Key result
Pharmacological treatment of systolic heart failure with ACE-inhibitors, beta-blockers, and mineralocorticoid receptor antagonists improves morbidity and mortality by antagonizing neuroendocrine activation.
This narrative review outlines the pathophysiological rationale and clinical trial evidence for guideline-directed medical therapy in chronic systolic heart failure.
Reinforces foundational GDMT in systolic HF; leaves open optimization with newer agents in contemporary practice.
Chronic heart failure is characterised by neuroendocrine activation as an attempt of the body to maintain pump function of the heart and blood pressure for the perfusion of peripheral tissues. While this neuroendocrine activation is beneficial in the short term, it induces maladaptive remodeling of the heart with continuous deterioration of left ventricular function. Accordingly, pharmacological treatment of patients with heart failure aims at protecting the heart from this neuroendocrine activation, which is represented in particular by the sympathetic nervous and the renin-angiotensin-aldosterone systems. While this concept is based on evidence from numerous large randomised placebo-controlled studies in patients with systolic heart failure, about half of the patients with heart failure have preserved systolic function, and most studies antagonising neuroendocrine activation were not successful in these latter patients. Here, we review the pathophysiological changes that occur in patients with heart failure and provide an overview on the mechanisms and clinical evidence of currently applied pharmacological treatment in patients with systolic heart failure.
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Maack et al. (2014) conducted a review in Chronic Systolic Heart Failure. Pharmacological treatments (ACE-inhibitors, beta-blockers, MRAs, ivabradine, diuretics) was evaluated. Pharmacological treatment of systolic heart failure with ACE-inhibitors, beta-blockers, and mineralocorticoid receptor antagonists improves morbidity and mortality by antagonizing neuroendocrine activation.
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