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[Hormonal theory of heart failure with altered systolic function]
1Service de physiologie-explorations fonctionnelles, hôpital Bichat, 75018 Paris, France. florence.arnoult@bch.aphp.fr
Insights
Heart failure therapies now focus on blocking harmful neurohormonal activation, improving survival. Targeting the renin-angiotensin-aldosterone and sympathetic systems is key for managing heart failure with systolic dysfunction.
Area of Science:
- Cardiology and Internal Medicine
- Pharmacology and Therapeutics
Context:
- Heart failure (HF) is a leading cause of death and disability globally, with increasing hospitalizations.
- Previous HF therapies focused on hemodynamic support, but failed to improve survival and sometimes increased mortality.
Purpose:
- To highlight the shift in heart failure treatment strategies from hemodynamic correction to counteracting detrimental neurohormonal activation.
- To emphasize the long-term benefits of blocking the renin-angiotensin-aldosterone system and sympathetic nervous system in systolic heart failure.
Summary:
- Neurohormonal activation, initially supportive in heart failure, proves detrimental long-term, exacerbating myocardial damage and increasing mortality.
- Current mainstays of medical therapy for systolic dysfunction heart failure involve blocking the renin-angiotensin-aldosterone system and the sympathetic system.
- This therapeutic approach significantly reduces mortality, hospitalizations, and enhances the quality of life for heart failure patients.
Impact:
- Established a new paradigm in heart failure management, prioritizing neurohormonal blockade over purely hemodynamic interventions.
- Demonstrated improved patient outcomes, including reduced mortality and hospitalizations, through targeted pharmacological interventions.
- Underscores the importance of differentiating treatment approaches for chronic versus acute heart failure.
Abstract:
Heart failure (HF) is a major cause of morbidity and mortality in the developed countries. Hospital discharges and deaths from HF are regularly increasing. Therapies initially aimed at reversing hemodynamic abnormalities in HF, increasing cardiac output, decreasing intracardiac pressures, and blocking vasoconstriction. However, none of these therapies improved survival and some actually increased mortality. Now therapies for HF related to left ventricular systolic dysfunction have focused on counteracting compensatory neurohormonal activation. Several neurohormonal activations are present in HF supporting hemodynamics, but they appear to be deleterious in the long term on the myocardium, increasing progression of the HF and mortality. Blocking the renin-angiotensin-aldosterone system and the sympathetic system are now the mainstay of medical therapy in HF related to systolic dysfunction as they decrease mortality, hospitalisation rate and improve quality of life. Hence, the approach to patient with chronic heart failure should differ from that of patient with acute heart failure.
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