Background Although MRI can discriminate the lipid core from the collagenous cap of atherosclerotic lesions in vitro with T2 contrast, it has not yet produced detailed in vivo images of these human plaque components Methods and Results We imaged seven lesions from six patients who required surgical carotid endarterectomy and calculated T2 in vivo before surgery in various plaque regions Using the same acquisition parameters, we repeated these measurements in vitro on the resected fragment and compared MR images with histology T2 values calculated in vivo correlate with in vitro measurements for each plaque component; the in vitro discrimination we demonstrated previously with T2 contrast can therefore be performed similarly in vivo Conclusions MRI is the first noninvasive imaging technique that allows the discrimination of lipid cores, fibrous caps, calcifications, normal media, and adventitia in human atheromatous plaques in vivo This technique also characterizes intraplaque hemorrhage and acute thr

Magnetic resonance images lipid, fibrous, calcified, hemorrhagic, and thrombotic components of human atherosclerosis in vivo.

In this article, we advance a hypothesis for the rupture of thin fibrous cap atheroma, namely that minute (10-μm-diameter) cellular-level microcalcifications in the cap, which heretofore have gone undetected because they lie below the visibility of current in vivo imaging techniques, cause local stress concentrations that lead to interfacial debonding. New theoretical solutions are presented for the local stress concentration around these minute spherical inclusions that predict a nearly 2-fold increase in interfacial stress that is relatively insensitive to the location of the hypothesized microinclusions in the cap. To experimentally confirm the existence of the hypothesized cellular-level microcalcifications, we examined autopsy specimens of coronary atheromatous lesions using in vitro imaging techniques whose resolution far exceeds conventional magnetic resonance imaging, intravascular ultrasound, and optical coherence tomography approaches. These high-resolution imaging modalities, which include confocal microscopy with calcium-specific staining and micro-computed tomography imaging, provide images of cellular-level calcifications within the cap proper. As anticipated, the minute inclusions in the cap are very rare compared with the numerous calcified macrophages observed in the necrotic core. Our mathematical model predicts that inclusions located in an area of high circumferential stress (>300 kPa) in the cap can intensify this stress to nearly 600 kPa when the cap thickness is <65 μm. The most likely candidates for the inclusions are either calcified macrophages or smooth muscle cells that have undergone apoptosis.

A hypothesis for vulnerable plaque rupture due to stress-induced debonding around cellular microcalcifications in thin fibrous caps

A detailed understanding of the mechanical procedure of balloon angioplasty requires three-dimensional (3D) modeling and efficient numerical simulations. We have developed a 3D model for eight distinct arterial components associated with specific mechanical responses. The 3D geometrical model is based on in vitro magnetic resonance imaging of a human stenotic postmortem artery and is represented by nonuniform rational B-spline surfaces. Mechanical tests of the corresponding vascular tissues provide a fundamental basis for the formulation of large strain constitutive laws, which model the typical anisotropic, highly nonlinear, and inelastic mechanical characteristics under supraphysiological loadings. The 3D finite-element realization considers the balloon–artery interaction and accounts for vessel-specific axial in situ prestretches. 3D stress states of the investigated artery during balloon expansion and stent deployment were analyzed. Furthermore, we studied the changes of the 3D stress state due to model simplifications, which are characterized by neglecting axial in situ prestretch, assuming plane strain states, and isotropic material responses, as commonly utilized in previous works. Since these simplifications lead to maximum stress deviations of up to 600%—where even the stress character may interchange—the associated models are, in general, inappropriate. The proposed approach provides a tool that has the potential (i) to improve procedural protocols and the design of interventional instruments on a lesion-specific basis, and (ii) to determine postangioplasty mechanical environments, which may be correlated with restenosis responses. © 2002 Biomedical Engineering Society.
 PAC2002: 8719Rr, 8761Lh, 8710+e

A layer-specific three-dimensional model for the simulation of balloon angioplasty using magnetic resonance imaging and mechanical testing.

Fibrous cap thickness is often considered as diagnostic of the degree of plaque instability. Necrotic core area (Core(area)) and the arterial remodeling index (Remod(index)), on the other hand, are difficult to use as clinical morphological indexes: literature data show a wide dispersion of Core(area) thresholds above which plaque becomes unstable. Although histopathology shows a strong correlation between Core(area) and Remod(index), it remains unclear how these interact and affect peak cap stress (Cap(stress)), a known predictor of rupture. The aim of this study was to investigate the change in plaque vulnerability as a function of necrotic core size and plaque morphology. Cap(stress) value was calculated on 5,500 idealized atherosclerotic vessel models that had the original feature of mimicking the positive arterial remodeling process described by Glagov. Twenty-four nonruptured plaques acquired by intravascular ultrasound on patients were used to test the performance of the associated idealized morphological models. Taking advantage of the extensive simulations, we investigated the effects of anatomical plaque features on Cap(stress). It was found that: 1) at the early stages of positive remodeling, lesions were more prone to rupture, which could explain the progression and growth of clinically silent plaques and 2) in addition to cap thickness, necrotic core thickness, rather than area, was critical in determining plaque stability. This study demonstrates that plaque instability is to be viewed not as a consequence of fibrous cap thickness alone but rather as a combination of cap thickness, necrotic core thickness, and the arterial remodeling index.

https://www.physiology.org/doi/pdf/10.1152/ajpheart.00005.2008

Necrotic core thickness and positive arterial remodeling index: emergent biomechanical factors for evaluating the risk of plaque rupture

Atherosclerosis remains a major cause of morbidity and mortality worldwide, and a thorough understanding of the underlying pathophysiological mechanisms is crucial for the development of new therapeutic strategies. Although atherosclerosis is a systemic inflammatory disease, coronary atherosclerotic plaques are not uniformly distributed in the vascular tree. Experimental and clinical data highlight that biomechanical forces, including wall shear stress (WSS) and plaque structural stress (PSS), have an important role in the natural history of coronary atherosclerosis. Endothelial cell function is heavily influenced by changes in WSS, and longitudinal animal and human studies have shown that coronary regions with low WSS undergo increased plaque growth compared with high WSS regions. Local alterations in WSS might also promote transformation of stable to unstable plaque subtypes. Plaque rupture is determined by the balance between PSS and material strength, with plaque composition having a profound effect on PSS. Prospective clinical studies are required to ascertain whether integrating mechanical parameters with medical imaging can improve our ability to identify patients at highest risk of rapid disease progression or sudden cardiac events.

/pdf/role-of-biomechanical-forces-in-the-natural-history-of-4v8pndsjch.pdf

Role of biomechanical forces in the natural history of coronary atherosclerosis

Computational structural analysis based on intravascular ultrasound imaging before in vitro angioplasty: Prediction of plaque fracture locations

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Computational structural analysis based on intravascular ultrasound imaging before in vitro angioplasty: Prediction of plaque fracture locations