Regional wall mechanics in the ischemic left ventricle: numerical modeling and dog experiments
01 Jan 1996-American Journal of Physiology-heart and Circulatory Physiology (American Physiological Society)-Vol. 270, Iss: 1
TL;DR: The mechanics of the ischemic left ventricle during a complete cardiac cycle were simulated using a finite-element model accounting for the thick-walled ventricular geometry, the fibrous nature of the myocardial tissue, and the dependency of active muscle fiber stress on time, strain, and strain rate.
Abstract: The mechanics of the ischemic left ventricle during a complete cardiac cycle were simulated using a finite-element model accounting for the thick-walled ventricular geometry, the fibrous nature of the myocardial tissue, and the dependency of active muscle fiber stress on time, strain, and strain rate. Ischemia was modeled by disabling the generation of active stress in a region comprising approximately 12% of total wall volume. In the model simulations, the approximately 12% reduction in the amount of normally contracting tissue resulted in an approximately 25% reduction in stroke work compared with the normal situation. The more-than-proportional loss of stroke work may partly be attributed to storage of elastic energy in the bulging ischemic region. Furthermore the mechanical performance in the nonischemic border zone deteriorated because of reduced systolic fiber stress (if fibers were in series with those in the ischemic region) or reduced fiber shortening (if fibers were parallel). The deformation pattern of the ventricle was asymmetric with respect to the ischemic region because of the anisotropy of the myocardial tissue. Epicardial fiber shortening in and around the ischemic region, as predicted from the model simulations, was in qualitative agreement with shortening, as measured in four dogs in which ischemia was induced by occlusion of the distal part of the left anterior interventricular coronary artery.
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01 Jan 2004
TL;DR: An interface is proposed which generates complex left ventricular simulation model which can be generated with 3D shapemodel, cell orientation model, cell electrophysiological model, coronary artery model and tissue mechanical property and model.
Abstract: Recent advances in constructing accurate cell models have enabled new research areas for establishing accurate tissue and organ models. One important target of such research is heart. However, although the accurate myocardial cell model is becoming available, many elements such as cell orientation, mechanical tissue properties are still not known. On the other hand, computer simulation is becoming important tool for biological research. In such research, biological model is constructed and evaluated with variety of parameters. However, for the organ models such as heart model, it becomes very complicated and difficult to generate and evaluate variety of heart models with different combinations of element models and their parameters. In this paper, we propose an interface which generates complex left ventricular simulation model. We can generate left ventricular simulation models with 3D shape model, cell orientation model, cell electrophysiological model, coronary artery model and tissue mechanical property and model. Obtained simulation results show the effectiveness of the system.
8 citations
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07 Jun 2007
TL;DR: Investigation of possible mechanisms for the characteristic strain patterns in moderately ischemic regions using a simulation model of the LV wall found they may be caused by slower mechanical activation and relaxation rates.
Abstract: Background: Myocardial ischemia in the left ventricular (LV) myocardium introduces non-uniform and pathological strain patterns. Total passive segments lengthen when pressure increases during early systole and shorten when pressure drops at the end of ejection. Moderately ischemic segments typically lengthen during isovolumic contraction, start shortening during ejection and continue shortening, usually at an increased rate, after aortic valve closure.
Aim: The aim of this study was to investigate possible mechanisms for the characteristic strain patterns in moderately ischemic regions using a simulation model of the LV wall.
Methods: A thick-walled truncated ellipsoidal finite element model was used to represent the LV geometry. The model included mathematical descriptions of fiber orientation, passive elastic properties, and actively generated fiber stress. A severely ischemic region and a moderately ischemic border zone were incorporated in the model. The severely ischemic region was made stiffer and generated no active fiber stress during systole. The border zone was made slightly stiffer, active fiber stress was reduced and generated at a slower rate while the relaxation rate was slower than in the normal regions. The cardiac cycle was simulated by applying physiological pressure-volume boundary conditions.
Results: The strain pattern in the severely ischemic region resembled the pressure curve with lengthening during pressure rise and shortening during pressure decrease, while the border zone started shortening after an initial early systolic lengthening and continued shortening during isovolumic relaxation at an increased rate.
Conclusion: The characteristic moderately ischemic strain pattern may be caused by slower mechanical activation and relaxation rates.
8 citations
7 citations
TL;DR: This method can be used to predict the effect of ischemia on the regional myocardium and promises to facilitate better understanding of FMR response to REVASC.
Abstract: Background: Functional Mitral Regurgitation (FMR) associated with coronary artery disease affects nearly 3 million patients in the United States. Both myocardial infarction (MI) and ischemia contribute to FMR development but uncertainty as to which patients will respond to revascularization (REVASC) of ischemia alone prevents rational decision making about FMR therapy. The aim of the study was to create patient-specific cardiac MRI (CMR) informed finite element (FE) models of the left ventricle (LV), calculate regional LV systolic contractility and then use optimized systolic material properties to simulate the effect of revascularization (virtual REVASC). Method: We describe a novel finite element method able to predict the effect of myocardial ischemia on regional left ventricular function. Cardiac MRI (CMR) was obtained in five patients with multi-vessel coronary disease and FMR before and 3 months after percutaneous REVASC and a single healthy volunteer. Patient-specific FE models were created and divided into 17 sectors where the systolic contractility parameter, T_max, of each sector was a function of regional stress perfusion (SP-CMR) and myocardial infarction (LGE-CMR) scores. Sector-specific circumferential and longitudinal end-systolic strain and LV volume from CSPAMM were used in a formal optimization to determine the sector based myocardial contractility, T_max, and ischemia effect, α. Virtual REVASC was simulated by setting α to zero. Results: The FE optimization successfully converged with good agreement between calculated and experimental end-systolic strain and LV volumes. Specifically, the optimized T_max for the healthy myocardium for five patients and the volunteer was 495.1 kPa, 336.8 kPa, 173.5 kPa, 227.9 kPa, 401.4 kPa, and 218.9 kPa. The optimized α was found to be 1.0, 0.44, and 0.08 for Patients 1, 2, and 3, and 0 for Patients 4 and 5. The calculated average of radial strain for the Patients 1, 2, and 3 at baseline and after virtual REVASC was 0.23 and 0.25, respectively. Conclusion: We developed a novel computational method able to predict the effect of myocardial ischemia in patients with FMR. This method can be used to predict the effect of ischemia on the regional myocardium and promises to facilitate better understanding of FMR response to REVASC.
7 citations
01 Jan 2004
TL;DR: The fibre structure of the human heart is studied and finite element models are presented which were developed to simulate the contraction of the left ventricle in three dimensions and the active fibre contraction processes are described.
Abstract: The healthy human myocardium represents a global syncytium consisting of myocytes or fibres which are attached to each other to form a spatial network with a well-defined mechanical functionality. In order that upon stimulation of the fibres and subsequent contraction a physiologic ejection volume of blood is reached, the arrangement of the fibres exhibits a systematic architecture, in particular, the fibrous network wraps both ventricles in a characteristic, rope-like fashion. Thereby, no beginning and end of fibre strands can be found in the myocardium; in contrast to the skeletal muscles where fibre strands are attached to ligaments, cardiac contractile pathways are essentially closed. In this work the fibre structure of the human heart is studied and finite element models are presented which were developed to simulate the contraction of the left ventricle in three dimensions. The anisotropy associated with the fibre arrangement within the myocardium is thereby included and the active fibre contraction processes are described. Finally, the relation between the local fibre structure in the myocardium and the systolic deformation patterns are studied.
7 citations