Electromechanical wavebreak in a model of the human left ventricle

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 299; no. 1; pp. H134 - H143
• Main Authors: Keldermann, R H, Nash, M P, Gelderblom, H, Wang, V Y, Panfilov, A V
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.07.2010
• Subjects: Animals; Biomechanical Phenomena; Cardiac arrhythmia; Cells; Computer Simulation; Dogs; Elasticity; Electrocardiography; Excitation Contraction Coupling; Feedback, Physiological; Finite Element Analysis; Heart; Heart Conduction System - pathology; Heart Conduction System - physiopathology; Heart Ventricles - pathology; Heart Ventricles - physiopathology; Humans; Mechanotransduction, Cellular; Models, Anatomic; Models, Cardiovascular; Myocardial Contraction; Numerical Analysis, Computer-Assisted; Physiology; Reproducibility of Results; Tachycardia, Ventricular - pathology; Tachycardia, Ventricular - physiopathology; Time Factors; Ventricular Fibrillation - pathology; Ventricular Fibrillation - physiopathology; Ventricular Function, Left
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00862.2009

In the present report, we introduce an integrative three-dimensional electromechanical model of the left ventricle of the human heart. Electrical activity is represented by the ionic TP06 model for human cardiac cells, and mechanical activity is represented by the Niederer-Hunter-Smith active contractile tension model and the exponential Guccione passive elasticity model. These models were embedded into an anatomic model of the left ventricle that contains a detailed description of cardiac geometry and the fiber orientation field. We demonstrated that fiber shortening and wall thickening during normal excitation were qualitatively similar to experimental recordings. We used this model to study the effect of mechanoelectrical feedback via stretch-activated channels on the stability of reentrant wave excitation. We found that mechanoelectrical feedback can induce the deterioration of an otherwise stable spiral wave into turbulent wave patterns similar to that of ventricular fibrillation. We identified the mechanisms of this transition and studied the three-dimensional organization of this mechanically induced ventricular fibrillation.