In response to an increased afterload, the myocardium undergoes a complex adaptation by which wall stress is normalized and cardiac output is maintained. Although the consensus suggests that the increase of the myocardial mass is a necessary adaptive process to accommodate the increased workload, there is growing evidence that hypertrophy ultimately results in pathological remodeling and deterioration of cardiac function. Despite intense investigation, our understanding of the cellular mechanisms that are responsible for the initiation and the maintenance of this adaptation is largely incomplete and preventing or regressing left ventricular hypertrophy (LVH) is a major challenge. This chapter provides a detailed description of the procedures necessary to induce LVH by coarctation of the transverse aorta and to analyze the effects of the increased hemodynamic load on cardiac mass, cardiomyocyte size, and cardiac performance.