The pathophysiology of right ventricular (RV) remodeling is a complex process and may include unique elements not observed in left ventricular (LV) remodeling. The RV also has a relatively irregular geometry not accounted for in LV analyses. RV remodeling includes basic changes in geometry, wall thickness, and ventricular pressure-volume relationships. Also, myocyte dimensions and number increase, and myocardial extracellular matrix and biochemical milieu are modified. Remodeling has been associated with such diseases as pulmonary hypertension, lung transplant, LV pathology, Chagas' disease, and arrhythmogenic right ventricular cardiomyopathy. Disease progression may lead to further RV changes, including hypertrophy, dilatation, and subsequently to variable alterations in RV hemodynamic status. The multiple methods to assess RV hypertrophy include cine magnetic resonance imaging and 3-D echocardiography. Each technique offers different precision in evaluating RV dimensions and functional performance characteristics. Strategies to prevent RV remodeling include pharmacological agents, such as vasodilators and angiotensin-converting enzyme inhibitors, as well as more invasive interventions, such as ventricular assist devices.