Defective cardiac muscle relaxation plays a causal role in heart failure. S
hown here is the new in vivo application of parvalbumin, a calcium-binding
protein that facilitates ultrafast relaxation of specialized skeletal muscl
es. Parvalbumin is not naturally expressed in the heart. We show that parva
lbumin gene transfer to the heart in vivo produces levels of parvalbumin ch
aracteristic of fast skeletal muscles, causes a physiologically relevant ac
celeration of heart relaxation performance in normal hearts, and enhances r
elaxation performance in an animal model of slowed cardiac muscle relaxatio
n. Parvalbumin may offer the unique potential to correct defective relaxati
on in energetically compromised failing hearts because the relaxation-enhan
cement effect of parvalbumin arises from an ATP-independent mechanism. Addi
tionally, parvalbumin gene transfer may provide a new therapeutic approach
to correct cellular disturbances in calcium signaling pathways that cause a
bnormal growth or damage in the heart or other organs.