Prediction of mechanical properties of human atherosclerotic tissue by high-frequency intravascular ultrasound imaging. An in vitro study.

Abstract

Intravascular ultrasound may be useful for studying the natural history of atherosclerotic lesions of different morphologies and for guiding interventional strategies. This study was designed to test the hypothesis that tissue appearance by intravascular ultrasound is related to the biomechanical properties of atheroma components. Forty-three atheroma caps were obtained from the abdominal aortas of 22 patients at autopsy and studied with an ultrasensitive, servo-controlled spectrometer. By measuring the static strain caused by increasing levels of compressive stress from 30 to 90 mm Hg, the uniaxial unconfined compression stiffness (ratio of stress to strain) was determined. After mechanical testing, specimens were imaged with a 6F, 20-MHz intravascular ultrasound transducer, and images were interpreted by an investigator who was unaware of the mechanical measurements. Specimens were classified as nonfibrous (n = 14), fibrous (n=18), or calcified (n=ll) based on intravascular ultrasound appearance. The static stiffnesses of the nonfibrous, fibrous, and calcified ultrasound classes were 41.2±18.8 kPa, 81.7±33.2 kPa, and 354.5±245.4 kPa, respectively (/?=0.0002 by analysis of variance). The times to reach static equilibrium (creep time) for the nonfibrous, fibrous, and calcified classes were 79.6±26.5 minutes, 50.2±20.0 minutes, and 19.4±8.1 minutes, respectively (/?=0.0007). Intravascular ultrasound appearance was most significantly related to biomechanical behavior when calcium deposits were noted; the differences in biomechanical behavior between nonfibrous and fibrous tissue appearances were less apparent Important biomechanical behavior of human atherosclerotic tissue can be predicted by intravascular ultrasound imaging; this technology may allow a detailed in vivo assessment of the stress-strain relation in diseased human arteries. (Arteriosclerosis and Thrombosis 1992;12:l-5) A therosclerotic lesions are often structurally / \ complex, with varying amounts of lipid, fi-J. \ -brous tissue, and calcium deposits. These components have different biomechanical behaviors that may explain why some plaques are more likely than others to rupture and cause occlusive thrombosis.1 Coronary angiography does not provide information about plaque structure beneath the endothelial surface (with the exception of severe calcification), so that evaluating the clinical importance of plaque structure antemortem has been limited to characterizing lumen geometry. 2Ultrasonic tissue-characterization methods can differentiate various pathological patterns of atherosclerosis, 3 and these patterns dramatically influence the biomechanical behavior of human plaque compo-

Viscoelastic Properties of Healthy Human Artery Measured in Saline Solution by AFM-Based Indentation Technique

“…Although the elastic modulus values reported by Gow et al [9,10] were obtained with indenters smaller in diameter than used here, information about the viscoelastic response is not provided. The technique used by Lee et al [11] used a 7 mm diameter indenter, and hence the results represent an average over an area more than 10 times larger than the area used in this study. In addition to providing local measurements of the elastic modulus of healthy, femoral artery (intimal) wall, to the best of the authors' knowledge, this investigation represents the first in vitro, localized assessment of the viscoelastic response of healthy inner arterial wall.…”

Noncollagenous Bone Matrix Proteins, Calcification, and Thrombosis in Carotid Artery Atherosclerosis

“…34 The use of undecalcified tissue allows observation of the earliest deposits, including cell association, therefore offering the possibility of linking descriptive morphology to mechanism. 35 Sample No. 7641 was heavily calcified and brittle and therefore was decalcified by chelation.…”

Characterizing Vulnerable Plaque Features With Intravascular Elastography

“…Although there is a difference between the static and dynamic mechanical properties of vascular tissue, the ratio between the different plaque components remains similar. 36,37 Nevertheless, in a pulsatile environment, the locations with increased strain may change between static or pulsatile experiments. However, the optimal threshold value (1.26% strain) for detecting a vulnerable plaque cannot be directly transferred from static in vitro experiments to pulsatile in patient recordings.…”