Modeling calcium-dependent passive cardiac mechanics in the mouse.

Area of Science:

• Cardiovascular Mechanics
• Biophysics
• Biomaterials

Background:

• Previous research focused on nonlinearity, anisotropy, and viscoelasticity in myocardial mechanics.
• Calcium was primarily thought to influence active, not passive, cardiac mechanics.
• Recent studies reveal calcium significantly affects passive myocardial viscoelasticity.

Purpose of the Study:

• To extend fractional viscoelastic constitutive models to include calcium-sensitive passive mechanics.
• To investigate the implications of calcium cycling on dynamic passive cardiac function.
• To model the contribution of altered passive mechanics to diastolic heart failure.

Main Methods:

• Developed extended fractional viscoelastic constitutive models.
• Incorporated additional Maxwell arms to capture calcium's effect on passive mechanics.
• Utilized a Hill curve to model calcium concentration dependence.

Main Results:

• Calcium's effect necessitates additional Maxwell arms in viscoelastic models.
• Calcium induces a pure viscoelastic response with a first-order exponential decay (time constant ~2.17s).
• This model accurately captures passive mechanics across various calcium levels.
• Calcium dependence acts as a scaling factor, potentially increasing passive mechanics sixfold in mouse trabeculae.

Conclusions:

• Calcium significantly modulates passive myocardial mechanics, challenging prior assumptions.
• The developed fractional viscoelastic model accurately represents calcium's influence.
• This work enables more precise computational cardiac models, particularly for diastolic dysfunction.