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 2017
TL;DR: Emerging models of wound healing in the infarct region and growth and remodeling in the surviving myocardium that are beginning to predict the long-term effects of infarction and post-infarction therapies hold great promise for designing novel therapies.
Abstract: Each year, over seven million people suffer a myocardial infarction (heart attack). For those who survive the initial event, the mechanical properties of the scar tissue that gradually replaces the damaged muscle are a critical determinant of many life-threatening sequelae, such as infarct rupture and the development of heart failure. Thus, understanding the mechanics of healing infarct scar, its interaction with the rest of the heart, and the resulting changes in heart function are critical to devising effective therapies. Computational models play an essential role in understanding these potentially complex interactions. The first section of this chapter reviews the structure and mechanical properties of the normal heart and the methods used to study those properties. The second section discusses the structure and mechanical properties of healing post-infarction scar. The remaining sections review landmark analytical and computational models that provided insight into the functional consequences of myocardial infarction and potential therapies. Finally, we briefly consider emerging models of wound healing in the infarct region and growth and remodeling in the surviving myocardium that are beginning to predict the long-term effects of infarction and post-infarction therapies. In the future, multi-scale models that capture such remodeling in addition to the beat-to-beat mechanics of the heart hold great promise for designing novel therapies, not only for myocardial infarction but also for a wide range of cardiac pathologies.
4 citations
Cites background or methods from "Regional wall mechanics in the isch..."
...Bovendeerd et al. (1996) published one of the last of this early class of models, integrating many of the most important features now common to modern models of the infarcted heart....
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...Bovendeerd et al. (1996) achieved an excellent match to experimentally measured fiber strains, then used their model to explore the impact of both transmural and non-transmural ischemia on regional work in the infarct borderzone....
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15 Nov 2001
TL;DR: This work has developed a framework, consisting of a graph network with nodes (compliant cavities) and edges (flow ducts) that facilitates tailored cardiac modeling using a toolkit of modules.
Abstract: Numerical models of various aspects of cardiac function are useful in simulating pathologies and therapies. Such models cannot be easily combined because of differences in input and output structure. To harbor the different models we have developed a framework, consisting of a graph network with nodes (compliant cavities) and edges (flow ducts). Thus using a toolkit of modules facilitates tailored cardiac modeling.
3 citations
TL;DR: A comparative analysis among the three MI groups showed that a larger infarct size was associated with larger remodeling strain, more serious impairment in the cellular structure and composition, and regional contractile function at regional tissue level and LV function at organ level.
Abstract: The surviving myocardium initially compensates the loss of injured myocardium after myocardial infarction (MI) and gradually becomes progressively dysfunctional. There have been limited studies on the effect of infarct size on temporal and spatial alterations in the myocardium during progressive myocardial remodeling. MI with three infarct sizes, i.e. 15, 25 and 35% of the left ventricular (LV) wall, was created in an ovine infarction model. The progressive LV remodeling over a 12-week period was studied. Echocardiography, sonomicrometry, and histological and molecular analyses were carried out to evaluate cardiac function, regional tissue contractile function, structural remodeling and cardiomyocyte hypertrophy, and calcium handling proteins. Twelve weeks after MI, the 15, 25 and 35% MI groups had normalized LV end diastole volumes of 1.4 ± 0.2, 1.7 ± 0.3 and 2.0 ± 0.4 ml/kg, normalized end systole volumes of 1.0 ± 0.1, 1.0 ± 0.2 and 1.3 ± 0.3 ml/kg and LV ejection fractions of 43 ± 3, 42 ± 6 and 34 ± 4%, respectively. They all differed from the sham group (p < 0.05). All the three MI groups exhibited larger wall areal expansion (remodeling strain), larger cardiomyocyte size and altered expression of calcium handing proteins in the adjacent myocardium compared to the remote counterpart from the infarct. A significant correlation was found between cardiomyocyte size and remodeling strain in the adjacent zone. A comparative analysis among the three MI groups showed that a larger infarct size (35 vs. 15% MI) was associated with larger remodeling strain, more serious impairment in the cellular structure and composition, and regional contractile function at regional tissue level and LV function at organ level.
3 citations
TL;DR: In this article, numerical simulations of blood flow and myocardium motion for an average canine left ventricle (LV) with fluid-structure interaction were performed and the temporal variations of the LV cavity pressure and wall stress during the cardiac cycle were consistent with previous literature.
Abstract: Numerical simulations of blood flow and myocardium motion for an average canine left ventricle (LV) with fluid-structure interaction were performed. The temporal variations of the LV cavity pressure and wall stress during the cardiac cycle were consistent with previous literature. LV cavity volume was conserved from one period to the next, despite sub-physiological ejection volumes and brief periods of backflow during early filling. This study improves on previous ones by presenting details of the models and results for both the fluid and solid components of the LV.
2 citations
01 Jan 1998
TL;DR: On the whole, a number of clinical settings are potentially associated with myocardial stunning, including the percutaneous transluminal coronary angioplasty, unstable, variant angina, acute myocardIAL infarction with early repercussion, exercise-induced ischemia, cardiac surgery, and cardiac transplantation.
Abstract: Although the ischemic dysfunction of the heart from coronary artery occlusion was observed before the 20th century, the concept of postischemic myocardial dysfunction was initially described by Vatner’s group in 1975 (33). Until 1982 the term myocardial stunning, related to the phenomenon of postischemic ventricular abnormality, was submitted and first coined by Braunwald and Kloner (11). They stated that the ischemic process may be “hit, run, and stun,”rather than a simple all-or-nothing process in which myocardial necrosis was caused when ischemia was prolonged and severe, but transient when brief or mild. In recent years it has been demonstrated experimentally that the mechanical dysfunction in postischemic or stunned myocardium persists after reperfusion despite the absence of irreversible damage and restoration of normal or near-normal coronary flow (6,7,9,39,60). In the other words, postischemic myocardial dysfunction is a fully reversible abnormality, if the reperfusion period is sufficient (11,14). On the whole, a number of clinical settings are potentially associated with myocardial stunning, including the percutaneous transluminal coronary angioplasty, unstable, variant angina, acute myocardial infarction with early repercussion, exercise-induced ischemia, cardiac surgery, and cardiac transplantation (7).
1 citations