Dimitrios Pleouras, A. Sakellarios, G. Karanasiou, S. Kyriakidis, Panagiota I. Tsompou, Vassiliki I. Kigka, D. Fotiadis
{"title":"应用多层次计算模型预测冠状动脉粥样硬化斑块生长:糖尿病的影响","authors":"Dimitrios Pleouras, A. Sakellarios, G. Karanasiou, S. Kyriakidis, Panagiota I. Tsompou, Vassiliki I. Kigka, D. Fotiadis","doi":"10.1109/BIBE.2019.00132","DOIUrl":null,"url":null,"abstract":"Atherosclerosis is the one of the major causes of mortality worldwide, urging the need for its treatment. This study is aiming to investigate the role of diabetes in the atherosclerotic plaque growth mechanisms through the utilization of a multi-level numerical model. To accomplish this, we developed a proof-of-concept mathematical model of the diabetes effect to plaque growth, that has been coupled to a stateof-the-art multi-level numerical model of plaque growth. Diabetes main effect is the increase of the average blood glucose concentration, which causes the decrease of the endothelial nitric oxide production rate by affecting several biologic pathways. Nitric oxide is a signaling molecule that regulates the endothelial flow rates, and any abnormal alteration leads to endothelial dysfunction, the major culprit of atherosclerosis. The derived model considers the modeling of blood flow in lumen and of species transport and reactions in the arterial wall. The considered factors include: (i) LDL, (ii) HDL, (iii) oxidized LDL, (iv) monocytes, (v) macrophages, (vi) cytokines, (vii) smooth muscle cells (contractile & synthetic), and (viii) collagen. The model is validated using 10 patients' reconstructed arterial data in two time-points. More specifically, baseline geometries are used as an input to our model, while follow-up geometries are used as benchmark for our model's output. The results presented a high coefficient of determination between the simulated with diabetes effect and the real follow-up geometries of 0.634.","PeriodicalId":318819,"journal":{"name":"2019 IEEE 19th International Conference on Bioinformatics and Bioengineering (BIBE)","volume":"26 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":"{\"title\":\"Atherosclerotic Plaque Growth Prediction in Coronary Arteries using a Computational Multi-level Model: The Effect of Diabetes\",\"authors\":\"Dimitrios Pleouras, A. Sakellarios, G. Karanasiou, S. Kyriakidis, Panagiota I. Tsompou, Vassiliki I. Kigka, D. Fotiadis\",\"doi\":\"10.1109/BIBE.2019.00132\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Atherosclerosis is the one of the major causes of mortality worldwide, urging the need for its treatment. This study is aiming to investigate the role of diabetes in the atherosclerotic plaque growth mechanisms through the utilization of a multi-level numerical model. To accomplish this, we developed a proof-of-concept mathematical model of the diabetes effect to plaque growth, that has been coupled to a stateof-the-art multi-level numerical model of plaque growth. Diabetes main effect is the increase of the average blood glucose concentration, which causes the decrease of the endothelial nitric oxide production rate by affecting several biologic pathways. Nitric oxide is a signaling molecule that regulates the endothelial flow rates, and any abnormal alteration leads to endothelial dysfunction, the major culprit of atherosclerosis. The derived model considers the modeling of blood flow in lumen and of species transport and reactions in the arterial wall. The considered factors include: (i) LDL, (ii) HDL, (iii) oxidized LDL, (iv) monocytes, (v) macrophages, (vi) cytokines, (vii) smooth muscle cells (contractile & synthetic), and (viii) collagen. The model is validated using 10 patients' reconstructed arterial data in two time-points. More specifically, baseline geometries are used as an input to our model, while follow-up geometries are used as benchmark for our model's output. The results presented a high coefficient of determination between the simulated with diabetes effect and the real follow-up geometries of 0.634.\",\"PeriodicalId\":318819,\"journal\":{\"name\":\"2019 IEEE 19th International Conference on Bioinformatics and Bioengineering (BIBE)\",\"volume\":\"26 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"2019 IEEE 19th International Conference on Bioinformatics and Bioengineering (BIBE)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1109/BIBE.2019.00132\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"2019 IEEE 19th International Conference on Bioinformatics and Bioengineering (BIBE)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1109/BIBE.2019.00132","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3
摘要
动脉粥样硬化是世界范围内死亡的主要原因之一,迫切需要对其进行治疗。本研究旨在通过多层次数值模型探讨糖尿病在动脉粥样硬化斑块生长机制中的作用。为了实现这一目标,我们开发了糖尿病对斑块生长影响的概念验证数学模型,该模型已与最先进的斑块生长多层次数值模型相结合。糖尿病的主要作用是平均血糖浓度升高,通过影响几种生物途径引起内皮细胞一氧化氮生成速率降低。一氧化氮是调节内皮血流速率的信号分子,任何异常改变都会导致内皮功能障碍,这是动脉粥样硬化的罪魁祸首。导出的模型考虑了管腔内血流和动脉壁内物质运输和反应的建模。考虑的因素包括:(i) LDL, (ii) HDL, (iii)氧化LDL, (iv)单核细胞,(v)巨噬细胞,(vi)细胞因子,(vii)平滑肌细胞(收缩和合成),(viii)胶原蛋白。利用10例患者在两个时间点的重建动脉数据对模型进行了验证。更具体地说,基线几何被用作模型的输入,而后续几何被用作模型输出的基准。结果表明,模拟的糖尿病效应与实际随访几何值之间的决定系数为0.634。
Atherosclerotic Plaque Growth Prediction in Coronary Arteries using a Computational Multi-level Model: The Effect of Diabetes
Atherosclerosis is the one of the major causes of mortality worldwide, urging the need for its treatment. This study is aiming to investigate the role of diabetes in the atherosclerotic plaque growth mechanisms through the utilization of a multi-level numerical model. To accomplish this, we developed a proof-of-concept mathematical model of the diabetes effect to plaque growth, that has been coupled to a stateof-the-art multi-level numerical model of plaque growth. Diabetes main effect is the increase of the average blood glucose concentration, which causes the decrease of the endothelial nitric oxide production rate by affecting several biologic pathways. Nitric oxide is a signaling molecule that regulates the endothelial flow rates, and any abnormal alteration leads to endothelial dysfunction, the major culprit of atherosclerosis. The derived model considers the modeling of blood flow in lumen and of species transport and reactions in the arterial wall. The considered factors include: (i) LDL, (ii) HDL, (iii) oxidized LDL, (iv) monocytes, (v) macrophages, (vi) cytokines, (vii) smooth muscle cells (contractile & synthetic), and (viii) collagen. The model is validated using 10 patients' reconstructed arterial data in two time-points. More specifically, baseline geometries are used as an input to our model, while follow-up geometries are used as benchmark for our model's output. The results presented a high coefficient of determination between the simulated with diabetes effect and the real follow-up geometries of 0.634.