Modeling cardiac energetics involves all of the elements of supply or demand. It is complicated: the exchange processes are distributed in space, heterogeneous, requiring parallel units interacting with each other. Multicomponent, multiscale models for the analysis of data are complicated. Using modular units aids building and maintenance. A convenient module is one in which the number of connecting variables is minimized, and the internal complexity is isolated.
Hypertensive heart disease
Two hypertrophic cardiomyopathy-associated cardiac troponin I (cTnI) mutations, R146G and R21C, are located in different regions of cTnI, the inhibitory peptide and the cardiac-specific N terminus. We recently reported that these regions may interact when Ser-23/Ser-24 are phosphorylated, weakening the interaction of cTnI with cardiac TnC. Little is known about how these mutations influence the affinity of cardiac TnC for cTnI (KC-I) or contractile kinetics during β-adrenergic stimulation.