sleep apnea; stroke; cardiovascular risk factors; outcome; blood pressure; oxidative stress; endothelial function; neuroimaging; cerebral hemodynamics; humoral factors; near-infrared spectrophotometry; magnetic resonance imaging; pulse wave analysis; Cerebrovascular events; Continuous Positive Airway Pressure; CPAP; Sleep disordered breathing
Cereda Carlo W, Tamisier Renaud, Manconi Maudo, Andreotti Jennifer, Frangi Jane, Pifferini Valeria, Bassetti Claudio L (2013), Endothelial Dysfunction and Arterial Stiffness in Ischemic Stroke : The Role of Sleep-Disordered Breathing, in Stroke
, 44, 1175-1178.
Pizza Fabio, Biallas Martin, Kallweit Ulf, Wolf Martin, Bassetti Claudio L (2012), Cerebral hemodynamic changes in stroke during sleep-disordered breathing, in Stroke
, 43(7), 1951-1953.
Cereda Carlo W, Bassetti Claudio L (2012), Sleep-disordered breathing in acute ischemic stroke and transient ischemic attack: effects on short- and long-term outcome and efficacy of treatment with continuous positive airways pressure--rational, in Int J Stroke
, 7(7), 597-603.
Bassetti Claudio L, Hermann Dirk M (2011), Sleep and stroke, in P. Montagna and S. Chokroverty Editors (ed.), 1051-1072.
Pizza Fabio, Biallas Marin, Wolf Martin, Werth Esther, Bassetti Claudio L (2010), Nocturnal cerebral hemodynamics in snorers and in patients with obstructive sleep apnea: a near-infrared spectroscopy study, in Sleep
, 33(2), 205-210.
Mauro Manconi, Ott Sebastian R, Bassetti Claudio L, Integrating the Review of Gottlieb et al. With the SAS-CARE Study, in Sleep
Manconi Mauro, Zavalko Irina, Cereda Carlo, Pisarenco Iraida, Ott Sebastian R, Fulda Stephany, Bassetti Claudio L, Longitudinal Polysomnographic Assessment from Acute to Subacute Phase in Infra- vs Supratentorial Stroke, in Cerebrovascular Diseases
Background: Sleep apnea (SA) has been recognized as independent risk factor for cardiovascular morbidity and mortality and is very frequent (more than 50%) in patients with acute stroke. Preliminary observations suggested that 1) stroke may cause (or worsen pre-existing) SA; 2) SA may adversely affect outcome of ischemic stroke. Possible mechanisms leading to this detrimental effect include cerebral hemodynamic, oxygen saturation, humoral (endothelial, coagulatory, metabolic and inflammatory) changes. It remains unclear how a) stroke may cause (or worsen) SA, and b) to what extent any by which mechanisms SA may affect outcome of ischemic stroke.Working Hypotheses: 1) Ischemic stroke leads to new-onset or worsening of pre-existing SA; 2) SA has a detrimental effect on MRI evolution (in the first hours after stroke onset) and clinical outcome of acute ischemic stroke (within the first 3 months); 3) These detrimental effects are related to changes in blood pressure/heart rate, cerebral hemodynamics/tissue oxygenation, endothelial function, and humoral factors.Specific aims: The four major specific aims of the project are to assess 1) the impact of topography and severity of acute stroke on SA; 2) the impact of SA on the evolution of the ischemic penumbra (as assessed by MRI) and on the clinical outcome of stroke in the first 3 months after its onset; 3) the effect of SA on cardiovascular variables (blood pressure/heart rate, cerebral hemodynamics, endothelial function, humoral factors) in the first 3 months after stroke.Experimental design/Methods: In this prospective cohort study 200 consecutive patients with acute ischemic stroke admitted within 48 hours after symptoms onset will be assessed. In the first week after stroke investigations will include: 1) clinical assessments (stroke severity, etiology outcome), 2) diffusion/perfusion and conventional brain MRI (at admission and 36h later), 3) registration of nocturnal breathing (including pCO2), 4) registration of blood pressure/heart rate, 5) measurements of oxygen, oxyhemoglobin and deoxyhemoglobin concentrations in the brain (near-infrared spectrophotometry), 6) a test of endothelial function (pulse wave analysis, PWA), 7) measurements of serum oxidative/inflammatory markers. Three months later the following investigations will be repeated: 1) clinical assessment (stroke outcome), 2) registration of nocturnal breathing, 3) registration of blood pressure/heart rate, 4) PWA, 5) measurements of serum oxidative/inflammatory markers.Expected Value of the proposed Project: This project will improve our understanding of the clinical relevance and pathophysiological implications of SA in acute stroke. The results of this prospective cohort study will offer the opportunity to identify a subpopulation of patients with acute stroke and SA at high risk for neurological/cardiovascular complications in whom early treatment may be considered.