Key result
Obstructive sleep apnea significantly reduced aortic wall systolic velocity compared to healthy controls (6.1 vs 8.5 cm/sec, p<0.001), indicating impaired aortic elasticity independent of hypertension.
Why the study?
Does obstructive sleep apnea syndrome impair aortic elastic properties and left ventricular function independently of hypertension?
Cross-Sectional (n=163)
No
Does obstructive sleep apnea syndrome impair aortic elastic properties and left ventricular function independently of hypertension?
Absolute Event Rate: 6.1% vs 8.5%
p-value: p=<0.001
Background: Obstructive sleep apnea syndrome (OSAS) has been linked to cardiovascular (CVS) complications. The diagnosis of effects of sleep apnea on heart may be difficult before apparent examination findings. Although the mechanisms underlying the association between OSAS and CVS disease are not known, it is believed that, the CVS effects of OSAS have a multifactorial pathogenesis. Objectives: To evaluate aortic elastic properties and left ventricular (LV) functions in patients with OSAS with and without systemic hypertension (HTN) and correlate these findings with brain natriuretic peptide (BNP) levels. Patients & methods: The study comprised 133 patients and 30 age and sex matched healthy volunteers as a control group (Group I). The patients were divided according to the presence of OSAS and HTN into 3 groups; Group II (42 patients) with HTN, Group III (44 patients) with OSAS and Group IV (47 patients) with both HTN and OSAS. All subjects included in the study underwent polysomnography and echocardiography. Assessment of LV function (systolic and diastolic), aortic strain (AS), distensibility (AD) and aortic wall systolic velocity (AWSV) was done using conventional echocardiography and Doppler tissue imaging (DTI). BNP levels were measured within 2 hours of echocardiography by rapid immunoassay. Results: Comparing control group to patients groups, AWSV (8.5±1.5 cm/sec vs. 6.04±2.4 cm/sec, 6.1±1.9 cm/sec, 5.01±1.5 cm/sec, p <0.001 for each), AS (17.2±9 % vs. 11.7±4%, 8.7±5%, 8.7±4%, p <0.001 for each) and AD (10±5 cm 2 /dyn/10 3 vs. 6±2 cm 2 /dyn/10 3 , 7±1 cm 2 /dyn/10 3 , 4±2 cm 2 /dyn/10 3 , p <0.01 for each) were significantly lower in all patients groups than control subjects. Long axis LV systolic function and LV diastolic function parameters were significantly impaired in all patients groups compared to control group, whereas LV Tei index and BNP levels were significantly higher in patients in comparison to control subjects. AWSV, AD and AS have strong significant positive correlations with mitral annular plane systolic excursion (MAPSE) ( r =.61, r =.55, r =.41 respectively, p <0.01 for each), Systolic mitral annular velocity (Sm)( r = .64, r = .48, r =.47 respectively, p <0.001 for each), mitral inflow E/A ratio( r =.49, r = .41, r = .39 respectively, p <0.05 for each) and DTI-derived mitral annular Em/Am ratio ( r = .60, r = .45, r = .42 respectively, p <0.01 for each) while the correlation was negative with Tei index ( r = - .61, r = - .5, r = - .45 respectively, p <0.01 for each) and BNP levels( r = - .67, r = - .59, r = - .5 respectively, p <0.001 for each). In multivariate analysis, age, HTN, OSAS and LV mass index are the independent predictors for impaired aortic elasticity. Conclusion: Aortic elasticity parameters (AWSV, AS and AD), Long axis LV systolic function (MAPSE and Sm), LV diastolic function parameters (derived by both conventional and tissue Doppler), Tei Index and BNP levels are all impaired in patients with OSAS, HTN or both. Accordingly subtle subclinical cardiac dysfunction is present in patients with OSAS independent from HTN.
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Elnoamany et al. (2012) conducted a cross-sectional in Obstructive sleep apnea syndrome and systemic hypertension (n=163). Obstructive sleep apnea vs. Healthy volunteers was evaluated on Aortic wall systolic velocity (AWSV) (p=<0.001). Obstructive sleep apnea significantly reduced aortic wall systolic velocity compared to healthy controls (6.1 vs 8.5 cm/sec, p<0.001), indicating impaired aortic elasticity independent of hypertension.
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