCED BY BALLOON ANGIOPLASTY

Citation
Mj. Vonesh et al., A HYPOTHESIS REGARDING VASCULAR ACOUSTIC-EMISSION ACCOMPANYING ARTERIAL INJURY-INDUCED BY BALLOON ANGIOPLASTY, Annals of biomedical engineering, 25(5), 1997, pp. 882-895
Citations number
30
Categorie Soggetti
Engineering, Biomedical
ISSN journal
00906964
Volume
25
Issue
5
Year of publication
1997
Pages
882 - 895
Database
ISI
SICI code
0090-6964(1997)25:5<882:AHRVAA>2.0.ZU;2-B
Abstract
Stress-induced structural damage is often accompanied by sound release . This behavior is known as acoustic emission (AE). We hypothesize tha t vascular injury such as that produced by balloon angioplasty is asso ciated with AE. Postmortem human peripheral arterial specimens were ra ndomly partitioned into test (n = 10) and control segments (n = 10). T est 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 w ere quantified. Test and matched control segments subsequently underwe nt identical histological processing. Pressure-induced tissue trauma w as estimated via computerized histomorphometric analysis of the result ing slides (n = 100). Vascular acoustic emission (VAE) signals exhibit ed an amplitude range of +/-5.0 mu-bars and were observed to occur dur ing periods of increasing intraluminal pressure. The VAE signal power within the monitored bandwidth was concentrated below 350 Hz. More tha n 25 times as much VAE energy was released during the first pressuriza tion 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 arter ial tissue rupture strength. Histomorphometric estimates of tissue tra uma was greater for the test than their matched control segments (p < 0.0001). These preliminary data suggest that detectable acoustic energ y is released by vascular tissue subjected to therapeutic stress level s. Histological analysis suggest that the underlying source of sound e nergy may be related to tissue trauma, independent of histological pre paration artifacts. From this preliminary work, we conclude that VAE m ay be a fundamental property accompanying vascular tissue trauma, whic h may have applications to improving balloon angioplasty outcomes.