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Coronary artery disease (CAD) risk and plaque scores are often subjective and biased, particularly in mid-age asymptomatic women, whose CAD risk assessment has been historically underestimated. In this study, a new automatic ascending aorta time-to-peak-distention (TPD) analysis was developed for fast screening and as an independent surrogate for subclinical atherosclerosis in asymptomatic women. CCTA was obtained in 50 asymptomatic adults. Plaque burden segment involvement score (SIS) and automatic TPD were obtained from all subjects. Logistic regression analyses were performed to investigate the association between CAD risk scores and TPD with severe coronary plaque burden (SIS>5). TPD, individually, was found to be a significant predictor of SIS>5. Additionally, sex was a significant effect modifier of TPD, with a stronger statistically significant association with women. Four-dimensional aortic time-to-peak distention could supplement conventional CCTA analysis and offer a quick objective screening tool for plaque burden severity and CAD risk stratification, especially in women., (© 2023. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Coronary plaque burden measured by coronary computerized tomography angiography (CCTA), independent of stenosis, is a significant independent predictor of coronary heart disease (CHD) events and mortality. Hence, it is essential to develop comprehensive CCTA plaque quantification beyond existing subjective plaque volume or stenosis scoring methods. The purpose of this study is to develop a framework for automated 3D segmentation of CCTA vessel wall and quantification of atherosclerotic plaque, independent of the amount of stenosis, along with overcoming challenges caused by poor contrast, motion artifacts, severe stenosis, and degradation of image quality. Vesselness, region growing, and two sequential level sets are employed for segmenting the inner and outer wall to prevent artifact-defective segmentation. Lumen and vessel boundaries are joined to create the coronary wall. Curved multiplanar reformation is used to straighten the segmented lumen and wall using lumen centerline. In-vivo evaluation included CCTA stenotic and non-stenotic plaques from 41 asymptomatic subjects with 122 plaques of different characteristics against the individual and consensus of expert readers. Results demonstrate that the framework segmentation performed robustly by providing a reliable working platform for accelerated, objective, and reproducible atherosclerotic plaque characterization beyond subjective assessment of stenosis; can be potentially applicable for monitoring response to therapy.

Background: Current guidelines for the primary prevention of atherosclerotic cardiovascular disease are based on the estimation of a predicted 10-year cardiovascular disease risk and the average relative risk reduction estimates from statin trials. In the clinical setting, however, decision-making is better informed by the expected benefit for the individual patient, which is typically lacking. Consequently, a personalized statin benefit approach based on absolute risk reduction over 10 years (ARR10 benefit threshold ≥2.3%) has been proposed as a novel approach. However, how this benefit threshold relates with coronary plaque burden in asymptomatic individuals with low/intermediate cardiovascular disease risk is unknown., Aims: In this study, we compared the predicted ARR10 obtained in each individual with plaque burden detected by coronary computed tomography angiography., Methods and Results: Plaque burden (segment volume score, segment stenosis score, and segment involvement score) was assessed in prospectively recruited asymptomatic subjects (n = 70; 52% male; median age 56 years [interquartile range 51-64 years]) with low/intermediate Framingham risk score (< 20%). The expected ARR10 with statin in the entire cohort was 2.7% (1.5-4.6%) with a corresponding number needed to treat over 10 years of 36 (22-63). In subjects with an ARR10 benefit threshold ≥2.3% (vs. < 2.3%), plaque burden was significantly higher (p = 0.02)., Conclusion: These findings suggest that individuals with higher coronary plaque burden are more likely to get greater benefit from statin therapy even among asymptomatic individuals with low cardiovascular risk., (This is a work of the US Government and is not subject to copyright protection in the USA. Foreign copyrights may apply. Published by S. Karger AG, Basel.)

Background and Aims: Autosomal dominant hyper-IgE (AD-HIES) is a primary immunodeficiency caused by mutations in STAT3. Elevated levels of IgE, an ineffective immune response, connective tissue abnormalities, and coronary arterial dilation and tortuosity characterize AD-HIES. To date, coronary artery evaluation in AD-HIES patients has been limited to lumenography measurements. Direct in vivo coronary vessel wall (VW) imaging may allow for better interrogation of coronary vessel abnormalities. The goal of this prospective study was to evaluate the coronary VW of AD-HIES patients using Magnetic Resonance Imaging (MRI) and histology. VW image findings were compared in healthy subjects and subjects with coronary atherosclerotic disease (CAD)., Methods: A total of 28 subjects (10 with AD-HIES, 8 healthy, 10 with CAD) were studied by coronary VW MRI imaging. Additionally, a post-mortem coronary artery from one VW imaged AD-HIES patient was examined., Results: Coronary VW in AD-HIES was thicker than in healthy controls but not significantly different from VW thickness in CAD subjects. AD-HIES coronaries showed increased VW area compared to healthy controls and CAD subjects. On histology, the AD-HIES coronary artery had findings consistent with atherosclerotic plaque, but had minimal luminal narrowing, deficient adventitia thickening and absence of both internal and external elastic laminae., Conclusions: This is the first study to demonstrate subclinical coronary atherosclerosis in AD-HIES patients on VW imaging by MRI. Histologic evaluation confirmed the presence of atherosclerosis with lack of supportive adventitial thickening and elastic components. These findings suggest mechanisms for coronary dilation in AD-HIES and thereby help direct clinical management., (Published by Elsevier B.V.)

Mouse models of atherosclerosis are extensively being used to study the mechanisms of atherosclerotic plaque development and the results are frequently extrapolated to humans. However, major differences have been described between murine and human atherosclerotic lesions and the determination of similarities and differences between these species has been largely addressed recently. This study takes over and extends previous studies performed by our group and related to the biomechanical characterization of both mouse and human atherosclerotic lesions. Its main objective was to determine the distribution and amplitude of mechanical stresses including peak cap stress (PCS) in aortic vessels from atherosclerotic apoE(-/-) mice, in order to evaluate whether such biomechanical data would be in accordance with the previously suggested lack of plaque rupture in this model. Successful finite element analysis was performed from the zero-stress configuration of aortic arch sections and mainly indicated (1) the modest role of atherosclerotic lesions in the observed increase in residual parietal stresses in apoE(-/-) mouse vessels and (2) the low amplitude of murine PCS as compared to humans. Overall, the results from the present study support the hypothesis that murine biomechanical properties and artery size confer less propensity to rupture for mouse lesions in comparison with those of humans., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Coronary atheroma develop in local sites that are widely variable among patients and are considerably variable in their vulnerability for rupture. This article summarizes studies conducted by our collaborative laboratories on predictive biomechanical modeling of coronary plaques. It aims to give insights into the role of biomechanics in the development and localization of atherosclerosis, the morphologic features that determine vulnerable plaque stability, and emerging in vivo imaging techniques that may detect and characterize vulnerable plaque. Composite biomechanical and hemodynamic factors that influence the actual site of development of plaques have been studied. Plaque vulnerability, in vivo, is more challenging to assess. Important steps have been made in defining the biomechanical factors that are predictive of plaque rupture and the likelihood of this occurring if characteristic features are known. A critical key in defining plaque vulnerability is the accurate quantification of both the morphology and the mechanical properties of the diseased arteries. Recently, an early IVUS based palpography technique developed to assess local strain, elasticity and mechanical instabilities has been successfully revisited and improved to account for complex plaque geometries. This is based on an initial best estimation of the plaque components' contours, allowing subsequent iteration for elastic modulus assessment as a basis for plaque stability determination. The improved method has also been preliminarily evaluated in patients with successful histologic correlation. Further clinical evaluation and refinement are on the horizon.

Coronary bifurcations represent specific regions of the arterial tree that are susceptible to atherosclerotic lesions. While the effects of vessel compliance, curvature, pulsatile blood flow, and cardiac motion on coronary endothelial shear stress have been widely explored, the effects of myocardial contraction on arterial wall stress/strain (WS/S) and vessel stiffness distributions remain unclear. Local increase of vessel stiffness resulting from wall-strain stiffening phenomenon (a local process due to the nonlinear mechanical properties of the arterial wall) may be critical in the development of atherosclerotic lesions. Therefore, the aim of this study was to quantify WS/S and stiffness in coronary bifurcations and to investigate correlations with plaque sites. Anatomic coronary geometry and cardiac motion were generated based on both computed tomography and MRI examinations of eight patients with minimal coronary disease. Computational structural analyses using the finite element method were subsequently performed, and spatial luminal arterial wall stretch (LW(Stretch)) and stiffness (LW(Stiff)) distributions in the left main coronary bifurcations were calculated. Our results show that all plaque sites were concomitantly subject to high LW(Stretch) and high LW(Stiff), with mean amplitudes of 34.7 ± 1.6% and 442.4 ± 113.0 kPa, respectively. The mean LW(Stiff) amplitude was found slightly greater at the plaque sites on the left main coronary artery (mean value: 482.2 ± 88.1 kPa) compared with those computed on the left anterior descending and left circumflex coronary arteries (416.3 ± 61.5 and 428.7 ± 181.8 kPa, respectively). These findings suggest that local wall stiffness plays a role in the initiation of atherosclerotic lesions.