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Genioglossus Stimulation in Sleep Apnea

Background:

The therapeutic value of transcutaneous electrical stimulation of the genioglossus muscle in patients with obstructive sleep apnea (OSA) to reduce sleep-disordered breathing is unclear.

 Methods:

Contraction of the genioglossus muscles during transcutaneous stimulation was investigated using ultrasonography in 11 healthy subjects (seven men, mean [SD] age 30 [6] years; BMI, 24.2 [3.5] kg/m2). Esophageal and gastric pressures were measured with balloon catheters, and transesophageal diaphragm electromyogram (EMGdi) was recorded during polysomnography in 11 patients with OSA (eight men, aged 51 [16] years; BMI, 42.0 [9.7] kg/m2) while transcutaneous electrical stimulation of the genioglossus was applied in non-rapid eye movement sleep (stage N2).

 Results:

Ultrasonography measurements showed a significant increase in tongue diameter during stimulation (sagittal: 10.0% [2.8%]; coronal: 9.4 % [3.7%]). The measurements were reproducible and repeatable. In patients with OSA, snoring decreased during stimulation (P < .001) and oxygenation improved (P = .001); the respiratory disturbance index (RDI) fell from 28.1 (26.3) to 10.2 (10.2) events per hour during stimulation (P = .002), returning to 26.6 (26.0) events per hour after stimulation was stopped. Transdiaphragmatic pressure swing decreased from 24.1 (13.5) cm H2O to 19.7 (7.1) cm H2O (P = .022), increasing to 24.2 (10.8) cm H2O afterward, and EMGdi fell from 23.8% max (12.6% max) to 15.7% max (6.4% max) (P < .001), rising to 22.6% max (10.4% max) post stimulation.

 Conclusions:

Continuous transcutaneous electrical stimulation of the genioglossus contracts the genioglossus muscle and reduces ventilatory load and neural respiratory drive in patients with OSA.

ECG Measurement of Right/Left Ventricular Function

Background:

Right ventricular (RV) function is predictive of outcome in patients with acute pulmonary embolism (PE). We assessed the possible incremental value of ventricular function with ECG-synchronized cardiac CT scanning over pulmonary CT scan angiography (CTA) for predicting short-term outcome in patients with suspected acute PE.

 Methods:

The local ethics committee approved the study, and informed consent was obtained. In addition to standard CTA, 430 consecutive patients (193 men, 237 women; age, 55 ± 17 years) with suspected acute PE underwent ECG-synchronized CT scanning to assess ventricular function. RV/left ventricular (LV) function ratio and pulmonary obstruction index were obtained from non-ECG-synchronized CTA. Ventricular function was used to predict adverse events (< 6 weeks). Receiver operating characteristic analysis was performed to determine differences between ECG-synchronized CT scan and CTA in predicting outcome.

 Results:

In 113 patients with PE, RV and LV ejection fraction (EF) and RV/LV diameter and volume ratios were associated with adverse outcome (P < .05), whereas vascular obstruction index was not. RVEF had the largest area under the receiver operating characteristic curve (0.75; 95% CI, 0.62-0.88) for predicting adverse outcome but had no significant incremental value over the RV/LV function ratio (0.72; 95% CI, 0.57-0.86; P = .25). All parameters revealed high negative predictive values (94%-98%) but low positive predictive values (13%-18%). For disease-specific outcome, areas under the curve were 0.80 (95% CI, 0.69-0.91) for RVEF vs 0.68 (95% CI, 0.48-0.88) for axial RV/LV ratio; the difference was not significant (P = .07). RVEF and RV/LV ratio proved better predictors for outcome than pulmonary obstruction index (both P < .001).

 Conclusions:

RVEF was the best predictor for clinical outcome in patients with acute PE. However, incremental value of RVEF over axial RV/LV ratio was not found.

Medication Adherence in the Asthmatic Child and Adolescent.

Asthma is a common inflammatory condition affecting more than 7 million children in the United States alone, and tens of millions more globally. Despite effective preventive medications, medication nonadherence in children and adolescents is alarmingly high. Nonadherence can result in poor asthma control, which leads to decreased quality of life, lost productivity, increased health care utilization, and even the risk of death. Nonadherence in children and adolescents deserves special attention because they face unique barriers to adherence that change with age.

Young children depend on adults for the delivery of asthma care, and their care is strongly influenced by parental motivation and attitudes and the home environment. As these children enter adolescence, they typically assume responsibility for their asthma care at the same time that they are claiming their independence and possibly experimenting with high-risk behaviors. Morbidity and mortality, as well as nonadherence, appear to be greatest among adolescents and minority children. Although no perfect tool for measuring adherence exists, objective methods, such as electronic monitoring, can provide valuable information to health care providers.

Beyond asthma self-management and education, no specific resource-heavy adherence interventions have proven consistently helpful. However, large-scale, well-designed studies on this subject are lacking. In light of the fact that nonadherence is a potentially modifiable factor that impacts on morbidity and mortality, it is worth pursuing further research to determine better interventions. It is likely, however, that no one answer exists, and interventions will need to be tailored to specific at-risk populations.

Targeting eosinophil biology in asthma therapy.

Due to their role as main effector cells in immune reactions against invading parasites, eosinophils have a plethora of molecules available to destroy these complex pathogens. Their role in allergic diseases such as bronchial asthma, where they do not have to conquer pathogens, is discussed controversially.

However, since eosinophils were identified by Paul Ehrlich in tissue and sputum of patients with asthma, it was regarded that their important defensive role turns into its direct opposite so that these cells cause destruction of the airway tissue, ultimately leading to the formation of disease phenotype. Thus, eosinophils were identified as a prime target in therapeutic intervention of bronchial asthma.

Over the last years, a number of mediators and receptors involved in the regulation of eosinophil recruitment, chemotaxis, activation, survival, and apoptosis have been identified. Some of these molecules have been addressed in vitro and in animal models of experimental asthma to evaluate their therapeutic potential in asthma. A few of these candidates have been tested in clinical studies, which produced surprising results questioning the role of eosinophils in asthma pathogenesis.

This article summarizes these approaches and gives a critical overview about further candidate molecules that have been recently discussed as targets for an eosinophil-specific asthma therapy.

Efficacy of Second-Generation Antihistamines in Patients with Allergic Rhinitis and Comorbid Asthma.

Allergic rhinitis (AR) and asthma share common mediators, cytokines, and chemokines from mast cells and basophils that are central to the complex cascade of events involved in the inflammatory response. Histamine is the salient mediator released after immunologic challenge, initiating multiple pathologic processes of the allergic reaction that result in bronchial smooth muscle contraction, vasodilation, mucus hypersecretion, and edema. The recent identification of a fourth histamine receptor has reinforced clinical interest in the pleiotropic effects of histamine and the relative roles of histamine receptors in mediating immune and inflammatory responses.

Material and methods. A comprehensive literature search was conducted for the following terms, alone or in combination: allergic rhinitis, asthma, antihistamines, histamine, and histamine receptors, and for the second-generation antihistamines azelastine, cetirizine, desloratadine, ebastine, fexofenadine, levocetirizine, loratadine, mizolastine, and rupatadine. Clinical trials were included that reported results for patients with AR and comorbid asthma who were treated with second-generation antihistamines. The search dates ranged from 1995 through 2010. Clinical studies that were not placebo controlled or double blinded were excluded from this review.

Results. A total of 14 clinical trials of second-generation nonsedating antihistamines were included in this review.

Conclusion. H1-antihistamines have been shown to attenuate the symptoms associated with early- and late-phase allergic reactions. Cumulative clinical evidence indicates that H1-antihistamines may have a beneficial effect on asthma symptoms and improve quality of life. Scientific significance. Mechanistic and clinical data suggest that the potential of H1-antihistamines to alleviate comorbid asthma symptoms in AR patients should be further investigated.

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