Objective: To explore the role of vagal nerve in obstructive sleep apnea hypopnea syndrome (OSAHS) associated hypertension.
Methods: A total of 104 patients were diagnosed OSAHS via polysomnography for at least 7 hours. Their blood pressures were measured before and after sleep. Pearson's and Spearman's correlation test were applied to analyze the relevance of body mass index (BMI), apnea-hypopnea index (AHI), nocturnal minimum of arterial oxygen saturation (nSaO2% min), percentage of dwell time of arterial oxygen saturation lower than 90% (DT90%), deviation between minimal heart rate and maximal heart rate during apnea (DHR) to systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial blood pressure (MAP) before and after sleep. Logistic regression was performed to examine the risk factors of morning diastolic hypertension and systolic hypertension. Moreover, odds ratio (OR) and 95% confidence interval (CI) of each risk factor were calculated.
Results: Morning SBP, DBP and MAP in 104 subjects were (128.3 +/- 17. 9), (88.6 +/- 10.6) and (101.8 +/- 12.3) mm Hg respectively. They were significantly elevated as compared with their pre-sleep levels [(123.5 +/- 17.8), (82.0 +/- 9.6) and (95.8 +/- 11.5) mm Hg respectively, all P < 0.01]. Thirty-seven cases (35.6%) met the diagnostic criteria of hypertension (SBP > or = 140 and/or DBP > or = 90 mm Hg) in their blood pressures before sleep while 49 cases (47.1%) in their morning blood pressures. Spearman's correlation analysis shows that DBP after sleep was correlated with DHR (r = 0.214, P < 0.05). DHR in OSAHS patients with diastolic hypertension increased as compared with those without diastolic hypertension (P < 0.05). After adjusting for age, BMI, AHI, nSaO2% min and DT90%, DHR was a predictor for the morning systolic hypertension (OR = 1.253, 95% CI: 1. 057 - 1.486, P < 0.01).
Conclusions: Sleep apnea-associated heart rate variability is correlated with morning DBP in OSAHS patients. And it is also an independent predictive factor for morning systolic hypertension. This suggests that vagal regulation may be involved in OSAHS associated hypertension.