ABSTRACT
This chapter reviews experimental data supporting the pathophysiologic roles of both angiotensin II (Ang II) and aldosterone in ventricular remodeling. In addition, experimental data exploring the effects and mechanisms of pharmacologic agents that block components of renin–angiotensin–aldosterone system (RAAS) signaling on ventricular remodeling are reviewed. The chapter presents pertinent clinical evidence supporting the utility of these agents to prevent remodeling and their benefits in the management of heart failure. Left ventricular (LV) remodeling refers to alterations in ventricular mass, chamber size, and geometry that result from myocardial injury, pressure, or volume overload. The ultrastructural changes of the remodeled ventricle are the direct result of myocyte hypertrophy, fibroblast proliferation, and abnormal accumulation of the extracellular matrix. The RAS consists of both circulating and local tissue compartments, the activation of which leads to the formation of Ang II, the primary hormonal mediator of the RAS.
