Obstructive sleep apnea and cerebral hemodinamics in acute phase of ischemic stroke

Abstract

Respiratory disorders and cerebrovascular diseases are highly prevalent worldwide, and there are mounting clinical and epidemiological evidence of a strong causal relation between them. A better comprehension of such interaction could result in advances in treatment and prevention of both conditions, with considerable public health impact.Stroke is the second leading cause of death and the main cause of disability among adults in the world. In Brazil, cerebrovascular diseases are the leading cause of death. Eighty five percent of strokes are ischemic, while hemorrhagic stroke answers for the remaining 15%. Obstructive sleep apnea (OSA) affects 2-5% of the population, and is frequent among patients with cerebrovascular diseases. Recent studies have found that 50 to 70% of acute stroke patients suffer OSA, suggesting that OSA may be an important risk factor for stroke. Indeed, OSA has been associated with a pro-thrombotic and pro-inflammatory state. However, the consequences of apnea episodes in patients with acute stroke have not been adequately clarified, and the pathophysiology underlying this interaction remains unexplored. In fact, if apnea episodes may result in changes in hemostasis, it could also have potential consequences for the success of recanalization therapies and for the occurrence of hemorrhagic transformation.In the present study, we aim to: search for possible associations between OSA and early acute neurological deterioration and clinical status at three and six months among patients with ischemic stroke; explore metabolic changes and oxidative stress markers serum levels in patients suffering apnea episodes during acute stroke, and correlate these changes with the patient's clinical evolution, and the occurrence of recanalization and hemorrhagic transformation.We will evaluate prospectively 60 adult consecutive patients with a first and only ischemic stroke. In the first night after the event. all patients will have full polysomnography done, and cerebral blood flow dynamics evolution will be assessed by transcranial Doppler. OSA severity will be plotted against clinical evolution, neuroimaging results and transcranial Doppler findings, and also with serum biomarkers levels (metalloproteinase-9, TIMP-1, d-dimer, thrombin, fibrinogen, C reactive protein, inteleukin-6, S100beta, alfa-2-antyplasmin, PAI-1 and vitronectin). The study will take place at the Emergency Unit of the Clinical Hospital, FMRP-USP. The data collected will be submitted to blind analysis by collaborating researchers from the Neurophysiology and Hemathology departments from the same institution. Patients will be reassessed at ambulatory consultations at our institution. Polysomnography will be repeated at three months. (AU)