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COPD patients hospitalized with exacerbations have greater cognitive impairment than patients hospitalized with decompensated heart failure

Authors Bajaj MPK, Burrage DR, Tappouni A, Dodd JW, Jones PW, Baker EH

Received 31 August 2018

Accepted for publication 31 October 2018

Published 18 December 2018 Volume 2019:14 Pages 1—8

DOI https://doi.org/10.2147/CIA.S185981

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Dr Richard Walker


Mohani-Preet K Bajaj,1 Daniel R Burrage,2 Andrew Tappouni,3 James W Dodd,4 Paul W Jones,2 Emma H Baker2

1Neurosciences Research Centre, Molecular and Clinical Sciences Research Institute, St George’s University of London, London, UK; 2Clinical Pharmacology, Institute of Infection and Immunity, St George’s University of London, London, UK; 3St George’s University of London, London, UK; 4Academic Respiratory Unit, University of Bristol, Bristol, UK

Purpose: People with COPD have cognitive dysfunction, which is greater in those hospitalized for exacerbations than in stable outpatients. We tested the hypothesis that cognitive dysfunction at exacerbation is a disease-specific feature of COPD, rather than a nonspecific feature of hospitalization for acute illness, by comparing cognition between patients hospitalized for acute COPD exacerbations and those with worsening heart failure (HF).
Patients and methods: A total of 40 hospital inpatients were recruited, 20 patients with COPD exacerbations and 20 patients with congestive or left-sided HF. Exclusion criteria included previous stroke, known neurological disease, and marked alcohol excess. Participants completed the Montreal cognitive assessment (MoCA) and Hospital Anxiety and Depression Scale (HADS) and underwent spirometry and review of clinical records.
Results: Age (mean±SD, COPD 73±10; HF 76±11 years), acute illness severity (Acute Physiology and Chronic Health Evaluation [APACHE]-II, COPD 15.4±3.5; HF 15.9±3.0), comorbidities (Charlson index, COPD 1.3±1.9; HF 1.6±1.5), and educational background were similar between COPD and HF groups. MoCA total was significantly lower in COPD than in HF (COPD 20.6±5.6; HF 24.8±3.5, P=0.007); however, significance was lost after correction for age, sex, and pack year smoking history. When compared with HF patients, the COPD cohort performed worse on the following domains of the MoCA: visuospatial function (median [IQR], COPD 0 [1]; HF 2 [1], P=0.003), executive function (COPD 2 [1]; HF 3 [1], P=0.035), and attention (COPD 4 [3]; HF 6 [2], P=0.020). Age (P=0.012) and random glucose concentration (P=0.041) were associated with cognitive function in whole group analysis, with pack year smoking history reaching borderline significance (P=0.050).
Conclusion: Total MoCA score for COPD and HF indicated that both groups had mild cognitive impairment, although this was greater in people with COPD. Mechanisms underlying the observed cognitive dysfunction in COPD remain unclear but appear related to blood glucose concentrations and greater lifetime smoking load.

Keywords: Montreal cognitive assessment, cognition, comorbidities, systemic, smoking, hyperglycemia

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