Oxidative Stress and Cardiovascular Morbidity in Sleep Apnea-Hypopnea Syndrome (SAHS)

Aim: To compare the levels of 8-isoprostane and other oxidative stress biomarkers in plasma and condensed exhaled air between patients with SAHS and cardiovascular complications, patients with SAHS without cardiovascular complications and control subjects. To evaluate the effect of three months of treatment with CPAP on the oxidative stress biomarkers.

Design: randomized, double blind, of parallel groups and controlled with placebo study.

Study subjects: 53 patients with SAHS (23 with cardiovascular complications and 30 without cardiovascular complications), 23 patients with cardiovascular diseases without SAHS and 23 control subjects.

Interventions: Three months of treatment with therapeutic CPAP or with sham CPAP (placebo).

Determinations: clinical (cardiovascular morbidity) and anthropometric data. Fat free corporal mass, echocardiography, spirometry, ambulatory monitoring of the arterial pressure, endothelial reactivity. Oxidative stress biomarkers (8-isoprostane, homocysteine, HIF-1, NFkB, AP-1, VEGF, ET-1, TNF-alpha, IL-1, IL-6, ICAM-1, VCAM-1, nitrates and nitrites) in plasma and condensed exhaled air.Peripheral sensitivity to hypoxia. Urinary excretion of catecholamines.

Inclusion criteria

• Sleep apnea-hypopnea syndrome (AHI > 5)
• Excessive sleepiness (ESS > 11)
• No previous CPAP treatment

Exclusion criteria

• Blood pressure > 180/120 mmHg.
• Secondary hypertension
• Professional driver
• COPD, asthma, bronchiectasis, lung cancer, restrictive lung disorder, chest wall disease
• Neuromuscular disease or thyroid function abnormalities
• Morbid obesity (BMI > 40 Kg/m2).
• Respiratory infection in the 2 last months.
• Anemia (Hb < 10 g/dl) or polyglobulia (Hct > 55%).
• Diurnal hypercapnia (PaCO2 > 45 mmHg) or moderate hypoxemia (PaO2 < 70 mmHg).