Key result
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
Absolute Event Rate: 2.26% vs 1.2%
p-value: p=<0.001
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.
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May enhance RV kinetics in congenital heart disease; hypothesis-generating from animal data, needs human validation.
Morano et al. (1996) conducted an 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.
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