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Pathophysiology and clinical evaluation of acute heart failure

Key Points

  • Acute heart failure (AHF) is a complex syndrome characterized by the worsening of signs and symptoms of heart failure

  • Clinical evaluation of patients with AHF involves a focused history and physical examination, along with ancillary data from laboratory and diagnostic tests

  • New team-based and device-based approaches to the clinical assessment and management of patients with AHF have improved outcomes and reduced hospitalization

  • Neurohormonal activation, venous congestion, endothelial dysfunction, myocardial injury, and renal dysfunction are central to the pathophysiology of AHF

  • Studies are currently underway to investigate the utility of identifying specific AHF phenotypes for targeted therapeutic interventions

Abstract

Acute heart failure (AHF) is a complex syndrome characterized by worsening heart failure (HF) symptoms that requires escalation of therapy. Intrinsic cardiac abnormalities and comorbid conditions, including lung and renal disease, and sleep-disordered breathing, can contribute to the development of AHF. In this Review, we summarize and discuss the literature on the clinical evaluation and underlying pathophysiology of AHF. Important features of AHF evaluation include identification of precipitating factors to the disease, and assessment of circulatory–renal limitations associated with use of HF medications, prior HF hospitalizations, congestion and perfusion profiles, and end-organ dysfunction. The pathophysiological contributions of endothelial dysfunction, neurohormonal activation, venous congestion, and myocardial injury to the development of AHF are also discussed. These potential causative mechanisms provide a framework for clinicians to evaluate and manage patients with AHF and highlight possible future targets for therapies designed to improve clinical outcomes.

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Figure 1: Assessment of haemodynamic profile using a colour gradient chart involving haemodynamic signs of patients presenting with heart failure.
Figure 2: Mechanisms of acute heart failure.

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Both authors researched data for the article, discussed its content, and wrote, reviewed, and edited the manuscript before submission.

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Correspondence to Robert J. Mentz.

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R.J.M. declares that he has received research support from Amgen, AstraZeneca, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Novartis, Otsuka, and ResMed. He has also received honoraria from Thoratec and has served on an advisory board for Luitpold Pharmaceuticals, Inc. C.M.O. receives research support from Astellas, Gilead, Otsuka, and Roche Diagnostics, and is a consultant for HeartWare.

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Mentz, R., O'Connor, C. Pathophysiology and clinical evaluation of acute heart failure. Nat Rev Cardiol 13, 28–35 (2016). https://doi.org/10.1038/nrcardio.2015.134

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