Endothelial Dysfunction and Pre-Existing Cognitive Disorders in Stroke Patients.


Journal

Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414

Informations de publication

Date de publication:
18 Jun 2024
Historique:
received: 01 04 2024
revised: 01 06 2024
accepted: 05 06 2024
medline: 27 6 2024
pubmed: 27 6 2024
entrez: 27 6 2024
Statut: epublish

Résumé

The origin of pre-existing cognitive impairment in stroke patients remains controversial, with a vascular or a degenerative hypothesis. To determine whether endothelial dysfunction is associated with pre-existing cognitive problems, lesion load and biological anomalies in stroke patients. Patients originated from the prospective STROKDEM study. The baseline cognitive state, assessed using the IQ-CODE, and risk factors for stroke were recorded at inclusion. Patients with an IQ-CODE score >64 were excluded. Endothelial function was determined 72 h after stroke symptom onset by non-invasive digital measurement of endothelium-dependent flow-mediated dilation and calculation of the reactive hyperemia index (RHI). RHI ≤ 1.67 indicated endothelial dysfunction. Different biomarkers of endothelial dysfunction were analysed in blood or plasma. All patients underwent MRI 72 h after stroke symptom onset. A total of 86 patients were included (52 males; mean age 63.5 ± 11.5 years). Patients with abnormal RHI have hypertension or antihypertensive treatment more often. The baseline IQ-CODE was abnormal in 33 (38.4%) patients, indicating a pre-existing cognitive problem. Baseline IQ-CODE > 48 was observed in 15 patients (28.3%) with normal RHI and in 18 patients (54.6%) with abnormal RHI ( A vascular mechanism may be responsible for cognitive problems pre-existing stroke. The measurement of endothelial dysfunction after stroke could become an important element of follow-up, providing an indication of the functional and cognitive prognosis of stroke patients.

Sections du résumé

BACKGROUND BACKGROUND
The origin of pre-existing cognitive impairment in stroke patients remains controversial, with a vascular or a degenerative hypothesis.
OBJECTIVE OBJECTIVE
To determine whether endothelial dysfunction is associated with pre-existing cognitive problems, lesion load and biological anomalies in stroke patients.
METHODS METHODS
Patients originated from the prospective STROKDEM study. The baseline cognitive state, assessed using the IQ-CODE, and risk factors for stroke were recorded at inclusion. Patients with an IQ-CODE score >64 were excluded. Endothelial function was determined 72 h after stroke symptom onset by non-invasive digital measurement of endothelium-dependent flow-mediated dilation and calculation of the reactive hyperemia index (RHI). RHI ≤ 1.67 indicated endothelial dysfunction. Different biomarkers of endothelial dysfunction were analysed in blood or plasma. All patients underwent MRI 72 h after stroke symptom onset.
RESULTS RESULTS
A total of 86 patients were included (52 males; mean age 63.5 ± 11.5 years). Patients with abnormal RHI have hypertension or antihypertensive treatment more often. The baseline IQ-CODE was abnormal in 33 (38.4%) patients, indicating a pre-existing cognitive problem. Baseline IQ-CODE > 48 was observed in 15 patients (28.3%) with normal RHI and in 18 patients (54.6%) with abnormal RHI (
CONCLUSIONS CONCLUSIONS
A vascular mechanism may be responsible for cognitive problems pre-existing stroke. The measurement of endothelial dysfunction after stroke could become an important element of follow-up, providing an indication of the functional and cognitive prognosis of stroke patients.

Identifiants

pubmed: 38927124
pii: biom14060721
doi: 10.3390/biom14060721
pii:
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : French Health Minister
ID : PHRC-API 19-01

Auteurs

Anne-Marie Mendyk-Bordet (AM)

Univ. Lille, CHU Lille, Inserm, Lille Neuroscience and Cognition, F-59000 Lille, France.

Thavarak Ouk (T)

Univ. Lille, CHU Lille, Inserm, Lille Neuroscience and Cognition, F-59000 Lille, France.

Anne Muhr-Tailleux (A)

Univ. Lille, CHU Lille, Inserm, Institut Pasteur de Lille, Nuclear Receptor, Metabolic and Cardiovascular Diseases, F-59000 Lille, France.

Maud Pétrault (M)

Univ. Lille, CHU Lille, Inserm, Lille Neuroscience and Cognition, F-59000 Lille, France.

Emmanuelle Vallez (E)

Univ. Lille, CHU Lille, Inserm, Institut Pasteur de Lille, Nuclear Receptor, Metabolic and Cardiovascular Diseases, F-59000 Lille, France.

Patrick Gelé (P)

Univ. Lille, CHU Lille, Inserm, Lille Neuroscience and Cognition, F-59000 Lille, France.

Thibaut Dondaine (T)

Univ. Lille, CHU Lille, Inserm, Lille Neuroscience and Cognition, F-59000 Lille, France.

Julien Labreuche (J)

Univ. Lille, CHU Lille, Inserm, Biostatistic Platform, F-59000 Lille, France.

Dominique Deplanque (D)

Univ. Lille, CHU Lille, Inserm, Lille Neuroscience and Cognition, F-59000 Lille, France.

Régis Bordet (R)

Univ. Lille, CHU Lille, Inserm, Lille Neuroscience and Cognition, F-59000 Lille, France.
Univ. Lille, CHU Lille, Inserm, Department of Medical Pharmacology, F-59000 Lille, France.

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Classifications MeSH