title: The effect of residual strain on the diastolic function of the left ventricle as predicted by a structural model.
abstract: The unloaded heart is not stress-free. It is subjected to residual stress and strain. Their extent and influence on the global performance of the left ventricle and on local phenomena in the ventricular wall are studied by model simulation. The analysis focuses on the equatorial region of the ventricle, with an approximate thick-walled cylindrical geometry. The in vivo myocardium is considered to be incompressible, consisting of fibers embedded in a fluid matrix, with transmurally varying anisotropic microstructure in accordance with morphological characteristics. The results show that residual strain is transmurally distributed with a pattern and magnitude which agree well with measurements. The calculated residual strains are within mean +/- one standard deviation of the measured ones. Their magnitude was found to increase with increasing opening angle and with increasing wall thickness. The residual strain was found to have several effects on ventricular function: At volumes higher than the reference one it gives rise to more uniform transmural distributions of stress and intramyocardial pressure; it causes about 50% increase in the ventricular compliance at high volumes and doubles the suction of atrial blood at low volumes, thus facilitating the diastolic filling. In addition, residual strains cause bias of in vivo measured strains from their true values. This may significantly affect physiological interpretation of measured ventricular deformations. In conclusion, the present structural analysis predicts that residual strain has favorable effect on left-ventricular diastolic performance, and gives rise to more uniform ventricular stress distribution.
authors: Department of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa.
authors: E
authors: E
authors: Nevo
authors: Y
authors: Y
authors: Lanir
mesh_terms: D016279:Atrial Function, Left / Q000502:physiology; D015982:Bias; D002302:Cardiac Output / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D003094:Collagen / Q000737:chemistry / Q000502:physiology; D003971:Diastole / Q000502:physiology*; D004548:Elasticity; D004699:Endocardium / Q000502:physiology; D005110:Extracellular Space / Q000502:physiology; D006352:Heart Ventricles / Q000033:anatomy & histology; D006801:Humans; D006874:Hydrostatic Pressure; D008955:Models, Cardiovascular; D008961:Models, Structural; D018485:Muscle Fibers, Skeletal / Q000502:physiology; D009206:Myocardium / Q000166:cytology / Q000648:ultrastructure; D010496:Pericardium / Q000502:physiology; D013314:Stress, Mechanical; D013329:Structure-Activity Relationship; D016276:Ventricular Function; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D003094:Collagen