O006 Early vascular ageing in children with sleep disordered breathing: evidence of vascular hypertrophy and hyperplasia

P Vokolos,D Kennedy, K Lushington,J Martin, D Wabnitz,A Kontos

SLEEP Advances(2021)

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摘要
Abstract Children with sleep disordered breathing (SDB) have evidence of increased blood flow velocity and sympathetic overactivity. Sympathetic overactivity leads to peripheral vasoconstriction, increased vascular resistance and consequently, increases blood flow velocity. Early vascular ageing involves premature arterial thickening and stiffening that leads to changes in vascular function. Both increased blood flow velocity and sympathetic overactivity are promoters of arterial remodelling and hence, early vascular ageing. No studies have directly histologically investigated arterial wall structure in children with SDB and how it relates to vascular function. Thirty-six children scheduled for tonsillectomy underwent polysomnography to determine SDB severity and resting brachial artery blood flow velocity (velocity time integral and peak systolic velocity) using Doppler ultrasound. The dorsal lingual artery (tonsil) was stained using hematoxylin and eosin techniques to examine arterial wall structures. Increased velocity time integral correlated with increased arterial medial thickness (r = 0.50, P<0.01), arterial smooth muscle cells (r =0.43, P<0.05) and arterial smooth muscle layers (r=0.45, P<0.01). These relationships remained significant after controlling for body-mass index (BMI). Increased BMI was associated with increased velocity time integral (r=0.61, P<0.01), arterial medial thickness (r=0.37, P<0.05) and arterial medial area (r=0.36, P<0.05). SpO2nadir (TST/REM) was inversely associated with arterial medial area (r=-0.35; r=-0.38, P<0.05). These results demonstrate that increased blood flow velocity is associated with changes in arterial wall composition in children with SDB. This suggests that paediatric SDB, a treatable disorder, is potentially a modifiable risk factor for early vascular ageing and resultant cardiovascular disease in adulthood.
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