Context-Systemic hypertension is prevalent among patients with obstructive sleep apnea (OSA). Short-term studies indicate that continuous positive airway pressure (CPAP) therapy reduces blood pressure in patients with hypertension and OSA.Objective-To determine whether CPAP therapy is associated with a lower risk of incident hypertension.Design, Setting, and Participants-A prospective cohort study of 1889 participants without hypertension who were referred to a sleep center in Zaragoza, Spain, for nocturnal polysomnography between January 1, 1994, and December 31, 2000. Incident hypertension was documented at annual follow-up visits up to January 1, 2011. Multivariable models adjusted for Corresponding Author: José M. Marin, MD, Respiratory Department, Hospital Universitario Miguel Servet, Avda Isabel la Católica, 1-3, 50006 Zaragoza, Spain (jmmarint@unizar.es).. Author Contribution: Dr Marin had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Conclusion-Compared with participants without OSA, the presence of OSA was associated with increased adjusted risk of incident hypertension; however, treatment with CPAP therapy was associated with a lower risk of hypertension. HHS Public AccessOBSTRUCTIVE SLEEP APNEA (OSA), a prevalent condition that is estimated to affect 17% of US adults, is associated with an increased risk for cardiovascular diseases and overall mortality. [1][2][3][4][5] Although treatment of OSA with continuous positive airway pressure (CPAP) therapy is associated with decreased overall cardiovascular risk, its efficacy in preventing new-onset hypertension is unknown. 2Several cross-sectional studies link OSA to arterial hypertension, a major risk factor for fatal and nonfatal cardiovascular events. [6][7][8][9][10] However, the association between OSA and increased rate of incident hypertension has not been observed consistently in prospective studies. 11,12 A relatively short follow-up period (<5 years) and a limited inclusion of patients with severe OSA hinder conclusions regarding the association of OSA with incident hypertension. 11,12 Further more, the contribution of change in body weight over time, a well-established risk factor for both hypertension and OSA, to the development of newonset hyper-tension has not been investigated in patients with OSA. 13 Treatment of OSA eliminates repetitive episodes of hypoxia associated with transient cessation of breathing and stabilizes cardiovascular function. 14 Short-term studies indicate that CPAP use is associated with a reduction in blood pressure in patients with hypertension and OSA. 15 Whether long-term CPAP therapy prevents or reduces the rate of new-onset hypertension in patients with OSA has not been investigated. We hypothesized that OSA is an independent risk factor for the development of new-onset hypertension and that longterm CPAP therapy reduces this risk regardless of change in body weight over time. Clinical DataDemographic, anthropomet...

T he vast majority of experimental stroke research has focused on animal models of large territorial infarction involving both cortical and subcortical grey and white matter. 1 However, 20% to 25% of strokes in humans are small, lacunarlike, involve subcortical white matter tracts, 2 are often recurrent, and may lead to cognitive decline, subcortical dementia, and major disability. 3 Moreover, white matter ischemic lesions are a main pathological manifestation of small vessel diseases, a subset of cerebrovascular alterations leading to stroke and cognitive decline. 4 Only a few experimental models investigating small white matter strokes have been reported. 5 Recently, Carmichael and collaborators 6 developed a model of selective white matter stroke by injecting the potent vasoconstrictor endothelin-1 into corpus callosum to create a small area of myelin and axonal degeneration. Although reproducibility has been a problem with this model, it generates a lesion confined to white matter and therefore offer advantages to other white matter injury models that in addition cause diffuse brain injury after global cerebral hypoperfusion.7 After adapting, improving, and extending this new experimental approach, we tested whether subcortical white matter ischemic injury is associated with cognitive impairment in wildtype (WT) mice. Furthermore, we tested whether a NOTCH3 gene deletion negatively affects tissue and functional outcome after selective white matter injury. NOTCH3 mutations are the most common cause of inherited strokes and vascular dementia in young and middle-aged adults. 8 We previously showed that NOTCH3 knockout mice seem especially vulnerable to ischemic injury after middle cerebral artery occlusion, probably because of vascular dysfunction and reduced collateral blood flow. 9 Here, we extended these findings to white matter susceptibility and provided a novel experimental approach to further dissect the relationship between genotype and ischemic phenotype in NOTCH3 mutants. Materials and MethodsExperiments were conducted according to protocols approved by the Animal Research Committee of Massachusetts General Hospital and the National Institutes of Health Guide for the Care and Use of Laboratory Animals (see online-only Data Supplement).Background and Purpose-Small subcortical white matter infarcts are a common stroke subtype often associated with cognitive deficits. The lack of relevant models confined to white matter has limited the investigation of its pathophysiology. Here, we examine tissue and functional outcome after an ischemic lesion within corpus callosum in wild-type (WT) mice and in mice null for a gene, NOTCH3, linked to white matter ischemic injury in patients. Methods-WT and NOTCH3 knockout mice were subjected to stereotactic microinjections of the potent vasoconstrictor endothelin-1 at the level of periventricular white matter to induce a focal ischemic lesion. Infarct location was confirmed by MRI, and brains were examined for lesion size and histology; behavioral deficits were a...

BackgroundSpinal cord infarction (SCI) is rarely caused by vertebral artery dissection (VAD), which is an important cause of posterior circulation stroke in young and middle-aged patients. We report the case of a middle-aged patient without obvious risk factors for atherosclerosis who had SCI from right VAD.Case presentationAn otherwise healthy 40-year-old man presented with acute right-sided body weakness. Six days earlier, he had experienced posterior neck pain without obvious inducement. Neurologic examination revealed a right Brown-Séquard syndrome. Magnetic resonance imaging (MRI) of the head was normal. Further, cervical spine MRI showed spinal cord infarction (SCI) on the right at the C1-C3 level. Three-dimensional high-resolution MRI (3D HR-MRI) volumetric isotropic turbo spin echo acquisition (VISTA) scan showed evidence of vertebral artery dissection (VAD). The patient was significantly relieved of symptoms and demonstrated negative imaging findings after therapy with anticoagulation (AC) and antiplatelets (AP) for 3 months.ConclusionsThe possibility of vertebral artery dissection (VAD) should be considered in the case of young and middle-aged patients without obvious risk factors for atherosclerosis. Furthermore the VISTA black blood sequence plays an important role in the pathological diagnosis of vertebral artery stenosis. Early correct diagnosis and active therapy are crucial to the prognosis.