Pathologic left ventricular (LV) remodeling as described by adverse changes in LV mass, volume, geometry, and composition in response to mechanical and systemic neurohormonal activation portends a poor prognosis in patients with underlying LV systolic dysfunction. Conversely, reversal of LV remodeling is associated with improved morbidity and mortality. Improvement in LV function and size may result from either change in loading conditions or reversal of remodeling (RR). When complete normalization of LV function and geometry occurs (ejection fraction >50% and indexed LV end-diastolic dimension <33 mm/m(2)), true reversal of LV alteration is likely to have occurred. Sustained improvement in function and dimensions after therapy withdrawal further supports RR. In the absence of complete RR one cannot readily differentiate incomplete RR from changes in loading conditions. In this review, we evaluate the role of renin-angiotensin-aldosterone system inhibition, beta-adrenergic receptor blockade, cardiac resynchronization therapy, and endovascular mitral repair on LVRR and improvement in LV geometry and function.