Abstract 3359: A Nocturnal Invader of Endothelium in Hypertensives with Obstructive Sleep Apnea Syndrome: from the Vulnerable Airway to the Vulnerable Endothelium
Hypothesis: We investigated the impairment of endothelial function by molecular means in hypertensives with obstructive sleep apnea syndrome (OSAS).
Methods: 62 consecutive subjects [49 men, aged 48±7 years, 31 smokers, body mass index (BMI) 31.9±4.9kg/m2) with stage I-II untreated-uncomplicated hypertension and OSAS diagnosed by polysomnography (PSG) [apnea/hypopnea index (AHI)> 5] and a control group of 70 untreated hypertensives with negative PSG (without OSAS) matched for age, sex, BMI, smoking status, and 24h systolic blood pressure (BP) were studied. All subjects underwent 24h ambulatory BP monitoring, echocardiography study while full metabolic profile and asymmetric dimethyl arginine (ADMA), were assessed. ADMA was measured twice (morning and evening values were finally averaged).
Results: Hypertensives with OSAS compared to hypertensives without OSAS had similar levels of 24h systolic BP, 24h pulse pressure and 24h heart rate (140±9 vs.138±6 mmHg, 53. ± 5 vs. 53±6 mmHg, and 80±6 vs. 79±7 b/min, p=NS in all cases), while 24h diastolic BP and nighttime pulse pressure were higher in OSAS group (87±6 vs. 84±7 mmHg, p<0.03 and 49±9 vs. 45±10, p<0.008). Left ventricle mass index was greater in hypertensives with OSAS compared to those without OSAS (109±23 vs. 100±25 gr/m2), while relative wall thickness (0.45±0.07 vs. 0.45±0.08, p=NS) and metabolic profile (regarding glucose levels, glucosided hemoglobin, low and high density lipoprotein cholesterol, and triglycerides) did not differ between the two groups (p=NS, in all cases). Levels of logADMA were increased in OSAS hypertensives compared to those without OSAS (−0.25±0.09 vs. −0.31±0.08 μmol/l, p<0.0001). In a covariance analysis model (ANCOVA) the difference in ADMA, remained significant even after adjustment for several confounders (p<0.05). ADMA levels were correlated with the presence of OSAS (r=0.33, p<0.0001), logAHI (r=0.41, p<0.0001) and minimum oxygen saturation during sleep (r=−0.38, p<0.0001)
Conclusions: OSAS has a detrimental effect on endothelial function in the setting of hypertension. Our findings suggest that early atherosclerosis in OSAS and hypertension may be driven by pronounced endothelial dysfunction impairment accelerating further vascular damage.