Obstructive sleep apnea and blood pressure. Interaction between the blood pressure-lowering effects of positive airway pressure therapy and antihypertensive drugs.

BACKGROUND: There is increasing evidence that obstructive sleep apnea is an independent risk factor for arterial hypertension. Previous studies on the antihypertensive effects of positive airway pressure therapy on daytime blood pressure (BP) revealed inconsistent results. METHODS: The relations between the apnea/hypopnea index (AHI) and BP or heart rate (HR) were investigated in a cohort of 540 consecutive patients (age, 55.4 +/-11.1 years) with moderate or severe obstructive sleep apnea (OSA). The mean AHI was 28.2 +/- 22.0 events/h before OSA therapy. A group of 196 patients in whom antihypertensive medication was kept unchanged was followed for 6 months during bilevel or continuous positive airway pressure (Bi-/CPAP) therapy. RESULTS: Significant associations were found between AHI and systolic BP (beta = 0.078, P = .014), diastolic BP (beta = 0.056, P = .003), HR (beta = 0.096, P < .001), and the prevalence of arterial hypertension (odds ratio = 0.015, P = .003), independent of age, body mass index, and gender. During the follow-up period with effective Bi-/CPAP therapy, the mean daytime systolic BP decreased from 130.7 +/- 15.5 mm Hg to 128.6 +/- 15.9 mm Hg (P = .051), diastolic BP from 80.2 +/- 9.3 mm Hg to 77.5 +/- 9.5 mm Hg (P = .001), and HR from 77.7 +/- 8.8 to 75.7 +/- 8.1 beats/min (P = .001). Multiple linear regression analysis revealed that the absence of antihypertensive drugs and the level of the initial BP are significant and independent predictors for the lowering effect of Bi-/CPAP therapy on systolic and diastolic BP. CONCLUSIONS: This study confirms an independent relationship between the severity of OSA and BP/HR. Absence of BP-lowering medication and BP values before treatment are independent predictors for the reduction of BP with Bi-/CPAP therapy.

Interaction of sleep disturbances and gastroesophageal reflux in chronic laryngitis.

BACKGROUND: A considerable percentage of patients with reflux laryngitis do not respond to conventional treatment with proton pump inhibitors or prokinetics. At the present time, the reasons for this are not well known. PURPOSE: To investigate whether nocturnal reflux associated with sleep-related respiratory disorders is the cause of refractory laryngitis. METHOD: The data from 227 patients (133 women, ages 18 to 75 years, body mass index 17.4 to 38.3, mean 32.1 kg/m(2)) with LG were analyzed retrospectively. All received laryngoscopy and gastroscopy. All patients initially received 40- to 80 mg omeprazole and underwent a follow-up laryngoscopy after 6 weeks. Of the patients, 202 showed a clear improvement, whereas 25 (11.1%) did not. All underwent 24-hour pH monitoring and cardiorespiratory polysomnography. RESULTS: All of the patients showed laryngoscopic signs of LG. Of the patients, 102 (45%) had a hiatal hernia and 53 (28%) suffered from reflux esophagitis. Forty-two patients (19%) were found to have Helicobacter pylori in the stomach. Among the 25 patients who failed to respond to omeprazole, pH monitoring showed nocturnal acid reflux in 15 (60%). Twenty-four patients (96%) showed a sleep-related respiratory disturbance manifesting as pathologic snoring (16 patients) or obstructive sleep apnea (8 patients, respiratory disturbance index [RDI] 11 to 33, mean 16.3/h). All received nasal continuous positive airway pressure (nCPAP) treatment, 16 with constant mask pressure (4 to 12, mean, 5.6 mbar) and 8 with autoadjusting pressure. One patient abandoned treatment; the other 23 showed clear subjective and objective improvement after 3 months of treatment. CONCLUSIONS: Even without pH monitoring evidence of nocturnal reflux, refractory LG is very often associated with sleep-related respiratory disorders and responds well to nCPAP treatment. Prospective studies are needed to clarify the details of this association.