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Subclinical sleep apnoea and plasma levels of endothelin-1 among young and healthy adults

View Article: PubMed Central - PubMed

ABSTRACT

Objective: Obstructive sleep apnoea (OSA) is a risk factor for vascular disease and other adverse outcomes. These associations may be at least partly due to early endothelin-1 (ET-1)-mediated endothelial dysfunction (ED). Therefore, we assessed the relationships between subclinical sleep apnoea and plasma levels of ET-1.

Methods: We performed a population-based study among 1255 young and healthy adults aged 25–41 years. Cardiovascular disease, diabetes or a body mass index >35 kg/m2 were exclusion criteria. Plasma levels of ET-1 were measured using a high-sensitivity, single-molecule counting technology. The relationships between subclinical sleep apnoea (OSA indices: respiratory event index (REI), oxygen desaturation index (ODI), mean night-time blood oxygen saturation (SpO2)) and ET-1 levels were assessed by multivariable linear regression analysis.

Results: Median age of the cohort was 35 years. Median ET-1 levels were 2.9 (IQR 2.4–3.6) and 2.5 pg/mL (IQR 2.1–3.0) among patients with (n=105; 8%) and without subclinical sleep apnoea (REI 5–14), respectively. After multivariable adjustment, subclinical sleep apnoea remained significantly associated with plasma levels of ET-1 (β=0.13 (95% CI 0.06 to 0.20) p=0.0002 for a REI 5–14; β=0.10 (95% CI 0.03 to 0.16) p=0.003 for an ODI≥5). Every 1% decrease in mean night-time SpO2 increased ET-1 levels by 0.1 pg/mL, an association that remained significant after multivariable adjustment (β=0.02 (95% CI 0.003 to 0.033) p=0.02).

Conclusions: In this study of young and healthy adults, we found that participants with subclinical sleep apnoea had elevated plasma ET-1 levels, an association that was due to night-time hypoxaemia. Our results suggest that ED may already be an important consequence of subclinical sleep apnoea.

No MeSH data available.


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Median levels of plasma ET-1 according to mean night-time SpO2. Dashed line=regression line adjusted for age, sex, body mass index, high-sensitivity C reactive protein, glomerular filtration rate, HbA1c, systolic and diastolic ambulatory blood pressure, low-density lipoprotein, high-density lipoprotein, triglycerides and smoking status. ET-1, endothelin-1; HbA1c, glycated haemoglobin; Mean SpO2, mean night-time blood oxygen saturation.
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OPENHRT2016000523F1: Median levels of plasma ET-1 according to mean night-time SpO2. Dashed line=regression line adjusted for age, sex, body mass index, high-sensitivity C reactive protein, glomerular filtration rate, HbA1c, systolic and diastolic ambulatory blood pressure, low-density lipoprotein, high-density lipoprotein, triglycerides and smoking status. ET-1, endothelin-1; HbA1c, glycated haemoglobin; Mean SpO2, mean night-time blood oxygen saturation.

Mentions: Linear regression models on the relationship between OSA indices and ET-1 levels are shown in table 3. In unadjusted models, subclinical sleep apnoea was significantly associated with log-transformed ET-1 (β=0.17 (95% CI 0.10 to 0.24) p<0.0001 for a REI 5–14). Multivariable adjustment slightly attenuated this relationship, but subclinical sleep apnoea remained strongly associated with ET-1 levels (β=0.13 (95% CI 0.06 to 0.20) p=0.0002 for a REI 5–14). A similar robust association was found between ET-1 levels and an elevated ODI, present in 124 participants (multivariable-adjusted β=0.10 (95% CI 0.03 to 0.16) p=0.003). Every 1% decrease in mean night-time SpO2 resulted in an increase in the plasma concentration of ET-1 of 0.1 pg/mL, as shown in figure 1. This association remained significant after multivariable adjustment (β=0.02 (95% CI 0.003 to 0.033) p=0.02) (table 3). In addition, the per cent of sleeping time with SpO2<90% was also associated with plasma levels of ET-1 (multivariable-adjusted β=0.012 (95% CI 0.002 to 0.023) p=0.02). Figure 2 summarises the effect sizes of the different sleep apnoea indices on log-transformed plasma levels of ET-1.


Subclinical sleep apnoea and plasma levels of endothelin-1 among young and healthy adults
Median levels of plasma ET-1 according to mean night-time SpO2. Dashed line=regression line adjusted for age, sex, body mass index, high-sensitivity C reactive protein, glomerular filtration rate, HbA1c, systolic and diastolic ambulatory blood pressure, low-density lipoprotein, high-density lipoprotein, triglycerides and smoking status. ET-1, endothelin-1; HbA1c, glycated haemoglobin; Mean SpO2, mean night-time blood oxygen saturation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5384465&req=5

OPENHRT2016000523F1: Median levels of plasma ET-1 according to mean night-time SpO2. Dashed line=regression line adjusted for age, sex, body mass index, high-sensitivity C reactive protein, glomerular filtration rate, HbA1c, systolic and diastolic ambulatory blood pressure, low-density lipoprotein, high-density lipoprotein, triglycerides and smoking status. ET-1, endothelin-1; HbA1c, glycated haemoglobin; Mean SpO2, mean night-time blood oxygen saturation.
Mentions: Linear regression models on the relationship between OSA indices and ET-1 levels are shown in table 3. In unadjusted models, subclinical sleep apnoea was significantly associated with log-transformed ET-1 (β=0.17 (95% CI 0.10 to 0.24) p<0.0001 for a REI 5–14). Multivariable adjustment slightly attenuated this relationship, but subclinical sleep apnoea remained strongly associated with ET-1 levels (β=0.13 (95% CI 0.06 to 0.20) p=0.0002 for a REI 5–14). A similar robust association was found between ET-1 levels and an elevated ODI, present in 124 participants (multivariable-adjusted β=0.10 (95% CI 0.03 to 0.16) p=0.003). Every 1% decrease in mean night-time SpO2 resulted in an increase in the plasma concentration of ET-1 of 0.1 pg/mL, as shown in figure 1. This association remained significant after multivariable adjustment (β=0.02 (95% CI 0.003 to 0.033) p=0.02) (table 3). In addition, the per cent of sleeping time with SpO2<90% was also associated with plasma levels of ET-1 (multivariable-adjusted β=0.012 (95% CI 0.002 to 0.023) p=0.02). Figure 2 summarises the effect sizes of the different sleep apnoea indices on log-transformed plasma levels of ET-1.

View Article: PubMed Central - PubMed

ABSTRACT

Objective: Obstructive sleep apnoea (OSA) is a risk factor for vascular disease and other adverse outcomes. These associations may be at least partly due to early endothelin-1 (ET-1)-mediated endothelial dysfunction (ED). Therefore, we assessed the relationships between subclinical sleep apnoea and plasma levels of ET-1.

Methods: We performed a population-based study among 1255 young and healthy adults aged 25&ndash;41&#8197;years. Cardiovascular disease, diabetes or a body mass index &gt;35&#8197;kg/m2 were exclusion criteria. Plasma levels of ET-1 were measured using a high-sensitivity, single-molecule counting technology. The relationships between subclinical sleep apnoea (OSA indices: respiratory event index (REI), oxygen desaturation index (ODI), mean night-time blood oxygen saturation (SpO2)) and ET-1 levels were assessed by multivariable linear regression analysis.

Results: Median age of the cohort was 35&#8197;years. Median ET-1 levels were 2.9 (IQR 2.4&ndash;3.6) and 2.5&#8197;pg/mL (IQR 2.1&ndash;3.0) among patients with (n=105; 8%) and without subclinical sleep apnoea (REI 5&ndash;14), respectively. After multivariable adjustment, subclinical sleep apnoea remained significantly associated with plasma levels of ET-1 (&beta;=0.13 (95% CI 0.06 to 0.20) p=0.0002 for a REI 5&ndash;14; &beta;=0.10 (95% CI 0.03 to 0.16) p=0.003 for an ODI&ge;5). Every 1% decrease in mean night-time SpO2 increased ET-1 levels by 0.1&#8197;pg/mL, an association that remained significant after multivariable adjustment (&beta;=0.02 (95% CI 0.003 to 0.033) p=0.02).

Conclusions: In this study of young and healthy adults, we found that participants with subclinical sleep apnoea had elevated plasma ET-1 levels, an association that was due to night-time hypoxaemia. Our results suggest that ED may already be an important consequence of subclinical sleep apnoea.

No MeSH data available.


Related in: MedlinePlus