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In the last 30 years, the concept of chronic heart failure (CHF) has changed. Before the 1970s, the fundamental pathophysiology of CHF was thought to be volumeoverload, and thereby the first line of drugs for CHF included digitalis and diuretics. In the 1970s, numerous experimental and clinical studies of cardiac function brought about the change in the concept of CHF that the main pathophysiology of CHF is regarded as pump failure and an increase in the afterload. In accordance with the concept change, positive inotropic agents and vasodilators became widely used. As is well known however, the positive inotropic agents did not improve survival but rather worsened it. In 1987, CONSENSUS study (1) for the first time disclosed the usefulness of the ACE inhibitor, enarapril; it improves survival of severe CHF compared with placebo. Also the V-Heft trail (2) proved that ACE-inhibitors have a more beneficial effect on cardiac function and survival than the so-called vasodilator, hydralaradine. This finding, together with many clinical studies, proves that blocking of the renin angiotensin system (RAS) improves cardiac function, left ventricular remodeling and survival. In the 1980s, numerous humoral factors, such as the natriuretic peptide family, all of which regulate cardiovascular homeostasis, were discovered and their receptors were also cloned. Moreover, development of their blockers or the mice overexpressing or lacking the gene encoding cardiovascular hormone has provided a better understanding of the molecular mechanism of the development and progression of CHF.

internal medicine

Clinical Pathology and Treatment of Renin-Angiotensin System 1. Usefulness of Blocking of the Renin-Angiotensin System in Treatment of Chronic Heart Failure