New Findings What is the topic of this review? This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex‐mediated pathophysiology in obstructive and central sleep apnoea. What advances does it highlight? Chemoreflex mechanisms are thought to contribute significantly to the pathophysiology and adverse outcomes seen in sleep apnoea. Clinical implications of altered chemoreflex function in sleep apnoea from recent studies in humans, including cardiac arrhythmias, coronary artery disease, systolic/diastolic heart failure and sudden cardiac death are highlighted. Activation of the chemoreflex in response to hypoxaemia results in an increase in sympathetic neural outflow. This process is predominantly mediated by the peripheral chemoreceptors in the carotid bodies and is potentiated by the absence of the sympatho‐inhibitory influence of ventilation during apnoea, as is seen in patients with sleep apnoea. In these patients, repetitive nocturnal hypoxaemia and apnoea elicit sympathetic activation, which may persist into wakefulness and is thought to contribute to the development of systemic hypertension and cardiac and vascular dysfunction. Chemoreflex activation could possibly lead to adverse cardiovascular outcomes, such as nocturnal myocardial infarction, systolic and/or diastolic heart failure, cardiac arrhythmias and sudden death in patients with sleep apnoea. This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex‐mediated pathophysiology in obstructive and central sleep apnoea. Measurement of the chemoreflex response may serve as a potential avenue for individualized screening for cardiovascular disease. Whether modulation of this response in sleep apnoea may aid in the prevention and treatment of adverse cardiovascular consequences will require further study.
Differential effects of insulin sensitization and insulin provision treatment strategies on concentrations of circulating adipokines in patients with diabetes and coronary artery disease in the BARI 2D trial
Diagnostic performance of body mass index to identify obesity as defined by body adiposity in children and adolescents: a systematic review and meta‐analysis
SummaryBackgroundThe ideal means of identifying obesity in children and adolescents has not been determined although body mass index (BMI) is the most widely used screening tool.ObjectiveWe performed a systematic review and meta‐analysis of studies assessing the diagnostic performance of BMI to detect adiposity in children up to 18 years.MethodsData sources were EMBASE, MEDLINE, Cochrane, Database of Systematic Reviews Cochrane CENTRAL, Web of Science and SCOPUS up to March 2013. Studies providing measures of diagnostic performance of BMI and using body composition technique for body fat percentage measurement were included.ResultsThirty‐seven eligible studies that evaluated 53 521 patients, with mean age ranging from 4 to 18 years were included in the meta‐analysis. Commonly used BMI cut‐offs for obesity showed pooled sensitivity to detect high adiposity of 0.73 (confidence interval [CI] 0.67–0.79), specificity of 0.93 (CI 0.88–0.96) and diagnostic odds ratio of 36.93 (CI 20.75–65.71). Males had lower sensitivity. Moderate heterogeneity was observed (I2 = 48%) explained in meta‐regression by differences across studies in race, BMI cut‐off, BMI reference criteria (Center for Disease Control vs. International Obesity Task Force) and reference standard method assessing adiposity.ConclusionBMI has high specificity but low sensitivity to detect excess adiposity and fails to identify over a quarter of children with excess body fat percentage.
Interatrial pressure gradients during simulated obstructive sleep apnea: A catheter‐based study
Objective Obstructive sleep apnoea (OSA) and obesity are both associated with endothelial dysfunction, which precedes the development of atherosclerosis. As obesity is highly prevalent in OSA, we wanted to test the hypothesis that OSA is associated with endothelial dysfunction independently of obesity. Design Cross-sectional, population-based study. Setting Norwegian university hospital. Patients Seventy-one subjects (median age 44 years, 35% female) were recruited from a population-based study in Norway. Participants were categorised as obese (body mass index (BMI) ≥30 kg/m2), non-obese (BMI<30 kg/m2) with OSA (apnoea–hypopnoea index (AHI)≥10), or non-obese without OSA (AHI<5). Interventions None. Main outcome measures Endothelial function measured by brachial artery ultrasound and expressed as percentage of flow-mediated dilation (FMD%). Results When non-obese subjects without OSA were used as the reference (FMD% (mean±SD) 10.1±6.3), endothelial function was found to be impaired in subjects with OSA (FMD% 6.4±3.2) (p=0.003). FMD% did not differ between obese (6.0±3.4) and non-obese (6.7±3.1) OSA subjects (p=0.3). By univariate linear regression analysis, AHI, BMI, gender and baseline brachial artery diameter were significantly associated with FMD%. When these variables were entered into a multivariate model, only AHI was significantly associated with FMD%. Conclusions OSA is associated with endothelial dysfunction independently of obesity and conventional risk factors.