TY - JOUR
T1 - Regional wall mechanics in the ischemic left ventricle
T2 - Numerical modeling and dog experiments
AU - Bovendeerd, P. H.M.
AU - Arts, T.
AU - Delhaas, T.
AU - Huyghe, J. M.
AU - Van Campen, D. H.
AU - Reneman, R. S.
PY - 1996
Y1 - 1996
N2 - 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 ~12% of total wall volume. In the model simulations, the ~12% reduction in the amount of normally contracting tissue resulted in an ~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.
AB - 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 ~12% of total wall volume. In the model simulations, the ~12% reduction in the amount of normally contracting tissue resulted in an ~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.
KW - contractile work
KW - finite-element model
KW - ischemic border zone
KW - left ventricular deformation
UR - http://www.scopus.com/inward/record.url?scp=0030022226&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.1996.270.1.h398
DO - 10.1152/ajpheart.1996.270.1.h398
M3 - Article
C2 - 8769776
AN - SCOPUS:0030022226
SN - 0363-6135
VL - 270
SP - H398-H410
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 1 39-1
ER -