Abstract
Increased myofilament Ca(2+) sensitivity is a common attribute of many inherited and acquired cardiomyopathies that are associated with cardiac arrhythmias. Accumulating evidence supports the concept that increased myofilament Ca(2+) sensitivity is an independent risk factor for arrhythmias. This review describes and discusses potential underlying molecular and cellular mechanisms how myofilament Ca(2+) sensitivity affects cardiac excitation and leads to the generation of arrhythmias. Emphasized are downstream effects of increased myofilament Ca(2+) sensitivity: altered Ca(2+) buffering/handling, impaired energy metabolism and increased mechanical stretch, and how they may contribute to arrhythmogenesis.