Heart failure, a complex disorder with heterogeneous aetiologies remains one of the most threatening diseases known. It is a clinical syndrome attributable to a multitude of factors that begins with the compensatory response known as hypertrophy, followed by a decompensated state that finally results in heart failure. Given the lack of a unified theory of heart failure, future research efforts are required to unify and synthesize our current understanding of the multiple mechanisms that control remodelling in heart under various stress conditions. During the past few decades, use of animal models has provided new insights into the complex pathogenesis of this syndrome. Rodents have contributed significantly in the understanding of the pathogenesis and progression of heart failure. With the advent of the transgenic era, rodent models have revolutionized preclinical research associated with heart failure. These models combined with physiological measurements of cardiac hemodynamics, are expected to yield more valuable information regarding the molecular mechanisms of heart failure and aid in the discovery of novel therapeutic targets. However, all animal models used have advantages and limitations, and the issues determining transfer from preclinical to clinical require critical evaluation. The present review focuses upon rodent models of heart failure.