Expression of atrial myosin light chain 1 (ALC-1) in the human right ventricle significantly increased maximal shortening velocity from 1.2 to 2.26 ML/s and accelerated isometric tension production.
Observational (n=27)
No
In patients with congenital heart disease, the expression of ALC-1 in the right ventricle modulates cross-bridge cycling kinetics, accelerating shortening velocity and isometric tension production.
Absolute Event Rate: 2.26% vs 1.2%
p-value: p=<0.001
Most of the patients with congenital heart diseases express the atrial myosin light chain 1 (ALC-1) in the right ventricle. We investigated the functional consequences of ALC-1 expression on the myosin cycling kinetics in the intact sarcomeric structure using multicellular demembranated fibers ("skinned fibers") from the right ventricular infundibulum of patients with Tetralogy of Fallot (TOF), double outlet right ventricle (DORV), and infundibular pulmonary stenosis (IPS), Force-velocity relation was analyzed by the constant-load technique at maximal Ca2+ activation (pCa 4.5). Half-time of tension development (t1/2) was investigated by monitoring contraction initiation upon photolytic release of ATP from caged-ATP in rigor. The patients investigated here expressed between 0 and 27% ALC-1. There was a statistically significant correlation between ALC-l and maximal shortening velocity (Vmax) which rose 1.87-fold from 1.2 muscle length per second (ML/s) to 2.25 ML/s in a normal (0% ALC-1) and diseased (19.9% ALC-1) ventricle. Half-time of tension development decreased 1.85-fold with increasing ALC-1 expression (t1/2) was 0.252 s and 0.136 s at 2 and 18.4% ALC-1, respectively). We conclude that the expression of ALC-1 in the human heart modulates cross-bridge cycling kinetics accelerating shortening velocity and isometric tension production.
Morano et al. (Mon,) conducted a observational in Congenital heart disease (Tetralogy of Fallot, double outlet right ventricle, infundibular pulmonary stenosis) (n=27). High ALC-1 expression (19.9%) vs. No ALC-1 expression (0%) was evaluated on Maximal shortening velocity (Vmax) (p=<0.001). Expression of atrial myosin light chain 1 (ALC-1) in the human right ventricle significantly increased maximal shortening velocity from 1.2 to 2.26 ML/s and accelerated isometric tension production.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: