Abstract

Cognitive impairment (CI) represents a common but often veiled comorbidity in patients with acute heart failure (AHF) that deserves more clinical attention. In the AHF setting, it manifests as varying degrees of deficits in one or more cognitive domains across a wide spectrum ranging from mild CI to severe global neurocognitive disorder. On the basis of the significant negative implications of CI on quality of life and its overwhelming association with poor outcomes, there is a compelling need for establishment of detailed consensus guidelines on cognitive screening methods to be systematically implemented in the population of patients with heart failure (HF). Since limited attention has been drawn exclusively on the field of CI in AHF thus far, the present narrative review aims to shed further light on the topic. The underlying pathophysiological mechanisms of CI in AHF remain poorly understood and seem to be multifactorial. Different pathophysiological pathways may come into play, depending on the clinical phenotype of AHF. There is some evidence that cognitive decline closely follows the perturbations incurred across the long-term disease trajectory of HF, both along the time course of stable chronic HF as well as during episodes of HF exacerbation. CI in AHF remains a rather under recognized scientific field that poses many challenges, since there are still many unresolved issues regarding cognitive changes in patients hospitalized with AHF that need to be thoroughly addressed.

Highlights

  • Acute heart failure (AHF) is a heterogeneous clinical syndrome characterized by abrupt onset or gradual deterioration of symptoms and signs of heart failure (HF), in contradiction to chronic HF which represents a state of a much more gradual onset of symptoms or an already established diagnosis of HF [1]

  • Cognitive status was assessed by means of the Short Portable Mental Status Questionnaire (SPMSQ) and the patients were categorized into three groups based on their performance on the particular test: 0–3 errors were considered as no Cognitive impairment (CI) or mild CI, 4–7 as moderate CI, and 8–10 as severe

  • In order to relate neuroanatomical alterations in the grey and white matter with cerebral metabolic changes that occur in certain cognitive areas of the brain, additional studies are warranted in HF patients, ideally with the application of more sophisticated imaging modalities, such as 18F-FDG positron emission tomography (PET), amyloid PET imaging, functional magnetic resonance imaging (MRI), and magnetic resonance spectroscopy [142,143,144,145]

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Summary

Introduction

Acute heart failure (AHF) is a heterogeneous clinical syndrome characterized by abrupt onset or gradual deterioration of symptoms and signs of heart failure (HF), in contradiction to chronic HF which represents a state of a much more gradual onset of symptoms or an already established diagnosis of HF [1]. AHF remains one of the most common causes of hospital admission in western societies accompanied by high readmission rates and accounting for considerable in-hospital and post-discharge mortality [3,4,5,6]. The close interaction between the heart and the brain has long been recognized, dating back to 1977 where the term ‘’cardiogenic dementia” was introduced to describe the cognitive deterioration observed in patients with heart disease [13]. Cognitive impairment (CI) is a well-established entity among patients with HF, encountered across a wide range of clinical presentations, that is both acute and stable chronic HF with either reduced or preserved ejection fraction [14]. HF-induced brain injury, outline aspects of epidemiology, explore potential pathogenic mechanisms in AHF that may underlie and predispose to the development of CI, describe the dynamic changes of CI during an episode of AHF, highlight the role of brain imaging modalities in the assessment of CI, and propose a therapeutic approach

Cognitive Screening Tools
Epidemiology
Pathophysiology
Trajectory of CI over the Time Course of HF
Therapeutic Strategy
Findings
Conclusions
Full Text
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