Jonathan F. Wenk
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Jonathan F. Wenk has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
Arthur W. Wallace
Department of Surgery, University of California, San Francisco, California. USA
2 shared publicationsJulius M. Guccione
Department of Surgery, University of California, San Francisco, California. USA
2 shared publicationsLiang Ge
Department of Surgery, University of California, San Francisco, California. USA
2 shared publicationsMark B. Ratcliffe
Department of Surgery, University of California, San Francisco, California. USA
2 shared publicationsMehrdad Soleimani
Department of Surgery, University of California, San Francisco, California. USA
2 shared publicationsZhihong Zhang
Department of Surgery, University of California, San Francisco, California. USA
2 shared publications
Latest Publications
- 1 August 2013
- Published by Taylor & Francis in Computer Methods in Biomechanics and Biomedical Engineering
- Vol. 16 (8) , 807-818
A coupled biventricular finite element and lumped-parameter circulatory system model of heart failure
Numerical modelling of the cardiovascular system is becoming an important tool for assessing the influence of heart disease and treatment therapies. In the current study, we present an approach for modelling the interaction between the heart and the circulatory system. This was accomplished by creating animal-specific biventricular finite element (FE) models, which characterise the mechanical response of the heart, and by coupling them to a lumped-parameter model that represents the systemic and pulmonic circulatory system. In order to minimise computation time, the coupling was enforced in a weak (one-way) manner, where the ventricular pressure–volume relationships were generated by the FE models and then passed into the circulatory system model to ensure volume conservation and physiological pressure changes. The models were first validated by tuning the parameters, such that the output of the models matched experimentally measured pressures and volumes. Then the models were used to examine cardiac function and the myofibre stress in a healthy canine heart and a canine heart with dilated cardiomyopathy. The results showed good agreement with experimental measurements. The stress in the case of cardiomyopathy was found to increase significantly, while the pump function was decreased, compared to the healthy case. The total runtime of the simulations is lesser than that of many fully coupled models presented in the literature. This will allow for a much quicker evaluation of possible treatment strategies for combating the effects of heart failure, especially in optimisation schemes that require numerous FE simulations.
- 1 August 2013
- Published by Taylor & Francis in Computer Methods in Biomechanics and Biomedical Engineering
- Vol. 16 (8) , 807-818
A coupled biventricular finite element and lumped-parameter circulatory system model of heart failure
Numerical modelling of the cardiovascular system is becoming an important tool for assessing the influence of heart disease and treatment therapies. In the current study, we present an approach for modelling the interaction between the heart and the circulatory system. This was accomplished by creating animal-specific biventricular finite element (FE) models, which characterise the mechanical response of the heart, and by coupling them to a lumped-parameter model that represents the systemic and pulmonic circulatory system. In order to minimise computation time, the coupling was enforced in a weak (one-way) manner, where the ventricular pressure–volume relationships were generated by the FE models and then passed into the circulatory system model to ensure volume conservation and physiological pressure changes. The models were first validated by tuning the parameters, such that the output of the models matched experimentally measured pressures and volumes. Then the models were used to examine cardiac function and the myofibre stress in a healthy canine heart and a canine heart with dilated cardiomyopathy. The results showed good agreement with experimental measurements. The stress in the case of cardiomyopathy was found to increase significantly, while the pump function was decreased, compared to the healthy case. The total runtime of the simulations is lesser than that of many fully coupled models presented in the literature. This will allow for a much quicker evaluation of possible treatment strategies for combating the effects of heart failure, especially in optimisation schemes that require numerous FE simulations.
- 17 February 2011
- Published by ASME International in Journal of Biomechanical Engineering
- Vol. 133 (4) , 044501
Regional Left Ventricular Myocardial Contractility and Stress in a Finite Element Model of Posterobasal Myocardial Infarction
Recently, a noninvasive method for determining regional myocardial contractility, using an animal-specific finite element (FE) model-based optimization, was developed to study a sheep with anteroapical infarction (Sun et al., 2009, “A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm,” ASME J. Biomech. Eng., 131(11), p. 111001). Using the methodology developed in the previous study (Sun et al., 2009, “A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm,” ASME J. Biomech. Eng., 131(11), p. 111001), which incorporates tagged magnetic resonance images, three-dimensional myocardial strains, left ventricular (LV) volumes, and LV cardiac catheterization pressures, the regional myocardial contractility and stress distribution of a sheep with posterobasal infarction were investigated. Active material parameters in the noninfarcted border zone (BZ) myocardium adjacent to the infarct , in the myocardium remote from the infarct , and in the infarct were estimated by minimizing the errors between FE model-predicted and experimentally measured systolic strains and LV volumes using the previously developed optimization scheme. The optimized was found to be significantly depressed relative to , while was found to be zero. The myofiber stress in the BZ was found to be elevated, relative to the remote region. This could cause further damage to the contracting myocytes, leading to heart failure.- 17 February 2011
- Published by ASME International in Journal of Biomechanical Engineering
- Vol. 133 (4) , 044501
Regional Left Ventricular Myocardial Contractility and Stress in a Finite Element Model of Posterobasal Myocardial Infarction
Recently, a noninvasive method for determining regional myocardial contractility, using an animal-specific finite element (FE) model-based optimization, was developed to study a sheep with anteroapical infarction (Sun et al., 2009, “A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm,” ASME J. Biomech. Eng., 131(11), p. 111001). Using the methodology developed in the previous study (Sun et al., 2009, “A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm,” ASME J. Biomech. Eng., 131(11), p. 111001), which incorporates tagged magnetic resonance images, three-dimensional myocardial strains, left ventricular (LV) volumes, and LV cardiac catheterization pressures, the regional myocardial contractility and stress distribution of a sheep with posterobasal infarction were investigated. Active material parameters in the noninfarcted border zone (BZ) myocardium adjacent to the infarct , in the myocardium remote from the infarct , and in the infarct were estimated by minimizing the errors between FE model-predicted and experimentally measured systolic strains and LV volumes using the previously developed optimization scheme. The optimized was found to be significantly depressed relative to , while was found to be zero. The myofiber stress in the BZ was found to be elevated, relative to the remote region. This could cause further damage to the contracting myocytes, leading to heart failure.- 23 December 2010
- Published by ASME International in Journal of Biomechanical Engineering
- Vol. 133 (1) , 014503
Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Parameter Sensitivity Study
As a follow-up to the work presented in Wenk et al. (2010, “Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Micromechanical Approximation,” ASME J. Biomech. Eng., 132, p. 091011), a formal sensitivity study was conducted in which several model parameters were varied. The previous work only simulated a few combinations of the parameters. In the present study, the fibrous cap thickness, longitudinal position of the region of microcalcifications, and volume fraction of microcalcifications were varied over a broader range of values. The goal of the present work is to investigate the effects of localized regions of microcalcifications on the stress field of atherosclerotic plaque caps in a section of carotid artery. More specifically, the variations in the magnitude and location of the maximum circumferential stress were assessed for a range of parameters using a global sensitivity analysis method known as Sobol' indices. The stress was calculated by performing finite element simulations of three-dimensional fluid-structure interaction models, while the sensitivity indices were computed using a Monte Carlo scheme. The results indicate that cap thickness plays a significant role in the variation in the magnitude of the maximum circumferential stress, with the sensitivity to volume fraction increasing when the region of microcalcification is located at the shoulder. However, the volume fraction played a larger role in the variation in the location of the maximum circumferential stress. This matches the finding of the previous study (Wenk et al., 2010, “Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Micromechanical Approximation,” ASME J. Biomech. Eng., 132, p. 091011), which indicates that the maximum circumferential stress always shifts to the region of microcalcification.
- 23 December 2010
- Published by ASME International in Journal of Biomechanical Engineering
- Vol. 133 (1) , 014503
Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Parameter Sensitivity Study
As a follow-up to the work presented in Wenk et al. (2010, “Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Micromechanical Approximation,” ASME J. Biomech. Eng., 132, p. 091011), a formal sensitivity study was conducted in which several model parameters were varied. The previous work only simulated a few combinations of the parameters. In the present study, the fibrous cap thickness, longitudinal position of the region of microcalcifications, and volume fraction of microcalcifications were varied over a broader range of values. The goal of the present work is to investigate the effects of localized regions of microcalcifications on the stress field of atherosclerotic plaque caps in a section of carotid artery. More specifically, the variations in the magnitude and location of the maximum circumferential stress were assessed for a range of parameters using a global sensitivity analysis method known as Sobol' indices. The stress was calculated by performing finite element simulations of three-dimensional fluid-structure interaction models, while the sensitivity indices were computed using a Monte Carlo scheme. The results indicate that cap thickness plays a significant role in the variation in the magnitude of the maximum circumferential stress, with the sensitivity to volume fraction increasing when the region of microcalcification is located at the shoulder. However, the volume fraction played a larger role in the variation in the location of the maximum circumferential stress. This matches the finding of the previous study (Wenk et al., 2010, “Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Micromechanical Approximation,” ASME J. Biomech. Eng., 132, p. 091011), which indicates that the maximum circumferential stress always shifts to the region of microcalcification.
- 1 September 2010
- Published by ASME International in Journal of Biomechanical Engineering
- Vol. 132 (9) , 091011
Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Micromechanical Approximation
Most finite element models of atherosclerotic arteries do not account for the heterogeneity of the plaque constituents at the microscale. Failure of plaque lesions has been shown to be a local event, linked to stress concentrations caused by cap thinning, inflammation, macroscopic heterogeneity, and recently, the presence of microcalcifications. There is growing evidence that microcalcifications exist in the fibrous cap of plaque lesions. However, their role is not yet fully understood. The goal of the present work is to investigate the effects of localized regions of microcalcifications on the stress field of atherosclerotic plaque caps in a section of carotid artery. This is achieved by performing finite element simulations of three-dimensional fluid-structure interaction models. The material response in the region of microcalcification is modeled using a combination of finite elements, homogenization theory, and a stress concentration function that approximates the average local stresses in the fibrous tissue and microcalcification phases. The results indicate that the circumferential stress in the fibrous tissue phase increases as the volume fraction of microcalcifications is increased, and that the stress exceeds a critical threshold when the fibrous cap thickness is decreased. Furthermore, the presence of the microcalcifications significantly influences the distribution of stress by shifting the maximum circumferential stress away from the cap shoulders, where failure is most common when the effective region of microcalcification is located at the center of the cap. This is a possible explanation of why 40% of plaque ruptures occur away from the shoulder region of the cap.
- 1 September 2010
- Published by ASME International in Journal of Biomechanical Engineering
- Vol. 132 (9) , 091011
Numerical Modeling of Stress in Stenotic Arteries With Microcalcifications: A Micromechanical Approximation
Most finite element models of atherosclerotic arteries do not account for the heterogeneity of the plaque constituents at the microscale. Failure of plaque lesions has been shown to be a local event, linked to stress concentrations caused by cap thinning, inflammation, macroscopic heterogeneity, and recently, the presence of microcalcifications. There is growing evidence that microcalcifications exist in the fibrous cap of plaque lesions. However, their role is not yet fully understood. The goal of the present work is to investigate the effects of localized regions of microcalcifications on the stress field of atherosclerotic plaque caps in a section of carotid artery. This is achieved by performing finite element simulations of three-dimensional fluid-structure interaction models. The material response in the region of microcalcification is modeled using a combination of finite elements, homogenization theory, and a stress concentration function that approximates the average local stresses in the fibrous tissue and microcalcification phases. The results indicate that the circumferential stress in the fibrous tissue phase increases as the volume fraction of microcalcifications is increased, and that the stress exceeds a critical threshold when the fibrous cap thickness is decreased. Furthermore, the presence of the microcalcifications significantly influences the distribution of stress by shifting the maximum circumferential stress away from the cap shoulders, where failure is most common when the effective region of microcalcification is located at the center of the cap. This is a possible explanation of why 40% of plaque ruptures occur away from the shoulder region of the cap.