The left ventricle can change its size and shape as a result of external load and/or loss of viable myocytes. This process, defined as remodeling, can be adaptive, as in compensatory hypertrophy and dilation secondary to myocardial infarction, or maladaptive in response to long-standing systemic hypertension. In addition to ventricular enlargement and cellular hypertrophy, extensive interstitial collagen deposition also occurs during this remodeling process. The increased fibrous tissue and hypertrophied myocytes can also lead to inappropriate energy production and utilization. Angiotensin-converting enzyme (ACE) inhibitors have the ability to modulate both cellular hypertrophy and collagen deposition. These effects represent, in part, the mechanism by which ACE inhibitors modify ventricular remodeling, the subsequent development and clinical expression of heart failure, and finally, the improvement in the mortality of patients with heart failure.