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Observational Study
. 2017 Sep 11;6(9):e006010.
doi: 10.1161/JAHA.117.006010.

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

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Free PMC article
Observational Study

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

Nadja Scherbakov et al. J Am Heart Assoc. .
Free PMC article

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.

Figures

Figure 1
Figure 1
Neurological deficit at baseline according to the National Institutes of Health Stroke Scale (NIHSS); (A); estimation of stroke‐related brain lesion according to the Alberta Stroke Program Early CT (ASPECT) score (B); functional impairment at baseline according to the modified Rankin scale (mRS) (C); functional disability at baseline according to the Barthel index (D) in patients without sleep‐disordered breathing (SDB) compared with the patients with SDB.
Figure 2
Figure 2
Peripheral endothelial function according to reactive hyperemia index (RHI) in patients without sleep‐disordered breathing (SDB) and in those with SDB after acute ischemic stroke (A). Association between the peripheral endothelial function according to RHI and the severity of SDB according to apnea‐hypopnea index (AHI) (B).
Figure 3
Figure 3
Severity of sleep‐disordered breathing (SDB) according to apnea‐hypopnea index (AHI) in patients without heart failure (HF), in those with left ventricular diastolic dysfunction (LVDD) and in those with left ventricular systolic dysfunction (LVSD).
Figure 4
Figure 4
Peripheral endothelial function according to reactive hyperemia index (RHI) in the follow‐up cohort at baseline and at 1‐year follow‐up examination. SDB indicates sleep‐disordered breathing.
Figure 5
Figure 5
Interaction between acute ischemic stroke, sleep‐disordered breathing, and peripheral endothelial dysfunction.

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