Homogeneity of cardiac contraction despite physiological asynchrony of depolarization: a model study.
The use of mathematical models combining wave propagation and wall mechanics may provide new insights in the interpretation of cardiac deformation toward various forms of cardiac pathology. In the present study we investigated whether combining accepted mechanisms on propagation of the depolarization wave, time variant mechanical properties of cardiac tissue after depolarization, and hemodynamic load of the left ventricle (LV) by the aortic impedance in a three-dimensional finite element model results in a physiological pattern of cardiac contraction. We assumed that the delay between depolarization for all myocytes and the onset of crossbridge formation was constant. Two simulations were performed, one in which contraction was initiated according to the regular depolarization pattern (NORM simulation), and another in which contraction was initiated after synchronous depolarization (SYNC simulation). In the NORM simulation propagation of depolarization was physiological, but wall strain was unphysiologically inhomogeneous. When simulating LV mechanics with unphysiological synchronous depolarization (SYNC) myofiber strain was more homogeneous and more physiologic. Apparently, the assumption of a constant delay between depolarization and onset of crossbridge formation results in an unrealistic contraction pattern. The present finding may indicate that electromechanical delay times are heterogeneously distributed, such that a contraction in a normal heart is more synchronous than depolarization.
Kerckhoffs
R C P
RC
Department of Biomedical Engineering, Eindhoven University of Technology, Whoog 4.105, P.O. Box 513, 5600 Eindhoven, The Netherlands.
Bovendeerd
P H M
PH
Kotte
J C S
JC
Prinzen
F W
FW
Smits
K
K
Arts
T
T
D016880:Anisotropy; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003198:Computer Simulation; D004548:Elasticity; D020342:Finite Element Analysis; D006329:Heart Conduction System / Q000502:physiology*; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D008955:Models, Cardiovascular; D008959:Models, Neurological; D009200:Myocardial Contraction / Q000502:physiology*; D009210:Myofibrils / Q000502:physiology*; D013314:Stress, Mechanical; D013318:Stroke Volume / Q000502:physiology; D016276:Ventricular Function; D016277:Ventricular Function, Left / Q000502:physiology*