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Heart failure therapy at a crossroad: are there limits to the neurohormonal model?

Mandeep R. Mehra, MD, FACC^*,*, Patricia A. Uber, PharmD^* and Gary S. Francis, MD, FACC

^* Department of Cardiovascular Medicine, Ochsner Clinic Foundation, New Orleans, Louisiana, USA
Department of Cardiology, Cleveland Clinic Foundation, Cleveland, Ohio, USA

View larger version (19K): [in a new window]   Figure 1 Saturation of benefits with incremental neurohormonal blockade in chronic heart failure (1975–2003). The curve represents directional tendency rather than exact point estimates of benefit or adverse outcomes. Spironolactone is not included because the supporting data are from a single large trial constructed in a distinct population of unstable and severe heart failure patients with low background use of beta-blockers. ACE = angiotensin-converting enzyme.

View larger version (26K): [in a new window]   Figure 2 Potential therapeutic targets beyond the neurohormonal model. Emerging investigations are focusing on amelioration of wall stress by using surgical remodeling and resynchronization therapy. Other important strategies are tackling myocardial metabolism, ischemia abrogation, sudden death prevention, anemia, sleep disorders, and renal insufficiency in heart failure.