https://orcid.org/0000-0003-3694-4559
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Christoph Maack, Gemma Vilahur, Marisol Ruiz-Meana, Derek Hausenloy, on behalf of the Core Group and Members of the Management Committee of EU-METAHEART, New COST Action ‘EUropean network to tackle METAbolic alterations in HEART failure’ (EU-METAHEART), European Heart Journal, Volume 45, Issue 42, 7 November 2024, Pages 4460–4463, https://doi.org/10.1093/eurheartj/ehae457
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Cardiovascular diseases (CVDs) are the main cause of morbidity and mortality in Europe, and heart failure (HF) is the terminal consequence of most CVD, making HF the largest disease burden in Europe. The prevalence of HF increases with age, and so does the prevalence of comorbidities. The most frequent comorbidities are chronic kidney disease, anaemia, and metabolic disorders, such as obesity and diabetes. Such metabolic (and also other) comorbidities adversely affect HF outcome, and vice versa, HF induces metabolic alterations and predisposes to the development of diabetes and other comorbidities.1 Therefore, HF is not a single-organ disease but a systemic disease that requires an interdisciplinary approach towards prevention, diagnostics, and treatment.
Major routes of communication between the heart and other organs are neuroendocrine activation, inflammation, and metabolism. Treatment of patients with HF has long been limited to drugs interfering with neuroendocrine activation, such as angiotensin-converting enzyme inhibitors, β-blockers, aldosterone antagonists, and angiotensin receptor/neprilysin inhibition. However, while these treatments are effective in patients with HF with reduced ejection fraction (HFrEF), they are not (or clearly less) effective in patients with HF with preserved ejection fraction (HFpEF).
