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5.4 Neurohormonal activation in heart failure
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Published:November 2023
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Abstract
Heart failure (HF) with reduced ejection fraction (HFrEF) has evolved over the past three decades from a mainly cardiac structural derangement to the result of deleterious effects of sustained neurohormonal activation on the heart and circulation. Some of the neurohormonal axes activated in HF have vasoconstrictor and antidiuretic effects (with growth-promoting properties), and include the sympathetic nervous system, the renin–angiotensin–aldosterone system, and the vasopressin–arginine system. In the acute setting, these adaptive responses may be beneficial, but long-term overactivation, such as that seen in patients with chronic HF, results in maladaptive processes such as left ventricular remodelling and disease progression. Other systems, including the natriuretic peptide system (with natriuretic and antimitogenic effects), exert opposing counter-regulatory vasodilatory pathways. The neurohormonal hypothesis of HF has been validated in multiple landmark clinical trials, which construe current evidence-based treatment for patients with HFrEF.
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