Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterise the profile of this blood pressure increase, to determine if it is sustained and to explore potential physiological mechanisms.We performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of IH exposure. We also assessed systemic haemodynamics, muscle sympathetic nerve activity (MSNA), ischaemic calf blood flow responses and baroreflex gain. We obtained blood samples for inflammatory markers before, during and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean¡SD MSNA increased across the exposure (17.2¡5.1 versus 21.7¡7.3 bursts?min -1 ; p,0.01) and baroreflex control of sympathetic outflow declined from -965.3¡375.1 to -598.4¡162.6 AIU?min -1 ?mmHg -1 (p,0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers. These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from reduced baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.
Obstructive sleep apnea (OSA) is associated with cardiovascular morbidity and mortality, largely as a result of myocardial anomalies. Numerous mechanisms cause OSA-related myocardial damage. The majority are initiated as a result of OSA-induced, chronic, intermittent hypoxia. The most-important mechanisms that lead to myocardial damage are increased sympathetic activity, endothelial dysfunction, systemic inflammation, oxidative stress, and metabolic anomalies. All these mechanisms promote the development of hypertension, which is common in patients with OSA. Hypertensive cardiomyopathy and coronary heart disease, as well as obesity-related, diabetic, and tachycardia-induced cardiomyopathies, are also associated with OSA. Left ventricular hypertrophy, myocardial fibrosis, atrial dilatation, and left ventricular systolic and diastolic dysfunction in patients with OSA explain the association of the disease with these clinical outcomes. The gold-standard treatment for OSA, nasal continuous positive airway pressure (CPAP), might improve cardiac symptoms and hemodynamic parameters in patients with the disease. However, large clinical trials are required to improve our understanding of the cardiac consequences of OSA, and determine the effect of treatment, particularly CPAP, on myocardial damage in symptomatic patients and primary prevention of cardiovascular disorders.
RationaleIn obstructive sleep apnea patients (OSA), continuous positive airway pressure (CPAP) adherence is crucial to improve symptoms and cardiometabolic outcomes. The choice of mask may influence CPAP adherence but this issue has never been addressed properly.ObjectiveTo evaluate the impact of nasal pillows, nasal and oronasal masks on CPAP adherence in a cohort of OSA.MethodsNewly CPAP treated OSA participating in “Observatoire Sommeil de la Fédération de Pneumologie”, a French national prospective cohort, were included between March 2009 and December 2011. Anthropometric data, medical history, OSA severity, sleepiness, depressive status, treatment modalities (auto-CPAP versus fixed pressure, pressure level, interface type, use of humidifiers) and CPAP-related side effects were included in multivariate analysis to determine independent variables associated with CPAP adherence.Results2311 OSA (age = 57(12) years, apnea+hypopnea index = 41(21)/h, 29% female) were included. Nasal masks, oronasal masks and nasal pillows were used by 62.4, 26.2 and 11.4% of the patients, respectively. In univariate analysis, oronasal masks and nasal pillows were associated with higher risk of CPAP non-adherence. CPAP non-adherence was also associated with younger age, female gender, mild OSA, gastroesophageal reflux, depression status, low effective pressure and CPAP-related side effects. In multivariate analysis, CPAP non-adherence was associated with the use of oronasal masks (OR = 2.0; 95%CI = 1.6; 2.5), depression, low effective pressure, and side effects.ConclusionAs oronasal masks negatively impact on CPAP adherence, a nasal mask should be preferred as the first option. Patients on oronasal masks should be carefully followed.
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