scholarly journals A prediction tool for plaque progression based on patient-specific multi-physical modeling

2021 ◽  
Vol 17 (3) ◽  
pp. e1008344
Author(s):  
Jichao Pan ◽  
Yan Cai ◽  
Liang Wang ◽  
Akiko Maehara ◽  
Gary S. Mintz ◽  
...  

Atherosclerotic plaque rupture is responsible for a majority of acute vascular syndromes and this study aims to develop a prediction tool for plaque progression and rupture. Based on the follow-up coronary intravascular ultrasound imaging data, we performed patient-specific multi-physical modeling study on four patients to obtain the evolutional processes of the microenvironment during plaque progression. Four main pathophysiological processes, i.e., lipid deposition, inflammatory response, migration and proliferation of smooth muscle cells (SMCs), and neovascularization were coupled based on the interactions demonstrated by experimental and clinical observations. A scoring table integrating the dynamic microenvironmental indicators with the classical risk index was proposed to differentiate their progression to stable and unstable plaques. The heterogeneity of plaque microenvironment for each patient was demonstrated by the growth curves of the main microenvironmental factors. The possible plaque developments were predicted by incorporating the systematic index with microenvironmental indicators. Five microenvironmental factors (LDL, ox-LDL, MCP-1, SMC, and foam cell) showed significant differences between stable and unstable group (p < 0.01). The inflammatory microenvironments (monocyte and macrophage) had negative correlations with the necrotic core (NC) expansion in the stable group, while very strong positive correlations in unstable group. The inflammatory microenvironment is strongly correlated to the NC expansion in unstable plaques, suggesting that the inflammatory factors may play an important role in the formation of a vulnerable plaque. This prediction tool will improve our understanding of the mechanism of plaque progression and provide a new strategy for early detection and prediction of high-risk plaques.

2020 ◽  
Author(s):  
Jichao Pan ◽  
Yan Cai ◽  
Liang Wang ◽  
Akiko Maehara ◽  
Gary S. Mintz ◽  
...  

AbstractAtherosclerotic plaque rupture is responsible for a majority of acute vascular syndromes and this study aims to develop a prediction tool for plaque progression and rupture. Based on the follow-up coronary intravascular ultrasound imaging data, we performed patient-specific multi-physical modeling study on four patients to obtain the evolutional processes of the microenvironment during plaque progression. Four main pathophysiological processes, i.e., lipid deposition, inflammatory response, migration and proliferation of smooth muscle cells (SMCs), and neovascularization were coupled based on the interactions demonstrated by experimental and clinical observations. A scoring table integrating the dynamic microenvironmental indicators with the classical risk index was proposed to differentiate their progression to stable and unstable plaques. The heterogeneity of plaque microenvironment for each patient was demonstrated by the growth curves of the main microenvironmental factors. The possible plaque developments were predicted by incorporating the systematic index with microenvironmental indicators. Five microenvironmental factors (LDL, ox-LDL, MCP-1, SMC, and foam cell) showed significant differences between stable and unstable group (p < 0.01). The inflammatory microenvironments (monocyte and macrophage) had negative correlations with the necrotic core (NC) expansion in the stable group, while very strong positive correlations in unstable group. The inflammatory microenvironment is strongly correlated to the NC expansion in unstable plaques, suggesting that the inflammatory factors may play an important role in the formation of a vulnerable plaque. This prediction tool will improve our understanding of the mechanism of plaque progression and provide a new strategy for early detection and prediction of high-risk plaques.Author summaryBesides the traditional systematic factors, the influences of the local microenvironmental factors on atherosclerotic plaque progression have been demonstrated. Mathematical and computational modeling is an important tool to investigate the complex interplay between plaque progression and the microenvironment, and provides a potential way toward the prediction of plaque vulnerability according to the comprehensive evaluation of both morphological and/or biochemical factors in tissue level with microenvironmental factors in cellular level. We performed patient-specific multi-physical modeling study on four patients to obtain the evolutional processes of the microenvironment during plaque progression and predicted the possible plaque developments. A scoring table integrating the dynamic microenvironmental indicators with the classical risk index was proposed to differentiate their progression to stable and unstable plaques. Based on patient-specific imaging data, the mathematical model will provide a novel method to predict the changes of plaque microenvironment and improve ability to access the personal therapeutic strategy for atherosclerotic plaque.


2021 ◽  
Vol 17 (12) ◽  
pp. e1009709
Author(s):  
Jichao Pan ◽  
Yan Cai ◽  
Liang Wang ◽  
Akiko Maehara ◽  
Gary S. Mintz ◽  
...  

Author(s):  
Chun Yang ◽  
Joseph D. Petruccelli ◽  
Zhongzhao Teng ◽  
Chun Yuan ◽  
Gador Canton ◽  
...  

Atherosclerotic plaque rupture and progression have been the focus of intensive investigations in recent years. The mechanisms governing plaque progression and rupture process are not well understood. Using computational models based on patient-specific multi-year in vivo MRI data, our recent results indicated that 18 out of 21 patients studied showed significant negative correlation between plaque progression measured by vessel wall thickness increase (WTI) and plaque wall (structural) stress (PWS) [1]. In this paper, a computational procedure based on meshless generalized finite difference (MGFD) method and serial magnetic resonance imaging (MRI) data was introduced to simulate plaque progression. Participating patients were scanned three times (T1, T2, and T3, at intervals of approximately 18 months) to obtain plaque progression data. Vessel wall thickness (WT) changes were used as the measure for plaque progression. Starting from T2 plaque geometry, plaque progression was simulated by solving the solid model and adjusting wall thickness using plaque growth functions iteratively until time T3 is reached. Numerically simulated plaque progression showed very good agreement with actual plaque geometry at T3 given by MRI data. We believe this is the first time plaque progression simulation results based on multi-year patient-tracking data are reported. Multi-year tracking data and MRI-based progression simulation add time dimension to plaque vulnerability assessment and will improve prediction accuracy.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Qingyu Wang ◽  
Dalin Tang ◽  
Gador Canton ◽  
Jian Guo ◽  
Xiaoya Guo ◽  
...  

It is hypothesized that artery stiffness may be associated with plaque progression. However, in vivo vessel material stiffness follow-up data is lacking in the literature. In vivo 3D multi-contrast and Cine magnetic resonance imaging (MRI) carotid plaque data were acquired from 8 patients with follow-up (18 months) with written informed consent obtained. Cine MRI and 3D thin-layer models were used to determine parameter values of the Mooney-Rivlin models for the 81slices from 16 plaques (2 scans/patient) using our established iterative procedures. Effective Young’s Modulus (YM) values for stretch ratio [1.0,1.3] were calculated for each slice for analysis. Stress-stretch ratio curves from Mooney-Rivlin models for the 16 plaques and 81 slices are given in Fig. 1. Average YM value of the 81 slices was 411kPa. Slice YM values varied from 70 kPa (softest) to 1284 kPa (stiffest), a 1734% difference. Average slice YM values by vessel varied from 109 kPa (softest) to 922 kPa (stiffest), a 746% difference. Location-wise, the maximum slice YM variation rate within a vessel was 306% (139 kPa vs. 564 kPa). Average slice YM variation rate within a vessel for the 16 vessels was 134%. Average variation of YM values from baseline (T1) to follow up (T2) for all patients was 61.0%. The range of the variation of YM values was [-28.4%, 215%]. For progression study, YM increase (YMI=YM T2 -TM T1 ) showed negative correlation with plaque progression measured by wall thickness increase (WTI), (r= -0.6802, p=0.0634). YM T2 showed strong negative correlation with WTI (r= -0.7764, p=0.0235). Correlation between YM T1 and WTI was not significant (r= -0.4353, p= 0.2811). Conclusion In vivo carotid vessel material properties have large variations from patient to patient, along the vessel segment within a patient, and from baseline to follow up. Use of patient-specific, location specific and time-specific material properties could potentially improve the accuracy of model stress/strain calculations.


2021 ◽  
Vol 3 (1) ◽  
pp. 104-130
Author(s):  
Sergey G. Sсherbak ◽  
Tatyana A. Kamilova ◽  
Svetlana V. Lebedeva ◽  
Dmitry A. Vologzhanin ◽  
Alexander S. Golota ◽  
...  

Early recognition of rupture-prone atherosclerotic lesions in patients with high-graded carotid stenosis is an important clinical problem for preventing ischemic stroke. Various pathophysiological mechanisms are responsible for the progression and instability of plaques, such as changes in lipid composition, infiltration by immunoinflammatory cells and degradation of the extracellular matrix of the vascular wall by matrix metalloproteinases, enhanced inflammatory response and plaque neovascularization. These features are the main cause of plaque rupture and, as a consequence, neurologic symptoms. Therefore, matrix metalloproteinases and inflammatory factors can serve as possible markers for patients with severe unstable stenosis of carotid arteries. Due to the heterogeneity of atherosclerotic lesions, only one biomarker is not enough to reliably predict the development of a stroke. The use of a combination of biomarkers is better correlated with clinical data and, therefore, exceeds the analysis of individual factors. To increase the overall sensitivity and specificity and more reliable diagnosis of stroke in patients with symptomatic and asymptomatic carotid stenosis, the biomarker panel should include independent biomarkers. Further preclinical experiments and clinical trials are needed to assess the significance and precise definition of the threshold levels of such biomarkers before they can be used in clinical practice.


2015 ◽  
Vol 20 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Nenad Filipovic ◽  
Igor Saveljic ◽  
Dalibor Nikolic ◽  
Zarko Milosevic ◽  
Pavle Kovacevic ◽  
...  

Author(s):  
Jinyu Xie ◽  
Qian Wang

Risk of having hypoglycemia is one of the biggest barriers preventing Type 1 Diabetes (T1D) patients from performing exercise. In addition, management of diet and exercise levels needs to be personalized for each patient to avoid hypoglycemia and to achieve a good glycemic control. In this paper, we developed a model-based diet and exercise recommender system that could be used to provide an (optimal) personalized intervention on diet and exercise for T1D patients. The recommender system makes prediction of blood glucose at each intervention time based on a patient-specific model of glucose dynamics, and then provides the optimal meal sizes, target heart rates during exercise, pre-exercise carbohydrate and bedtime snack by minimizing a clinical risk function under constraints. Patient-specific models of glucose dynamics were identified for 30 virtual subjects generated from a modified UVa/Padova simulator with an added exercise-glucose subsystem. The performance of the recommender system was then compared to two self-management schemes (the Starter and the Skilled). The latter represents an off-line optimal solution providing a lower bound on the risk index. The average clinical risk under the recommender system was reduced by 49% compared to that under the Starter, and it was comparable to the risk of the Skilled. In addition, the recommender system had less number of post-exercise/nocturnal hypoglycemia events occurred than that under the Starter or the Skilled. Such recommender system can be implemented as an “App” patient advisor to improve T1D patients’ self-management of glucose control.


Author(s):  
У.А. Халилова ◽  
В.В. Скворцов

Сердечно-сосудистые заболевания, особенно ишемическая болезнь сердца (ИБС), являются наиболее распространенными заболеваниями во всем мире. Более 50% смертности приходится на данную патологию. В последние десятилетия существует тенденция к «омоложению» сердечно-сосудистых заболеваний – прежде всего гипертонической болезни и ИБС, что вызывает особую тревогу. Общепризнано, что основным этиологическим моментом развития ИБС является атеросклероз. ИБС включает в себя целый ряд клинических диагнозов (стенокардия, инфаркт миокарда и т. д.) и связана с атеросклерозом, распространенным дегенеративным заболеванием, при котором липиды и фиброзный матрикс откладываются в артериальной стенке с формированием атероматозной бляшки. Разрыв нестабильных бляшек в коронарных артериях приводит к высвобождению тромбогенного содержимого в просвет сосуда, приводя к тромбозу коронарных артерий, окклюзии и последующему инфаркту миокарда – критическому состоянию с высокой смертностью [5]. Несмотря на большое количество известных факторов риска, влияющих на развитие данного заболевания, существуют данные, подтвержденные крупными исследованиями, о наличии генетической предрасположенности к нему. Cardiovascular diseases, especially coronary heart disease (CHD), are the most common diseases worldwide. More than 50% of mortality occurs in this pathology. In recent decades, there is a tendency to «rejuvenate» cardiovascular diseases – primarily hypertension and СHD, which is of particular concern [6, 8]. It is generally recognized that atherosclerosis is the main etiological moment in the development of coronary heart disease. CHD includes a number of clinical diagnoses (angina pectoris, myocardial infarction, etc.) and is associated with atherosclerosis, a common degenerative disease in which lipids and the fibrous matrix are deposited in the arterial wall with the formation of an atheromatous plaque. Rupture of unstable plaques in the coronary arteries leads to the release of thrombogenic contents into the lumen of the vessel, leading to coronary artery thrombosis, occlusion and subsequent myocardial infarction, critical state with high mortality [5]. Despite the large number of known risk factors affecting the development of this disease, there is evidence, confirmed by large studies, about the presence of a genetic predisposition to this disease.


2021 ◽  
Vol 12 ◽  
Author(s):  
Milad Ghasemi ◽  
Robert D. Johnston ◽  
Caitríona Lally

Atherosclerotic plaque rupture in carotid arteries can lead to stroke which is one of the leading causes of death or disability worldwide. The accumulation of atherosclerotic plaque in an artery changes the mechanical properties of the vessel. Whilst healthy arteries can continuously adapt to mechanical loads by remodelling their internal structure, particularly the load-bearing collagen fibres, diseased vessels may have limited remodelling capabilities. In this study, a local stress modulated remodelling algorithm is proposed to explore the mechanical response of arterial tissue to the remodelling of collagen fibres. This stress driven remodelling algorithm is used to predict the optimum distribution of fibres in healthy and diseased human carotid bifurcations obtained using Magnetic Resonance Imaging (MRI). In the models, healthy geometries were segmented into two layers: media and adventitia and diseased into four components: adventitia, media, plaque atheroma and lipid pool (when present in the MRI images). A novel meshing technique for hexahedral meshing of these geometries is also demonstrated. Using the remodelling algorithm, the optimum fibre patterns in various patient specific plaques are identified and the role that deviations from these fibre configurations in plaque vulnerability is shown. This study provides critical insights into the collagen fibre patterns required in carotid artery and plaque tissue to maintain plaque stability.


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