Role of myocardial viscoelasticity in disturbances of electrical and mechanical activity in calcium overloaded cardiomyocytes: mathematical modeling.

Cardiomyocyte Ca(2+) overload is closely linked to cardiac arrhythmias. We have earlier shown in a mathematical model that myocardium mechanical activity may contribute to rhythm disturbances induced by Ca(2+) overload in cardiomyocytes with reduced Na(+)-K(+) pump work (Sulman et al., 2008). The same model is used here to address possible contribution of the passive mechanical properties of cardiac muscle (i.e. myocardial viscous and elastic properties) to the arrhythmogenesis. In a series of contractions at regular pacing rate of 75 beats/min a model with higher viscosity demonstrated essentially earlier appearance of extrasystoles due to a faster cardiomyocyte Ca(2+) loading up to a level triggering spontaneous Ca(2+) releases from the sarcoplasmic reticulum. The model predicts that myocardial elasticity also may affect arrhythmogenesis in cardiomyocytes overloaded with Ca(2+). Contribution of the mechanical properties of the myocardial tissue to the arrhythmia has been analyzed for wide ranges of both viscosity and elasticity coefficients. The results suggest that myocardial viscoelastic properties may be a factor affecting Ca(2+) handling in cardiomyocytes and contributing to cardiac mechano-electric feedback in arrhythmogenesis.