; for the Spanish Sleep Network IMPORTANCE More than 70% of patients with resistant hypertension have obstructive sleep apnea (OSA). However, there is little evidence about the effect of continuous positive airway pressure (CPAP) treatment on blood pressure in patients with resistant hypertension. OBJECTIVE To assess the effect of CPAP treatment on blood pressure values and nocturnal blood pressure patterns in patients with resistant hypertension and OSA. DESIGN, SETTING, AND PARTICIPANTS Open-label, randomized, multicenter clinical trial of parallel groups with blinded end point design conducted in 24 teaching hospitals in Spain involving 194 patients with resistant hypertension and an apnea-hypopnea index (AHI) of 15 or higher. Data were collected from June 2009 to October 2011. INTERVENTIONS CPAP or no therapy while maintaining usual blood pressure control medication. MAIN OUTCOMES AND MEASURES The primary end point was the change in 24-hour mean blood pressure after 12 weeks. Secondary end points included changes in other blood pressure values and changes in nocturnal blood pressure patterns. Both intention-to-treat (ITT) and per-protocol analyses were performed. RESULTS A total of 194 patients were randomly assigned to receive CPAP (n = 98) or no CPAP (control; n = 96). The mean AHI was 40.4 (SD, 18.9) and an average of 3.8 antihypertensive drugs were taken per patient. Baseline 24-hour mean blood pressure was 103.4 mm Hg; systolic blood pressure (SBP), 144.2 mm Hg; and diastolic blood pressure (DBP), 83 mm Hg. At baseline, 25.8% of patients displayed a dipper pattern (a decrease of at least 10% in the average nighttime blood pressure compared with the average daytime blood pressure). The percentage of patients using CPAP for 4 or more hours per day was 72.4%. When the changes in blood pressure over the study period were compared between groups by ITT, the CPAP group achieved a greater decrease in 24-hour mean blood pressure (3.1 mm Hg [95% CI, 0.6 to 5.6]; P = .02) and 24-hour DBP (3.2 mm Hg [95% CI, 1.0 to 5.4]; P = .005), but not in 24-hour SBP (3.1 mm Hg [95% CI, −0.6 to 6.7]; P = .10) compared with the control group. Moreover, the percentage of patients displaying a nocturnal blood pressure dipper pattern at the 12-week follow-up was greater in the CPAP group than in the control group (35.9% vs

Abstractsistent pulmonary hypertension of the newborn. 5 In many patients with acute respiratory Background -Inhaled nitric oxide (NO) is a selective pulmonary vasodilator which distress syndrome (ARDS) inhaled NO reduces the pulmonary artery pressure and increases can improve gas exchange in acute lung injury. However, it is uncertain that this arterial oxygenation by lessening intrapulmonary shunt. 6 Experimentally, inhaled NO effect on arterial oxygenation can be generalised to all lung diseases.reverses hypoxic pulmonary vasoconstriction. 7Inhaled NO, however, can worsen gas exchange Methods -The effects of inhaled NO on gas exchange were studied in nine patients by overcoming the usual physiological mechanisms of matching ventilation (V) and perwith chronic obstructive pulmonary disease (COPD), 11 patients with severe pul-fusion (Q). Whilst inhaled NO acts as a selective pulmonary vasodilator in some monary hypertension, and 14 healthy volunteers. A randomised sequence of patients with chronic obstructive pulmonary disease (COPD), it fails to improve 40 ppm of NO or air was inhaled for 20 minutes through an orofacial mask.oxygenation. 8 9 It is important to establish in which diseases inhaled NO fails to improve Results -Inhaled NO reduced mean (SE) transcutaneous arterial oxygen tension gas exchange. We have studied the change in arterial oxygenation during NO inhalation in (TcPO 2 ) from 9.6 (0.3) to 8.9 (0.4) kPa in healthy volunteers and from 7.4 (0.6) to patients with COPD and compared it with normal volunteers and patients with severe pul-7.0 (0.5) kPa in patients with COPD. There was no change in TcPO 2 in patients with monary hypertension. severe pulmonary hypertension. During inhalation of NO and air no change occurred in transcutaneous arterial carbon Methods dioxide tension (TcPCO 2 ), arterial oxygen Nine patients with COPD, 11 with severe pulsaturation (SaO 2 ) measured by pulse oxi-monary hypertension, and 14 healthy vometer, or cardiac output determined by lunteers were studied. All gave their informed the transthoracic impedance method. consent and the study was approved by the Conclusions -Inhaled NO does not im-local hospital ethics committee. The diagnosis prove TcPO 2 nor increase cardiac output in of COPD was established from a history of normal subjects and patients with COPD, clinical and physiological evidence of irsuggesting that inhaled NO worsens gas reversible airway obstruction. All patients with exchange. This could represent inhaled Section of Respiratory COPD ceased bronchodilators 12 hours before NO overriding hypoxic pulmonary vasoMedicine, the study. The diagnosis of severe pulmonary

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A significant incidence of subclinical optic nerve involvement, not detected with other structural and psychophysics diagnostic techniques was seen by means of the mfVEP. In this sense, the mfVEP may be a useful diagnostic tool in the clinic for early diagnosis and monitoring of optic nerve function abnormalities in patients with OSAS.

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