Blood vessels interact with their mechanical environments in a comprehensive way. Local mechanical stimuli outside the biological range play important roles in various human cardiovascular diseases. Although many mechanobiological studies of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) in vitro have been reported in mimicking cellular dysfunctions, their quantitative correlations to the in vivo vascular conditions remain unclear. In order to interpret the stress-modulated dysfunctions of vascular cells and explore the key mechanical factors in vascular diseases, it is important to investigate the mechanical environments of vessel walls in vivo under various physiological conditions. Based on nonlinear continuum mechanics, we analyzed the variations of the mechanical stress, strain, and wall stiffness in human blood vessels at different blood pressures. We adopted nine middle-aged arteries located at different physiological sites for stress analysis including three aortas (ascending thoracic, descending thoracic, and abdominal), and five arterial branches (common iliac, femoropopliteal, subclavian, common carotid, and renal, and left anterior descending coronary artery). The femoropopliteal arteries aged from 11 to 70 years were also adopted for investigating the aging effects. It is found that 1) the vascular cells experience various mechanical stimuli along the arterial tree; 2) the intima and adventitia exhibit distinct variations in stress and strain during the femoropopliteal artery aging; and 3) the magnitude of wall stiffness seems to depend on the arterial locations rather than aging. Although it is reported that stress concentration usually occurs in intima causing EC dysfunctions, our results suggest that the adventitia is more likely to bear high stresses in middle-aged aortas and aged femoropopliteal arteries, triggering the vascular inflammation. We conclude that the mechanical niches of vascular cells strongly depend on the physiological site and aging process. The present results contribute to a better understanding of the mechanical environments in vessel walls, which could serve as a reference for studying the vascular cell mechano-transduction.
{"title":"An Analytical Investigation of in Vivo Mechanical References for Mechanobiological Experiments of Vascular Cells","authors":"Shaoxiong Yang, X. Gong, Ying‐Xin Qi, Zong-Lai Jiang","doi":"10.32604/MCB.2019.05701","DOIUrl":"https://doi.org/10.32604/MCB.2019.05701","url":null,"abstract":"Blood vessels interact with their mechanical environments in a comprehensive way. Local mechanical stimuli outside the biological range play important roles in various human cardiovascular diseases. Although many mechanobiological studies of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) in vitro have been reported in mimicking cellular dysfunctions, their quantitative correlations to the in vivo vascular conditions remain unclear. In order to interpret the stress-modulated dysfunctions of vascular cells and explore the key mechanical factors in vascular diseases, it is important to investigate the mechanical environments of vessel walls in vivo under various physiological conditions. Based on nonlinear continuum mechanics, we analyzed the variations of the mechanical stress, strain, and wall stiffness in human blood vessels at different blood pressures. We adopted nine middle-aged arteries located at different physiological sites for stress analysis including three aortas (ascending thoracic, descending thoracic, and abdominal), and five arterial branches (common iliac, femoropopliteal, subclavian, common carotid, and renal, and left anterior descending coronary artery). The femoropopliteal arteries aged from 11 to 70 years were also adopted for investigating the aging effects. It is found that 1) the vascular cells experience various mechanical stimuli along the arterial tree; 2) the intima and adventitia exhibit distinct variations in stress and strain during the femoropopliteal artery aging; and 3) the magnitude of wall stiffness seems to depend on the arterial locations rather than aging. Although it is reported that stress concentration usually occurs in intima causing EC dysfunctions, our results suggest that the adventitia is more likely to bear high stresses in middle-aged aortas and aged femoropopliteal arteries, triggering the vascular inflammation. We conclude that the mechanical niches of vascular cells strongly depend on the physiological site and aging process. The present results contribute to a better understanding of the mechanical environments in vessel walls, which could serve as a reference for studying the vascular cell mechano-transduction.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89429721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Peng Wu, Q. Gao, Wei Runjie, Wang Hongping, Lizhong Wang
Cardiovascular diseases are the leading cause of human deaths worldwide. Traditional diagnostic tools of cardiovascular diseases are either based on 2D static medical images, or invasive, bringing troubles to both patients and doctors. Our team is committed to the development of image-based non-invasive diagnostic system for cardiovascular diseases. We have made progress mainly in the following areas: 1) 4D flow technology for heart and large blood vessels. According to MRI 4D Flow data, three-dimensional velocity fields within blood vessels were constructed. Divergence-fee smoothing (DFS) was proposed to eliminate the high frequency noise in the hemodynamic flow field, and make the smoothed velocity field to satisfy the divergence-free condition. The vascular wall shear stress, pressure and other physiological indicators were obtained, their accuracy can meet the need of clinical applications. 2) Accurate noninvasive diagnostic techniques for coronary arterial disease. According to coronary CTA imaging data, 3D reconstruction of coronary arteries was achieved coronary stenosis and plaque lesion were identified and analyzed. Coronary microcirculation was modeled using a 0d model; the coronary artery FFR were computed through the Fast FFR technique, which was based on the reduced-order computational fluid dynamics (CFD). The Fast FFR technique can compute the FFR within 5 minutes. Similar techniques have been used in the preoperative evaluation of intraluminal artery bypass. 3) In vitro evaluation of artificial heart valves and blood-contacting artificial organs. High-fidelity CFD and PIV technique were developed to study the flow field in the artificial heart valve and blood pumps. In vitro platform for experimentally and numerically evaluate the blood damage were also developed.
{"title":"On the Image-Based Non-Invasive Diagnosis of Cardiovascular Diseases","authors":"Peng Wu, Q. Gao, Wei Runjie, Wang Hongping, Lizhong Wang","doi":"10.32604/MCB.2019.05711","DOIUrl":"https://doi.org/10.32604/MCB.2019.05711","url":null,"abstract":"Cardiovascular diseases are the leading cause of human deaths worldwide. Traditional diagnostic tools of cardiovascular diseases are either based on 2D static medical images, or invasive, bringing troubles to both patients and doctors. Our team is committed to the development of image-based non-invasive diagnostic system for cardiovascular diseases. We have made progress mainly in the following areas: \u00001) 4D flow technology for heart and large blood vessels. According to MRI 4D Flow data, three-dimensional velocity fields within blood vessels were constructed. Divergence-fee smoothing (DFS) was proposed to eliminate the high frequency noise in the hemodynamic flow field, and make the smoothed velocity field to satisfy the divergence-free condition. The vascular wall shear stress, pressure and other physiological indicators were obtained, their accuracy can meet the need of clinical applications. \u00002) Accurate noninvasive diagnostic techniques for coronary arterial disease. According to coronary CTA imaging data, 3D reconstruction of coronary arteries was achieved coronary stenosis and plaque lesion were identified and analyzed. Coronary microcirculation was modeled using a 0d model; the coronary artery FFR were computed through the Fast FFR technique, which was based on the reduced-order computational fluid dynamics (CFD). The Fast FFR technique can compute the FFR within 5 minutes. Similar techniques have been used in the preoperative evaluation of intraluminal artery bypass. \u00003) In vitro evaluation of artificial heart valves and blood-contacting artificial organs. High-fidelity CFD and PIV technique were developed to study the flow field in the artificial heart valve and blood pumps. In vitro platform for experimentally and numerically evaluate the blood damage were also developed.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90055158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Common carotid arteries (CCAs) are the major arteries supplying blood to the brain, and the hemodynamic variables in which are closely associated with the cardiovascular diseases. Exercise can induce the hemodynamic responses in the CCAs, including variations in blood pressure, circumferential stretch, and wall shear stress (WSS). Mechanosensors in the endothelial cells (ECs) are able to sense and distinguish these variations as mechanical signal, and transmit them into the interior of cells to affect cellular morphology and gene expression. Notably, reasonable exercises improve arterial structure and function, while unreasonable exercises cause endothelial dysfunction. Therefore, studies on the modulation of common carotid arterial structure and function by exercises are quite necessary, and it’s significant to choose reasonable exercise modalities for improving arterial structure and function and preventing cardiovascular diseases. In this work, firstly, we studied the acute and chronic effects of different exercise modalities on the carotid arterial elasticity and hemodynamic variables. The results showed that the acute exercise caused the increases in arterial elastic modulus, blood pressure and the magnitude and frequency of WSS, and led to the decrease of arterial diameter; moreover, the changes in these hemodynamic variables exhibited an exercise-intensity-dependent manner. Additionally, the responses of intracellular nitric oxide (NO), reactive oxygen species (ROS) and the autophagy flux to WSS waveforms induced by different intensity exercise were also studied in a multi-component parallel-plate flow chamber system. The experimental results indicated that autophagy regulated intracellular NO and ROS production, and the magnitude and frequency of WSS induced by the moderate intensity exercise were more beneficial to improve arterial endothelial function than the high intensity exercise. Finally, the feasibility of quantitative regulation of the intracellular Ca2+ concentration in ECs by WSS was preliminarily investigated and confirmed in a microfluidic chip. In summary, our work indicated that it is feasible to choose reasonable exercise modalities to accurately modulate the hemodynamic variables, including blood pressure, blood flow and WSS in the CCAs, and then to improve the structure and function of the CCAs.
{"title":"Modulation of Common Carotid Arterial Function by Exercise: A Hemodynamics Study","authors":"K. Qin","doi":"10.32604/MCB.2019.05703","DOIUrl":"https://doi.org/10.32604/MCB.2019.05703","url":null,"abstract":"Common carotid arteries (CCAs) are the major arteries supplying blood to the brain, and the hemodynamic variables in which are closely associated with the cardiovascular diseases. Exercise can induce the hemodynamic responses in the CCAs, including variations in blood pressure, circumferential stretch, and wall shear stress (WSS). Mechanosensors in the endothelial cells (ECs) are able to sense and distinguish these variations as mechanical signal, and transmit them into the interior of cells to affect cellular morphology and gene expression. Notably, reasonable exercises improve arterial structure and function, while unreasonable exercises cause endothelial dysfunction. Therefore, studies on the modulation of common carotid arterial structure and function by exercises are quite necessary, and it’s significant to choose reasonable exercise modalities for improving arterial structure and function and preventing cardiovascular diseases. In this work, firstly, we studied the acute and chronic effects of different exercise modalities on the carotid arterial elasticity and hemodynamic variables. The results showed that the acute exercise caused the increases in arterial elastic modulus, blood pressure and the magnitude and frequency of WSS, and led to the decrease of arterial diameter; moreover, the changes in these hemodynamic variables exhibited an exercise-intensity-dependent manner. Additionally, the responses of intracellular nitric oxide (NO), reactive oxygen species (ROS) and the autophagy flux to WSS waveforms induced by different intensity exercise were also studied in a multi-component parallel-plate flow chamber system. The experimental results indicated that autophagy regulated intracellular NO and ROS production, and the magnitude and frequency of WSS induced by the moderate intensity exercise were more beneficial to improve arterial endothelial function than the high intensity exercise. Finally, the feasibility of quantitative regulation of the intracellular Ca2+ concentration in ECs by WSS was preliminarily investigated and confirmed in a microfluidic chip. In summary, our work indicated that it is feasible to choose reasonable exercise modalities to accurately modulate the hemodynamic variables, including blood pressure, blood flow and WSS in the CCAs, and then to improve the structure and function of the CCAs.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81917035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To quantitatively analyze the aerodynamic changes in patient's trachea after the resection operation of hyperplastic granulation tissue, computational fluid dynamic (CFD) method was utilized to perform the simulation. Firstly, three dimensional finite element model of the patient’s trachea before and after surgery were reconstructed based on CT images; secondly, the numerical simulation based on CFD method was performed to investigate the changes in aerodynamic changes in patient's trachea after excision. Results indicated that the dyspnea symptom was largely alleviated after the removal surgery, the abnormal morphology was obviously improved and the resistance of trachea was decreased significantly. Present research also demonstrates that CFD methods can be used to quantitatively evaluate the postoperative effects of the granulation tissue resection operation.
{"title":"Numerical Simulation of the Granulation Tissue Resection Operation in Human Trachea","authors":"Zhiguo Zhang, Chenying Jiang","doi":"10.32604/MCB.2019.05749","DOIUrl":"https://doi.org/10.32604/MCB.2019.05749","url":null,"abstract":"To quantitatively analyze the aerodynamic changes in patient's trachea after the resection operation of hyperplastic granulation tissue, computational fluid dynamic (CFD) method was utilized to perform the simulation. Firstly, three dimensional finite element model of the patient’s trachea before and after surgery were reconstructed based on CT images; secondly, the numerical simulation based on CFD method was performed to investigate the changes in aerodynamic changes in patient's trachea after excision. Results indicated that the dyspnea symptom was largely alleviated after the removal surgery, the abnormal morphology was obviously improved and the resistance of trachea was decreased significantly. Present research also demonstrates that CFD methods can be used to quantitatively evaluate the postoperative effects of the granulation tissue resection operation.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75728218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study examines the effects of P53 in transdifferentiation of endothelial progenitor cells (EPCs) into smooth muscle cells induced by oscillatory shear stress. Endothelial progenitor cells (EPCs) were planted on slide and treated with 4 dyne/cm2 oscillatory shear stress (OSS). Results showed that the expression P53 was decreased time dependent after OSS. The OSS also attenuated the endothelial cells marker vWF and CD31 expression but enhanced the marker of smooth muscle cell α-SMA and SM22 expression in EPCs. After EPCs were pretreated with P53 agonist, the changes of angiogenesis in vitro were detected by matrix gel, and the expressions of alpha-SMA and SM22 were detected by Western blot. The results showed that simple oscillatory shear stress could decrease but P53 agonist could improve the ability of angiogenesis on EPCs, and down-regulate the expression of α-SMA and SM22. From the above results, we speculate that P53 may play a role in the transdifferentiation of EPCs into smooth muscle cells induced by OSS.
{"title":"The Role of P53 in Transdifferentiation of EPCs into Smooth Muscle Cells Induced by Oscillatory Shear Stress","authors":"Yu Gao, Meiyue Wang, Yanting He, Lanlan Li, Xiaodong Cui, Min Cheng, Xiaoyun Zhang","doi":"10.32604/mcb.2019.05758","DOIUrl":"https://doi.org/10.32604/mcb.2019.05758","url":null,"abstract":"This study examines the effects of P53 in transdifferentiation of endothelial progenitor cells (EPCs) into smooth muscle cells induced by oscillatory shear stress. Endothelial progenitor cells (EPCs) were planted on slide and treated with 4 dyne/cm2 oscillatory shear stress (OSS). Results showed that the expression P53 was decreased time dependent after OSS. The OSS also attenuated the endothelial cells marker vWF and CD31 expression but enhanced the marker of smooth muscle cell α-SMA and SM22 expression in EPCs. After EPCs were pretreated with P53 agonist, the changes of angiogenesis in vitro were detected by matrix gel, and the expressions of alpha-SMA and SM22 were detected by Western blot. The results showed that simple oscillatory shear stress could decrease but P53 agonist could improve the ability of angiogenesis on EPCs, and down-regulate the expression of α-SMA and SM22. From the above results, we speculate that P53 may play a role in the transdifferentiation of EPCs into smooth muscle cells induced by OSS.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85002254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Na Liu, Xiaoyun Zhang, Yuzhen Ding, Hong Li, Xiumei Guan, Min Cheng, Xiaodong Cui
Endothelial progenitor cells (EPCs) play a vital role in postnatal vascular injury and repair, especially vasculogenesis and angiogenesis. The purpose of this study was to investigate the effect of laminar shear stress in attenuating the decreased-expression of complement regulatory protein CD59 and the mechanism of cytoskeleton F-actin. Methods: EPCs were isolated from human umbilical vein blood and planted on glass slides, which applied to the laminar shear stress force (12 dyne/cm2) in a high glucose (20 mM) culture environment. The gene and protein expression of CD59 were detected by SYBGreen quantitative PCR and fluorescence activated cell sorter (FACS) respectively. The rearrangement of cytoskeleton F-actin was detected by FITC-phalloidin staining. Results: The elevated effect of shear stress on the expression of CD59 was significantly reduced in high glucose condition. Moreover, we found that F-actin was disorganized by high glucose, while rearrangement of cytoskeleton would be reversed by a moderate concentration of jasplakinolide (JAS) intervention. Conclusion: Our study indicated that high glucose inhibiting the rearrangement of EPCs cytoskeleton resulted the sensitivity of EPCs to laminar shear stress which should elevate the expression of complement regulatory protein CD59. As a result, EPCs was sensitive to membrane attack complex (MAC) -mediated cell autolysis.
{"title":"High Glucose Reduces the Shear Stress-Induced CD59 Expression on EPCs through F-Actin Alteration","authors":"Na Liu, Xiaoyun Zhang, Yuzhen Ding, Hong Li, Xiumei Guan, Min Cheng, Xiaodong Cui","doi":"10.32604/MCB.2019.05751","DOIUrl":"https://doi.org/10.32604/MCB.2019.05751","url":null,"abstract":"Endothelial progenitor cells (EPCs) play a vital role in postnatal vascular injury and repair, especially vasculogenesis and angiogenesis. The purpose of this study was to investigate the effect of laminar shear stress in attenuating the decreased-expression of complement regulatory protein CD59 and the mechanism of cytoskeleton F-actin. Methods: EPCs were isolated from human umbilical vein blood and planted on glass slides, which applied to the laminar shear stress force (12 dyne/cm2) in a high glucose (20 mM) culture environment. The gene and protein expression of CD59 were detected by SYBGreen quantitative PCR and fluorescence activated cell sorter (FACS) respectively. The rearrangement of cytoskeleton F-actin was detected by FITC-phalloidin staining. Results: The elevated effect of shear stress on the expression of CD59 was significantly reduced in high glucose condition. Moreover, we found that F-actin was disorganized by high glucose, while rearrangement of cytoskeleton would be reversed by a moderate concentration of jasplakinolide (JAS) intervention. Conclusion: \u0000Our study indicated that high glucose inhibiting the rearrangement of EPCs cytoskeleton resulted the sensitivity of EPCs to laminar shear stress which should elevate the expression of complement regulatory protein CD59. As a result, EPCs was sensitive to membrane attack complex (MAC) -mediated cell autolysis.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90746144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Coronary artery disease (CAD) is the leading cause of mortality and morbidity worldwide. It is the disease of the blood vessels supplying the heart muscle. The fatty plaques built within the walls of the coronary arteries might rupture, creating a thrombus, thereby blocking the entire flow through the vessel, which is followed by a heart attack. Patients who suffer from CAD with documented ischemia are predominately sent to the catheterization laboratory for an invasive procedure (PCI, or percutaneous coronary intervention) to open the vessel by the placement of a “stent” as a scaffolding device to release from ischemia. Identifying the culplit lesions that cause the actual ischemia is crucial for PCI optimization. It has been shown in many clinical trials that the integration of coronary imaging and physiology is better in guiding PCI compared to imaging alone. Over the past years, we have developed approaches to derive coronary physiological data using image reconstruction and biomechanical analysis, thus realizing seamless co-registration between imaging and physiology without using extra invasive devices to measure coronary physiology. Some of these approaches are being transferred into clinical applications that have potential to increase the utility of physiological assessment in patients with CAD. In this talk, I will present these activities and our efforts in developing practical solutions for tailored treatment strategies.
{"title":"Research and Clinical Applications of Biomechanical Analysis in Optimization of Coronary Interventions","authors":"S. Tu","doi":"10.32604/MCB.2019.05704","DOIUrl":"https://doi.org/10.32604/MCB.2019.05704","url":null,"abstract":"Coronary artery disease (CAD) is the leading cause of mortality and morbidity worldwide. It is the disease of the blood vessels supplying the heart muscle. The fatty plaques built within the walls of the coronary arteries might rupture, creating a thrombus, thereby blocking the entire flow through the vessel, which is followed by a heart attack. Patients who suffer from CAD with documented ischemia are predominately sent to the catheterization laboratory for an invasive procedure (PCI, or percutaneous coronary intervention) to open the vessel by the placement of a “stent” as a scaffolding device to release from ischemia. Identifying the culplit lesions that cause the actual ischemia is crucial for PCI optimization. It has been shown in many clinical trials that the integration of coronary imaging and physiology is better in guiding PCI compared to imaging alone. Over the past years, we have developed approaches to derive coronary physiological data using image reconstruction and biomechanical analysis, thus realizing seamless co-registration between imaging and physiology without using extra invasive devices to measure coronary physiology. Some of these approaches are being transferred into clinical applications that have potential to increase the utility of physiological assessment in patients with CAD. In this talk, I will present these activities and our efforts in developing practical solutions for tailored treatment strategies.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81511112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Coronary angiography is the traditional standard imaging modality for visual evaluation of coronary anatomy and guidance of percutaneous coronary interventions (PCI). However, the 2-dimensional lumenogram cannot depict the arterial vessel per se and plaque characteristics, or directly assess the stenting result. Intracoronary imaging by means of intravascular ultrasound (IVUS) and optical coherence tomography (OCT) provides valuable incremental information that can be used clinically to optimize stent implantation and thereby minimize stent-related problems. Beyond guidance of stent selection and optimisation, imaging provides critical insights into the pathophysiology of acute coronary syndrome (ACS), greater clarity when confronted with angiographically ambiguous lesions and highlights the dynamic nature and significance of atherosclerotic coronary plaque. For several decades, most physicians have believed that ACS is caused by coronary thrombosis resulting from rupture of vulnerable plaque characterized by a thin fibrous cap overlying a large necrotic core and massive inflammatory cell infiltration. However, nearly one-third of ACS cases are caused by plaque erosion characterized by intact fibrous cap, less or absent necrotic core, less inflammation, and large lumen. Because of the limitations of current imaging modalities, including angiography and intravascular ultrasound, the importance of plaque erosion as a cause of acute coronary events is less well known. OCT as an emerging modality with extremely high resolution is the only intravascular imaging modality available for identification of plaque erosion in vivo, which provides new insight into the mechanism of ACS. More importantly, the introduction of OCT to clinical practice enables us to differentiate the patients with ACS caused by plaque erosion from those caused by plaque rupture, thereby providing precise and personalized therapy based on the different underlying mechanisms. This presentation will systematically review the morphological characteristics of plaque erosion identified by OCT and its implications for the management of ACS.
{"title":"Role of Intracoronary OCT in Diagnosis and Treatment of Acute Coronary Syndrome","authors":"H. Jia, Bo Yu","doi":"10.32604/MCB.2019.05708","DOIUrl":"https://doi.org/10.32604/MCB.2019.05708","url":null,"abstract":"Coronary angiography is the traditional standard imaging modality for visual evaluation of coronary anatomy and guidance of percutaneous coronary interventions (PCI). However, the 2-dimensional lumenogram cannot depict the arterial vessel per se and plaque characteristics, or directly assess the stenting result. Intracoronary imaging by means of intravascular ultrasound (IVUS) and optical coherence tomography (OCT) provides valuable incremental information that can be used clinically to optimize stent implantation and thereby minimize stent-related problems. Beyond guidance of stent selection and optimisation, imaging provides critical insights into the pathophysiology of acute coronary syndrome (ACS), greater clarity when confronted with angiographically ambiguous lesions and highlights the dynamic nature and significance of atherosclerotic coronary plaque. For several decades, most physicians have believed that ACS is caused by coronary thrombosis resulting from rupture of vulnerable plaque characterized by a thin fibrous cap overlying a large necrotic core and massive inflammatory cell infiltration. However, nearly one-third of ACS cases are caused by plaque erosion characterized by intact fibrous cap, less or absent necrotic core, less inflammation, and large lumen. Because of the limitations of current imaging modalities, including angiography and intravascular ultrasound, the importance of plaque erosion as a cause of acute coronary events is less well known. OCT as an emerging modality with extremely high resolution is the only intravascular imaging modality available for identification of plaque erosion in vivo, which provides new insight into the mechanism of ACS. More importantly, the introduction of OCT to clinical practice enables us to differentiate the patients with ACS caused by plaque erosion from those caused by plaque rupture, thereby providing precise and personalized therapy based on the different underlying mechanisms. This presentation will systematically review the morphological characteristics of plaque erosion identified by OCT and its implications for the management of ACS.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77713887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Han Yu, P. J. Nido, T. Geva, Chun Yang, Zheyang Wu, R. Rathod, Xueying Huang, K. Billiar, D. Tang
Ventricle mechanical stress and strain calculations play an important role in cardiovascular investigations. Patients with repaired tetralogy of Fallot (TOF) account for the majority of cases with late onset right ventricular (RV) failure. The current surgical approach, including pulmonary valve replacement(PVR), has yielded mixed results with some patients recover RV function after pulmonary valve insertion with or without concomitant RV remodeling surgery but some do not[Therrien, Siu and McLaughlin (2000);]. Cardiac magnetic resonance (CMR) data were collected from 6 healthy volunteers and 12 Tetralogy of Fallot (TOF) patients before PVR with consent obtained. 12 patients were divided into two groups depending on right ventricle post-surgery recover( 6 for each group). 3D patient-specific CMR-based ventricle models with different zero-load diastole and systole geometries were constructed to qualify right ventricle (RV) stress and strain values at begin-filling, end-filling, begin-ejection, and end-ejection, respectively. The models are solved with ADINA. Our new models (called 2G models) could provide end-diastole and end-systole stress/strain values which the old models with only one zero-load geometries (called 1G models) could not provide[Tang, Del Nido, Yang, et al., 2016]. Logistic regression with 5-fold cross validation was adopted to predict pulmonary valve replacement outcome. The results showed 2G mean end-ejection stress value from the 18 participants was 321.4% higher than that from 1G models (p=0.0002). 2G mean strain values was 230% higher than that of 1G models (p=0.0002). TOF group (TG) end-ejection mean stress value was 105.4% higher than that of healthy group (HG) (17.54±7.42kPa vs. 8.54±0.92kPa, p=0.0245). Worse outcome group (WG) begin-ejection mean stress was 57.4% higher than that of better outcome group (BG, 86.94±26.29 vs. 52.93±22.86 kPa; p=0.041). Among 7 chosen parameters (stress, strain, age, gender, right volume end-diastole volume index, right volume end-systole volume index and ejection fracture), end-filling stress was the best predictor to differentiate BG patients from WG patients with prediction accuracy = 0.8208. 2G models may provide more accurate stress/strain results than 1G models and be applied in clinical situation, potentially. Large scale studies are still needed for validation.
心室机械应力和应变计算在心血管研究中起着重要作用。修复性法洛四联症(TOF)患者占晚发型右心室(RV)衰竭病例的大多数。目前的手术方法，包括肺动脉瓣置换术(PVR)，产生了不同的结果，一些患者在肺动脉瓣置入后恢复了右心室功能，并伴有或不伴有右心室重塑手术，但有些患者没有[Therrien, Siu和McLaughlin(2000)]。6名健康志愿者和12名法洛四联症(TOF)患者经同意后，在PVR前采集心脏磁共振(CMR)数据。12例患者根据术后右心室恢复情况分为两组(每组6例)。构建具有不同零负荷舒张和收缩几何形状的三维患者cmr心室模型，分别在填充开始、填充结束、弹射开始和弹射结束时确定右心室(RV)的应力和应变值。用ADINA对模型进行求解。我们的新模型(称为2G模型)可以提供只有一个零载荷几何形状的旧模型(称为1G模型)无法提供的舒张末期和收缩末期应力/应变值[Tang, Del Nido, Yang等，2016]。采用五重交叉验证的Logistic回归预测肺瓣膜置换术的预后。结果显示，18名参与者的2G平均弹射应力值比1G模型高321.4% (p=0.0002)。2G平均应变值比1G模型高230% (p=0.0002)。TOF组(TG)射血终末平均应激值较健康组(HG)高105.4%(17.54±7.42kPa vs. 8.54±0.92kPa, p=0.0245)。结果较差组(WG)开始射血平均应激比结果较好组(BG, 86.94±26.29 vs 52.93±22.86 kPa)高57.4%;p = 0.041)。在选取的7个参数(应力、应变、年龄、性别、右容积舒张末期容积指数、右容积收缩末期容积指数、射血骨折)中，充盈末期应力是区分BG和WG患者的最佳预测指标，预测准确率为0.8208。2G模型可能比1G模型提供更准确的应力/应变结果，有应用于临床的潜力。仍然需要大规模的研究来验证。
{"title":"Ventricle Stress/Strain Comparison Between Models Using Different Zero-Load Diastole and Systole Morphologies and Models Using Only One Zero-Load Morphologies","authors":"Han Yu, P. J. Nido, T. Geva, Chun Yang, Zheyang Wu, R. Rathod, Xueying Huang, K. Billiar, D. Tang","doi":"10.32604/MCB.2019.05837","DOIUrl":"https://doi.org/10.32604/MCB.2019.05837","url":null,"abstract":"Ventricle mechanical stress and strain calculations play an important role in cardiovascular investigations. Patients with repaired tetralogy of Fallot (TOF) account for the majority of cases with late onset right ventricular (RV) failure. The current surgical approach, including pulmonary valve replacement(PVR), has yielded mixed results with some patients recover RV function after pulmonary valve insertion with or without concomitant RV remodeling surgery but some do not[Therrien, Siu and McLaughlin (2000);]. Cardiac magnetic resonance (CMR) data were collected from 6 healthy volunteers and 12 Tetralogy of Fallot (TOF) patients before PVR with consent obtained. 12 patients were divided into two groups depending on right ventricle post-surgery recover( 6 for each group). 3D patient-specific CMR-based ventricle models with different zero-load diastole and systole geometries were constructed to qualify right ventricle (RV) stress and strain values at begin-filling, end-filling, begin-ejection, and end-ejection, respectively. The models are solved with ADINA. Our new models (called 2G models) could provide end-diastole and end-systole stress/strain values which the old models with only one zero-load geometries (called 1G models) could not provide[Tang, Del Nido, Yang, et al., 2016]. Logistic regression with 5-fold cross validation was adopted to predict pulmonary valve replacement outcome. The results showed 2G mean end-ejection stress value from the 18 participants was 321.4% higher than that from 1G models (p=0.0002). 2G mean strain values was 230% higher than that of 1G models (p=0.0002). TOF group (TG) end-ejection mean stress value was 105.4% higher than that of healthy group (HG) (17.54±7.42kPa vs. 8.54±0.92kPa, p=0.0245). Worse outcome group (WG) begin-ejection mean stress was 57.4% higher than that of better outcome group (BG, 86.94±26.29 vs. 52.93±22.86 kPa; p=0.041). Among 7 chosen parameters (stress, strain, age, gender, right volume end-diastole volume index, right volume end-systole volume index and ejection fracture), end-filling stress was the best predictor to differentiate BG patients from WG patients with prediction accuracy = 0.8208. 2G models may provide more accurate stress/strain results than 1G models and be applied in clinical situation, potentially. Large scale studies are still needed for validation.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75962927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Observational studies have identified angiogenesis from the adventitial vasa vasorum and intraplaque hemorrhage (IPH) as critical factors in atherosclerotic plaque progression and destabilization. Here we propose a mathematical model incorporating intraplaque neo vascularization and hemodynamic calculation for the quantitative evaluation of atherosclerotic plaque hemorrhage. An angiogenic microvasculature based on histology of a patient’s carotid plaque is generated by two - dimensional nine - point model of endothelial cell migration. Three key cells (endothelial cells, smooth muscle cells and macrophages) and three key chemicals (vascular endothelial growth factors, extracellular matrix and matrix metalloproteinase) are involved in the intraplaque angiogenesis model, and described by the reaction - diffusion partial equations. The hemodynamic calculation of the microcirculation on the generated microvessel network is carried out by coupling the intravascular, interstitial and transvascular flow. The plasma concentration in the interstitial domain is defined as the description of IPH area according to the diffusion and convection with the interstitial fluid flow, as well as the extravascular movement across the leaky vessel wall. The simulation results demonstrate a series of pathophysiological phenomena during the progression of an atherosclerotic plaq ue, including the high microvessel density (MVD) region at the shoulder areas, the transvascular flow through the capillary wall and the intraplaque hemorrhage. The hemodynamic results show significant consistency with both the histology data and the MR im aging data in quality and quantity. In addition, the sensitivity analysis of IPH to model parameters reveals that the decreased MVD and the vessel permeability may reduce the IPH area dramatically.
{"title":"Neovascularization and Intraplaque Hemorrhage in Atherosclerotic Plaque Destabilization-A Mathematical Model","authors":"Muyi Guo, Y. Cai, Zhiyong Li","doi":"10.32604/MCB.2019.05727","DOIUrl":"https://doi.org/10.32604/MCB.2019.05727","url":null,"abstract":"Observational studies have identified angiogenesis from the adventitial vasa vasorum and intraplaque hemorrhage (IPH) as critical factors in atherosclerotic plaque progression and destabilization. Here we propose a mathematical model incorporating intraplaque neo vascularization and hemodynamic calculation for the quantitative evaluation of atherosclerotic plaque hemorrhage. An angiogenic microvasculature based on histology of a patient’s carotid plaque is generated by two - dimensional nine - point model of endothelial cell migration. Three key cells (endothelial cells, smooth muscle cells and macrophages) and three key chemicals (vascular endothelial growth factors, extracellular matrix and matrix metalloproteinase) are involved in the intraplaque angiogenesis model, and described by the reaction - diffusion partial equations. The hemodynamic calculation of the microcirculation on the generated microvessel network is carried out by coupling the intravascular, interstitial and transvascular flow. The plasma concentration in the interstitial domain is defined as the description of IPH area according to the diffusion and convection with the interstitial fluid flow, as well as the extravascular movement across the leaky vessel wall. The simulation results demonstrate a series of pathophysiological phenomena during the progression of an atherosclerotic plaq ue, including the high microvessel density (MVD) region at the shoulder areas, the transvascular flow through the capillary wall and the intraplaque hemorrhage. The hemodynamic results show significant consistency with both the histology data and the MR im aging data in quality and quantity. In addition, the sensitivity analysis of IPH to model parameters reveals that the decreased MVD and the vessel permeability may reduce the IPH area dramatically.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77639128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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