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

https://doi.org/10.1016/S0735-1097(03)00245-6Get rights and content
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Abstract

The advent of neurohormonal blockade in heart failure (HF) has been an overwhelming success, but current evidence points to a ceiling effect as newer neurohormonal targets are exploited in an incremental manner. This has lead us to question whether the neurohormonal model of HF can be sustained by simply stacking multiple neurohormonal or cytokine blockers together as treatment. A unifying theme in some of these disparate trials relates to either a lack of efficacy or, more importantly, adversity resulting in regression of already achieved benefits. It is our contention that the available evidence has uncovered the remarkable complexity of interaction within the context of the neurohormonal construct. As we stand at a crossroad in HF and begin to fervently pursue non-neurohormonal therapeutic targets, we must also direct attention at navigating the multifaceted labyrinth of the neurohormonal model that has led to the current imbroglio.

Abbreviations

ACE
angiotensin-converting enzyme
ARB
angiotensin receptor antagonists
HF
heart failure
NEP
neutral endopeptidase
NYHA
New York Heart Association
RAAS
renin-angiotensin-aldosterone system
TNF
tumor necrosis factor

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Drs. Mehra and Francis have both served as consultants or received honoraria from Bristol Myers Squibb, Merck, Astra Zeneca, and Glaxo Smith Kline.