Ventricular interaction in the pathologic heart. A model based study.
The effects of direct ventricular interaction and interaction mediated by the pericardium on the diastolic left ventricle (LV) were quantified using idealized models of five pathologic conditions. Two-dimensional (2D) mathematical models were constructed in long and short axis views of four pathologic LV conditions and the normal heart (NL): dilated cardiomyopathy (DCM), concentric LV hypertrophy (HYP), chronic anterior-apical infarction in a normal shaped LV (CAINL), and CAI in a dilated LV (CAID). To assess the effects of RV pressure increase on the LV mechanical state, RV pressure was systematically increased for several LV pressures and changes in the LV diastolic pressure-area relationships, and LV free wall and septal principal stresses and strains were quantified. At higher RV pressures, with pericardial effects included in the models, the pressure-area relationship was similar for all models, indicating that, at these higher pressures, the effects of RV and pericardial pressures are more important than global LV shape, wall thickness, or material properties in determining the pressure-area relationship. There were significant differences among models in the changes in LV free wall and septal stress and strain after an increase in RV pressure. These models may be of use in predicting interaction in the corresponding clinical state.
Moulton
M J
MJ
Department of Surgery, Washington University, St. Louis, Missouri, USA.
Creswell
L L
LL
Downing
S W
SW
Actis
R L
RL
Myers
K W
KW
Szabó
B A
BA
Vannier
M W
MW
Pasque
M K
MK
D000818:Animals; D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000473:pathology / Q000503:physiopathology; D003971:Diastole / Q000502:physiology; D006331:Heart Diseases / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology; D010496:Pericardium / Q000473:pathology / Q000503:physiopathology; D016276:Ventricular Function / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology