Ventricular remodeling is a repair process. It can follow myocardial infarction, mechanical overload (for example, in hypertension or valvular heart disease), and also occurs in inflammation and dilated cardiomyopathy. Remodeling can be an (early) adaptive process followed by a maladaptive (late) phase and involves all cells that are present in the myocardium - the myocyte, the interstitial cells, the vascular endothelium, and the immune cells. Despite the varying etiopathology that these different aspects of heart disease share, a similar sequence of molecular, biochemical and mechanical events that can lead to heart failure, myocyte hypertrophy, extensive extracellular matrix production and fibrosis, even in patients who were previously unaffected by the original disease process (for example, inflammation or infarction). Heart failure can be influenced by treatment of the underlying disease and by modification of the remodeling process, for example, by ACE inhibitors (cardioreparation). In experimental animals it has been clearly demonstrated that ACE inhibitors may even prevent a genetically predetermined left ventricular hypertrophy (cardioprevention).