Rationale: Obstructive sleep apnea (OSA) is a risk factor for cardiovascular disease. We hypothesized that patients with OSA and no cardiovascular disease have oxidant-related microcirculatory endothelial dysfunction. Objectives: To evaluate the microcirculation in OSA. Methods: This study included seven patients with OSA and seven ageand weight-matched control subjects (mean age, 38 yr; mean body mass index, 32.5 kg/m 2 ). All participants were free of cardiovascular risk factors. Participants received measurement of brachial artery flow-mediated dilation and forearm subcutaneous biopsy. Patients underwent repeated tests 12 weeks after treatment. Microcirculatory endothelial cells were isolated, and immunohistochemistry staining for peroxynitrite in the microcirculation was performed. Measurements and Main Results: Flow-mediated dilation was lower in patients than in control subjects at baseline (mean 6 SEM: 5.7 6 0.5 vs. 9.5 6 0.6; P 5 0.02) and increased after treatment (5.7-7.3; change, 1.7 6 0.6; P 5 0.04). Microcirculatory peroxynitrite deposit was higher in patients compared with control subjects (44.0 6 1.6 vs. 21.8 6 1.9 stain density units; P , 0.001) and decreased after treatment from 44.0 to 30.5 stain density units (change, 213.5 6 2.9; P 5 0.009). In patients, transcription of endothelial nitric oxide synthase decreased from 5.2 to 21.3 after treatment (change, 6.5 6 2.5; P 5 0.05), and transcription of superoxide dismutase1 decreased from 24.0 to 212.3 after treatment (change, 28.3 6 2.1; P 5 0.01). These changes persisted after adjustment for weight and underlying severity of OSA. Conclusions: This is the first direct evaluation of the microcirculation in OSA. Patients with OSA with low cardiovascular risk status had increased oxidant production in the microcirculation and endothelial dysfunction, both of which improved with treatment. Endothelial nitric oxide synthase transcription decreased with treatment.
Background-Sleep Disordered Breathing (SDB) is present in over 50% of ambulatory patients with chronic heart failure. The prevalence and type of SDB in hospitalized patients with acutely decompensated heart failure (ADHF) are not known.
Obstructive sleep apnea (OSA) is increasingly recognized as a novel cardiovascular risk factor. OSA is implicated in the pathogenesis of hypertension, left ventricular dysfunction, coronary artery disease and stroke. OSA exerts its negative cardiovascular consequences through its unique pattern of intermittent hypoxia. Endothelial dysfunction, oxidative stress, and inflammation are all consequences of OSA directly linked to intermittent hypoxia and critical pathways in the pathogenesis of cardiovascular disease in patients with OSA. This review will discuss the known mechanisms of vascular dysfunction in patients with OSA and their implications for cardiovascular disease.
Background: Treatment of obstructive sleep apnea (OSA) in outpatients with systolic heart failure improves cardiac function. We evaluated the impact of immediate inpatient diagnosis and treatment of OSA in hospitalized patients with acutely decompensated heart failure (ADHF) on in-hospital cardiac outcomes.
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