STUDIO SULLA REGOLAZIONE NEURO-UMORALE DEL RITMO CIRCADIANO DELLA PRESSIONE ARTERIOSA IN PAZIENTI CON SINDROME DELLE APNEE OSTRUTTIVE DEL SONNO

CIRCADIAN RHYTHM OF BLOOD PRESSURE AND ITS NEUROHUMORAL REGULATION IN OBSTRUCTIVE SLEEP APNEA SYNDROME Background. Obstructive sleep apnea syndrome (OSAS) is a treatable cause of secondary and resistant hypertension, that must be taken in serious consideration to better estimate the cardiovascular (CV) risk in hypertensive (HT) patients. Untreated OSAS can worsen the CV function through several mechanisms, including sympathetic activation, oxidative stress, inflammation and endothelial dysfunction. Although the blood pressure control is significantly improved by continous positive airway pressure (CPAP), the activation of the renin angiotensin system (RAAS) in OSAS patients and its modification after CPAP are still an object of debate. Objective. To evaluate 1) the prevalence of OSAS, detected by polysomnography, in a cohort of resistant HT or moderate-severe HT patients, 2) the association between OSAS and the circadian rhytm of blood pressure assessed by ambulatory blood pressure monitoring (ABPM), 3) the association between OSAS and plasma renin activity (PRA), plasma aldosterone and urinary catecholamines, 4) the effect of CPAP on circadian rhytm of blood pressure and previous neurohumoral parameters. Methods. 17 consecutive hypertensive patients admitted at the Hypertension Clinic of S. Giuseppe Hospital, Milan, were screened for OSAS and circadian rhythm of blood pressure between July 2007 and August 2010. RAAS and catecholamins were assessed at the study entry. Among OSAS patients RAAS and catecholamines were further assesed one day after the initiation of CPAP. Results. Among the 17 enrolled patients, 13 (76.5%) resulted affected by OSAS. A dipper profile was observed in only 30% of the 10 OSAS patients evaluated by ABPM. PRA (ng/ml/min) was lower in non-OSAS compared to OSAS patients (0.5 + 0.2 vs 1.6 + 0.7 in mild OSAS and 1.5 + 2.3 in severe OSAS, p < 0.05). Catecholamines (mcg/8h) were lower in non-OSAS compared to severe OSAS (11 + 1 vs 17 + 7, p < 0.05). 24-hours systolic blood pressure (24h SBP), sleep systolic blood pressure (sleep SBP) and sleep heart rate (sleep HR) were lowered after the first day of CPAP (24h SBP 135 + 18 vs 140 + 17 mmHg, p < 0.05; sleep SBP 132 + 20 vs 138 + 19 mmHg; sleep HR 62 + 5 vs 65 + 6). CPAP was not associated with significant modifications of neurohumoral parameters. Conclusions. OSAS is highly prevalent in hypertensive population and it is associated with a non-dipper profile, a greater activation of the RAAS and the sympathetic system. CPAP improves the blood pressure control, probably via multiple pathways more complex then simple RAAS and sympathetic system.