Key result
In silico muscle force models reproduce the Frank-Starling mechanism as an alternative to elastance models.
This study provides a compact computational model of the Frank-Starling mechanism based on muscle force-length relations, offering an alternative to time-varying elastance models.
Provides computational support for force-based cardiac models; leaves open clinical applicability pending further validation.
Otto Frank's observation that fixed volume ventricles generate increased pressure with increased filling, and Ernest Starling's subsequent finding that the heart ejects more blood with increased filling, are incorporated as the Frank-Starling mechanism. In this study, the importance of muscle's underlying force-length relation is revealed as the source of these phenomena, using in silico models of cardiac muscle, isolated canine ventricles, and a complete, closed-loop cardiovascular model. Model parameters were extracted from experiments, and from literature data. In essence, treating muscle as a time- and length-dependent force generator, and the heart chambers as time- and volume-dependent pressure generators, leads to the Frank-Starling mechanism for both fixed length or volume contractions, and for shortening or ejecting beats, respectively. These models are alternatives to time-varying elastance based lumped models. A wide range of muscle and ventricle dynamics is embodied in a compact equation for each.
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Joseph L. Palladino (2024) studied Cardiac muscle and ventricle dynamics. In silico models of cardiac muscle and ventricles vs. Time-varying elastance based lumped models was evaluated on Frank-Starling mechanism phenomena. In silico models treating muscle as a time- and length-dependent force generator successfully reproduce the Frank-Starling mechanism, offering an alternative to time-varying elastance models.
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