Key result
Neurohormonal blockers, including ACE inhibitors, beta-blockers, and ARBs, prevent the progression of left ventricular remodeling and favorably influence the natural history of heart failure.
This historical review highlights the foundational role of the University of Minnesota in establishing the neurohormonal hypothesis and subsequent standard pharmacologic therapies for heart failure.
Supports neurohormonal blockade in HF; leaves open optimization with contemporary agents.
For nearly three decades, starting in the early 1970s, the cardiology research laboratories at the University of Minnesota served as the focal point for the discovery and implementation of much of the information we now apply to the management of heart failure. Director Jay Cohn, building on his expertise in hypertension and hemodynamics, led many creative and committed investigators in the exploration of the mechanisms responsible for increased sensitivity to afterload in heart failure. The neurohormonal hypothesis of heart failure led to the development of several pharmacologic tools, such as angiotensin-converting enzyme inhibitors, β-adrenergic blockers, and, later, angiotensin-receptor blockers. By the late 1990s, it was understood that neurohormonal antagonists could prevent the progression of left ventricular remodeling and favorably influence the natural history of heart failure. Neurohormonal blockers are now considered standard therapy. Issues remain to be addressed, including early identification and treatment of patients at risk.
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Gary S. Francis (2011) conducted a review in Heart failure. Neurohormonal blockers was evaluated. Neurohormonal blockers, including ACE inhibitors, beta-blockers, and ARBs, prevent the progression of left ventricular remodeling and favorably influence the natural history of heart failure.
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