Significance Modulation of actin filament architecture underlies a plethora of cellular processes including cell shape, division, adhesion, and motility. In heart muscle cells actin-containing thin filaments form highly organized structures with precisely regulated lengths. This precision is required for efficient interaction with myosin-containing filaments and provides the basis for contraction. The mechanism whereby heart muscle cells regulate thin filament assembly and its consequences for cardiac physiology are largely unknown. We discovered that Leiomodin 2 (Lmod2) elongates thin filaments to a proper length. Mice lacking Lmod2 have abnormally short thin filaments, experience severe contractile dysfunction and ventricular chamber enlargement consistent with dilated cardiomyopathy, and die at age ∼3 wk. Therefore, Lmod2 and proper thin filament lengths are essential for heart function.