title: Modeling of mechanical dysfunction in regional stunned myocardium of the left ventricle.
abstract: Reversible mechanical dysfunction of the myocardium after a single or multiple episode(s) of coronary artery occlusion has been observed in previous studies and is termed myocardial stunning. The hypothesis that stunning could be represented by a decrease in maximum available muscle force in the stunned region was examined by means of a mathematical model that incorporates series viscoelastic elements. A canine experimental model was also employed to demonstrate depressed contractility and a consistent delay of shortening in the stunned region. The mechanical model of the left ventricle was designed to include a normal and stunned region, for which the stunned region was allowed to have variable size. Each region consisted of a volume and time dependent force generator in parallel with a passive elastic force element. The passive elastic element was placed in series with a constant viscosity component and a series elastic component. The model was solved by means of a computer. Passive and active properties of each region could be altered independently. The typical regional measures of muscle performance such as percent shortening, percent bulge, percent thickening, delay of shortening, percent increase in end-diastolic length and other hemodynamic measures were computed. These results were similar to those observed in animal models of stunning. In addition, a nearly linear relationship with end-diastolic length and delay of shortening was predicted by the model. It was concluded that a decrease in the peak isovolumic elastance and augmentation of viscosity effect of creep during stunning can explain mechanical abnormalities of stunned myocardium.
authors.affiliation: Department of Biomedical Engineering, Rutgers University, Piscataway, NJ 08855-0909, USA. drzewiec@biomed.rutgers.edu
authors.forename: G
authors.initials: G
authors.lastname: Drzewiecki
authors.forename: J J
authors.initials: JJ
authors.lastname: Wang
authors.forename: J K
authors.initials: JK
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Kedem
authors.forename: H
authors.initials: H
authors.lastname: Weiss
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D003187:Compliance; D003198:Computer Simulation; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology*; D017682:Myocardial Stunning / Q000503:physiopathology*; D012044:Regression Analysis; D013314:Stress, Mechanical; D013599:Systole / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*