Composition- and history-dependent radial compressive behavior of human atherosclerotic plaque

Abstract

Invasive procedures to revascularize occluded blood vessels rely on the mechanical response of the diseased tissue. Failure rates associated with such procedures show the need for improvement. to understand the associated mechanics, the material properties of atherosclerotic plaque should be known; yet data are scant. The purpose of this study was to investigate the different mechanical responses exhibited by plaques with different compositions, focusing specifically on radial compressive behavior. A custom-built experimental system was developed that was fully computer controlled with a broad range of loading capabilities. A temperature-controlled, physiologic specimen bath allowed testing at 37 degrees C. Monotonically loaded specimens showed that plaque behavior was nonlinear under finite deformations. A multiple cycle protocol, executed in two phases, distinguished three types of mechanical response of different plaques. The differences in behavior were associated with histologic differences in plaque composition, and mechanically characterized by different "repeatability" (the stabilization of the cyclic response) and "recoverability" (the second loading phase retracing the first loading phase behavior). Type 1 behavior was categorized by repeatability and recoverability. Type 2 behavior displayed repeatability but only partial recovery during the second loading phase. Recovery was absent in type 3 behavior. The histologic observations demonstrated that calcified tissue was present only in specimens displaying type 1 behavior. Fibrous tissue and part of a modified media (due to disease) were present in specimens displaying type 2 behavior. An atheroma, along with a relatively thin modified media, was present in specimens displaying type 3 behavior. The differences in the maximum stretches attained at the end of phase I loading, the stretch offset from the first to the 15th cycle of phase I loading, and the hysteresis in the first and 15th cycles of phase I loading distinguished the specimen behaviors with statistical significance. These compression data showed that plaques exhibit composition- and history-dependent nonlinear and inelastic responses under finite deformations.

The influence of plaque composition on underlying arterial wall stress during stent expansion: The case for lesion-specific stents

“…Each plaque was assumed to be isotropic and homogenous. Artherosclerotic plaques have, however, been shown to be heterogeneous [34], viscoelastic [10] and significantly stiffer in tension compared with compression [8,9]. Finite element models have been developed of such inhomogenous plaque structures [11,35].…”

A comparison of the mechanical performance characteristics of seven drug‐eluting stent systems

“…The crossability will also depend, in part, on the stiffness of the lesion. The stiffness, or mechanical responses, of a lesion (that is, how easy is it to push the lesion out of the way as the stent progresses through) is lesion dependent [24, 25]. This effect was not simulated in our model.…”

Mineralized Blood Vessels in the Capsules of Human Pineal Glands

“…We have found no histopathological reports of blood vessel lumens entirely filled with mineralized deposits, except for brushite within the blood vessels of human primary molars 19 and a cow tooth 20 , although mineralized plaque fragments scattered within vessel lumens have been reported in arteriosclerosis [21][22][23] . Transverse planes of the vascular lumens showing mineralized deposits in this study resembled the capsular concretions with their rough concentric laminations.…”

“…Transverse planes of the vascular lumens showing mineralized deposits in this study resembled the capsular concretions with their rough concentric laminations. The peripheral substances might be smooth muscle cells, collagen and elastic fibers, and / or amorphous organic plaques that have been mineralized 11,[16][17][18] , whereas the blood vessel lumens filled with mineralized deposits may result from the calcification of organic contents such as plaque when a patient is affected by atherosclerosis or thrombosis [21][22][23][24] . Regrettably, we could not determine a clear relationship between the MSD showing a hyper-mineralization and the smaller mineralized round-shaped deposits attached to the blood vessels, as shown in Fig.…”