Ventilatory neural drive in chronically hypercapnic patients with COPD: effects of sleep and nocturnal noninvasive ventilation.

Sleep brings major challenges for the control of ventilation in humans, particularly the regulation of arterial carbon dioxide pressure ( ). In patients with COPD, chronic hypercapnia is associated with increased mortality. Therefore, nocturnal high-level noninvasive positive-pressure ventilation (NIV) is recommended with the intention to reduce down to normocapnia.

V̇/Q̇ Mismatch: A Novel Target for COPD Treatment.

In people with COPD, pulmonary gas-exchange efficiency may be impaired because of abnormal alveolar ventilation (V˙A), capillary perfusion (Q˙c), or both. Both have been reported in early and mild stages of the disease. Such derangements often accompany significant clinical consequences such as activity-related dyspnea and exercise intolerance.

Compensatory responses to increased mechanical abnormalities in COPD during sleep.

Purpose: To assess whether night-time increases in mechanical loading negatively impact respiratory muscle function in COPD and whether compensatory increases in inspiratory neural drive (IND) are adequate to stabilize ventilatory output and arterial oxygen saturation, especially during sleep when wakefulness drive is withdrawn.

Methods: 21 patients with moderate-to-severe COPD and 20 age-/sex-matched healthy controls (CTRL) participated in a prospective, cross-sectional, one-night study to assess the impact of COPD on serial awake, supine inspiratory capacity (IC) measurements and continuous dynamic respiratory muscle function (esophageal manometry) and IND (diaphragm electromyography, EMGdi) in supine sleep.

Results: Supine inspiratory effort and EMGdi were consistently twice as high in COPD versus CTRL (p < 0.

Non-dipping nocturnal blood pressure correlates with obstructive sleep apnoea severity in normotensive subjects and may reverse with therapy.

Background: Obstructive sleep apnoea (OSA) is strongly associated with systemic hypertension, but there are limited data on the relationship with blood pressure (BP) in normotensive subjects. Here, we examined the relationship of OSA with nocturnal BP in a documented diurnal normotensive cohort, explored potential intermediate pathways and assessed the effects on BP of continuous positive airways pressure (CPAP) therapy.

Methods: 65 males referred for assessment of possible OSA and normotensive on 24-hour BP monitoring underwent overnight inpatient polysomnography (age 41±7 years, body mass index (BMI) 34±6 kg·m, apnoea-hypopnoea index (AHI) 14 (interquartile range 5-26)).

Deterioration of Nighttime Respiratory Mechanics in COPD: Impact of Bronchodilator Therapy.

Background: COPD is associated with nighttime respiratory symptoms, poor sleep quality, and increased risk of nocturnal death. Overnight deterioration of inspiratory capacity (IC) and FEV have been documented previously. However, the precise nature of this deterioration and mechanisms by which evening bronchodilation may mitigate this occurrence have not been studied.

Nondipping Nocturnal Blood Pressure Predicts Sleep Apnea in Patients With Hypertension.

Study Objectives: Systemic hypertension is highly prevalent in obstructive sleep apnea (OSA) but there are limited data on OSA prevalence in cohorts with hypertension comparing dippers and nondippers. We investigated this relationship in a clinic-based cohort of patients with hypertension who were not screened for any pretest possibility of OSA.

Methods: A total of 100 patients with hypertension aged (mean ± SD) 58 ± 10 years, body mass index 30.

Ambulatory detection of sleep apnea using a non-contact biomotion sensor.

The high prevalence of obstructive sleep apnea has led to increasing interest in ambulatory diagnosis. The SleepMinder™ (SM) is a novel non-contact device that employs radiofrequency wave technology to assess the breathing pattern, and thereby estimate obstructive sleep apnea severity. We assessed the performance of SleepMinder™ in the home diagnosis of obstructive sleep apnea.

Intermittent hypoxia in obstructive sleep apnoea mediates insulin resistance through adipose tissue inflammation.

Obstructive sleep apnoea (OSA) is increasingly associated with insulin resistance. The underlying pathophysiology remains unclear but intermittent hypoxia (IH)-mediated inflammation and subsequent dysfunction of the adipose tissue has been hypothesised to play a key role.We tested this hypothesis employing a comprehensive translational approach using a murine IH model of lean and diet-induced obese mice, an innovative IH system for cell cultures and a tightly controlled patient cohort.

Diagnostic accuracy of carotid intima media thickness in predicting coronary plaque burden on coronary computed tomography angiography in patients with obstructive sleep apnoea.

Aim: To assess the diagnostic accuracy of common carotid artery intima media thickness (CIMT) for coronary artery disease (CAD) detection in patients with obstructive sleep apnoea (OSA).

Materials & Methods: Patients with clinically suspected OSA prospectively underwent polysomnography (PSG), ultrasound CIMT measurement and coronary computed tomography angiography (CTA). An average CIMT of ≥0.

Human adipocytes are highly sensitive to intermittent hypoxia induced NF-kappaB activity and subsequent inflammatory gene expression.

Introduction: Intermittent hypoxia (IH)-induced activation of pro-inflammatory pathways is a major contributing factor to the cardiovascular pathophysiology associated with obstructive sleep apnea (OSA). Obesity is commonly associated with OSA although it remains unknown whether adipose tissue is a major source of inflammatory mediators in response to IH. The aim of this study was to test the hypothesis that IH leads to augmented inflammatory responses in human adipocytes when compared to cells of non-adipocyte lineages.

Sleep-related disorders in chronic obstructive pulmonary disease.

Sleep may have several negative consequences in patients with chronic obstructive pulmonary disease (COPD). Sleep is typically fragmented with diminished slow wave and rapid-eye-movement sleep, which likely represents an important contributing factor to daytime symptoms such as fatigue and lethargy. Furthermore, normal physiological adaptations during sleep, which result in mild hypoventilation in normal subjects, are more pronounced in COPD, which can result in clinically important nocturnal oxygen desaturation.