Chest
Volume 119, Issue 4, April 2001, Pages 1085-1091
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Clinical Investigations: Sleep
Impairment of Vascular Endothelial Function and Left Ventricular Filling: Association With the Severity of Apnea-Induced Hypoxemia During Sleep

https://doi.org/10.1378/chest.119.4.1085Get rights and content

Study objective

To investigate whether a dose-effect relationship exists between the severity of obstructive sleep apnea (OSA) and subclinical indicators of myocardial or vascular dysfunction.

Design

Cross-sectional study using correlation analysis.

Participants

Twenty subjects referred to our sleep laboratory for screening or therapy of OSA but without regular medication and without known cardiovascular disease.

Measurements

Severity of OSA was quantified by polysomnography. Moreover, nocturnal excretion of norepinephrine was determined. Left ventricular (LV) myocardial function was assessed with Doppler echocardiography. Using ultrasonographic measurements, endothelium-dependent and endothelium-independent conduit artery dilation were measured as flow-mediated and glyceryltrinitrate-induced changes in brachial artery diameter.

Results

Worsening nocturnal hypoxemia, measured as nocturnal oxygen saturation nadir or percentage of sleep time spent in hypoxemia (< 90% hemoglobin oxygen saturation), predicted increased interventricular septum thickness (corrected for age and body mass index), prolonged isovolumetric relaxation time, decreased ratio between peak early and late mitral flow velocities, as well as reduced endothelium-dependent dilatory capacity of the brachial artery (all relationships corrected for cofactor age and with p < 0.05) were observed. Associations between these cardiovascular function markers and nocturnal excretion of norepinephrine followed the same trend, but relations with interventricular septum thickness and flow-mediated artery dilation missed significance (p = 0.064 and p = 0.061, respectively). LV posterior wall thickness, measures of LV systolic function, early mitral flow deceleration time, and endothelium-independent artery dilation were not significantly related to the degree of nocturnal hypoxemia or norepinephrine excretion. None of the correlations with apnea-hypopnea index were statistically significant.

Conclusions

The severity of apnea-related hypoxemia is associated with a gradual deterioration of LV diastolic function as well as large-artery endothelial function.

Section snippets

Patients

All male nonsmokers without regular medication and without history of diseases known to affect the cardiovascular system were selected from a total of 81 subjects consecutively referred to the Sleep Laboratory of the Pulmonary Department of Sahlgrenska University Hospital, Gothenburg, Sweden, for either implementation of nasal continuous positive airway pressure therapy or diagnostic sleep apnea screening. None of the participants received continuous positive airway pressure therapy before or

Sample Characteristics

Characteristics of the study sample are outlined in Table 1. Correlations between measures of OSA severity as well as NE excretion are described in Table 2. While the two measures of hypoxemia were found to be highly redundant (R2 = 93.7%), their variance explained only between 48.8% and 67.7% of the variance in AHI and nocturnal NE excretion. AHI was significantly related to BMI (r = 0.509, p = 0.022) whereas all remaining correlations between AHI, SATMIN, HYPOX%, or NE excretion on the one

Discussion

The results of the current study suggest that the severity of apnea-induced HbO2 desaturations in OSA is associated with a gradual but significant tendency toward reduced LV diastolic function and toward an impaired endothelium-dependent dilatory capacity of conduit arteries.

Considering the relatively small sample size of the present study, narrow sampling criteria providing a relatively homogeneous study group as well as statistical control of the remaining influence of confounding variables

ACKNOWLEDGMENT

We gratefully acknowledge the assistance of Anita Morath-Riha.

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    This work was supported by grants from the Swedish Medical Research Council (grant No. 9892), the Medical Faculty of Gothenburg University, and the Swedish Heart and Lung Foundation.

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