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J Am Heart Assoc. 2017 Sep 11;6(9). pii: e006010. doi: 10.1161/JAHA.117.006010.

Sleep-Disordered Breathing in Acute Ischemic Stroke: A Mechanistic Link to Peripheral Endothelial Dysfunction.

Author information

1
Center for Stroke Research Berlin (CSB), Charité-Universitätsmedizin Berlin, Berlin, Germany nadja.scherbakov@charite.de.
2
Innovative Clinical Trials, Department of Cardiology and Pneumology, University Medicine Goettingen (UMG), Goettingen, Germany.
3
Center for Stroke Research Berlin (CSB), Charité-Universitätsmedizin Berlin, Berlin, Germany.
4
Department of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland.
5
Cardiology Department, Military Hospital, Wroclaw, Poland.
6
Department of Intensive Care Medicine, Inselspital, University Hospital of Bern, Switzerland.
7
Interdisciplinary Center of Sleep Medicine, Charité-Universitätsmedizin Berlin, Berlin, Germany.
8
Department of Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
9
Department of Cardiology, Charité-Universitätsmedizin Berlin, Berlin, Germany.

Abstract

BACKGROUND:

Sleep-disordered breathing (SDB) after acute ischemic stroke is frequent and may be linked to stroke-induced autonomic imbalance. In the present study, the interaction between SDB and peripheral endothelial dysfunction (ED) was investigated in patients with acute ischemic stroke and at 1-year follow-up.

METHODS AND RESULTS:

SDB was assessed by transthoracic impedance records in 101 patients with acute ischemic stroke (mean age, 69 years; 61% men; median National Institutes of Health Stroke Scale, 4) while being on the stroke unit. SDB was defined by apnea-hypopnea index ≥5 episodes per hour. Peripheral endothelial function was assessed using peripheral arterial tonometry (EndoPAT-2000). ED was defined by reactive hyperemia index ≤1.8. Forty-one stroke patients underwent 1-year follow-up (390±24 days) after stroke. SDB was observed in 57% patients with acute ischemic stroke. Compared with patients without SDB, ED was more prevalent in patients with SDB (32% versus 64%; P<0.01). After adjustment for multiple confounders, presence of SDB remained independently associated with ED (odds ratio, 3.1; [95% confidence interval, 1.2-7.9]; P<0.05). After 1 year, the prevalence of SDB decreased from 59% to 15% (P<0.001). Interestingly, peripheral endothelial function improved in stroke patients with normalized SDB, compared with patients with persisting SDB (P<0.05).

CONCLUSIONS:

SDB was present in more than half of all patients with acute ischemic stroke and was independently associated with peripheral ED. Normalized ED in patients with normalized breathing pattern 1 year after stroke suggests a mechanistic link between SDB and ED.

CLINICAL TRIAL REGISTRATION:

URL: https://drks-neu.uniklinik-freiburg.de. Unique identifier: DRKS00000514.

KEYWORDS:

clinical trial; endothelial dysfunction; sleep disorders; sympathetic nervous system

PMID:
28893762
PMCID:
PMC5634268
DOI:
10.1161/JAHA.117.006010
[Indexed for MEDLINE]
Free PMC Article

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