To date, cardiac resynchronization therapy remains the only treatment that enhances systolic function while improving long-term outcome and survival. Dyssynchronous heart failure is characterized by profound global as well as regional cellular and molecular changes, many of which are not observed in synchronous heart failure. The beneficial effects of CRT on myofilament function, G protein-coupled receptor signaling, and adrenergic response are important components for restoring cardiac reserve and reducing arrhythmia, both major limitations in heart failure. Here, we review the molecular alterations associated with dyssynchronous heart failure and their reversibility induced by cardiac resynchronization therapy.
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