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Computational and Mathematical Methods in Medicine
Volume 2012, Article ID 138401, 9 pages
Research Article

Simulation of Exercise-Induced Syncope in a Heart Model with Severe Aortic Valve Stenosis

1Department of Hematology, Faculty of Medicine, University of Ljubljana, 1104 Ljubljana, Slovenia
2Institute of Pathophysiology, Faculty of Medicine, University of Ljubljana, 1104 Ljubljana, Slovenia

Received 22 June 2012; Revised 8 October 2012; Accepted 15 October 2012

Academic Editor: Gangmin Ning

Copyright © 2012 Matjaž Sever et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Severe aortic valve stenosis (AVS) can cause an exercise-induced reflex syncope (RS). The precise mechanism of this syncope is not known. The changes in hemodynamics are variable, including arrhythmias and myocardial ischemia, and one of the few consistent changes is a sudden fall in systemic and pulmonary arterial pressures (suggesting a reduced vascular resistance) followed by a decline in heart rate. The contribution of the cardioinhibitory and vasodepressor components of the RS to hemodynamics was evaluated by a computer model. This lumped-parameter computer simulation was based on equivalent electronic circuits (EECs) that reflect the hemodynamic conditions of a heart with severe AVS and a concomitantly decreased contractility as a long-term detrimental consequence of compensatory left ventricular hypertrophy. In addition, the EECs model simulated the resetting of the sympathetic nervous tone in the heart and systemic circuit during exercise and exercise-induced syncope, the fluctuating intra-thoracic pressure during respiration, and the passive relaxation of ventricle during diastole. The results of this simulation were consistent with the published case reports of exertional syncope in patients with AVS. The value of the EEC model is its ability to quantify the effect of a selective and gradable change in heart rate, ventricular contractility, or systemic vascular resistance on the hemodynamics during an exertional syncope in patients with severe AVS.