Longitudinal Changes in Symptom Cluster Membership in Inflammatory Bowel Disease

Purpose: To describe changes in symptom cluster membership over 1 year and to examine which demographic and clinical factors predict changes in symptom cluster membership among adults with inflammatory bowel disease. Design: A retrospective longitudinal study of the Crohn's & Colitis Foundation of America Partners Cohort from 2012 to 2015. Methods: We measured symptoms of pain interference, fatigue, sleep disturbance, depression, and anxiety. We used latent transition analysis to describe changes in symptom cluster membership (baseline, 6 months, and 12 months) and multinomial regressions to examine factors associated with symptom cluster membership transition. Findings: Four groups were identified (N = 5,296): high symptom burden (32.3%–35.3%), low symptom burden (24.2%–27.1%), physical symptoms (19.0%–20.9%; pain, fatigue, sleep disturbance), and psychological symptoms (20.0%–21.5%; depression, anxiety). The probability of staying in the same group was.814 to.905. Moving from active disease into remission was associated with moving from the high burden to low burden and psychological symptom groups. Conclusions: Symptom cluster membership was quite stable over 1 year. Research is needed to understand the underlying etiology of symptom clusters better and to develop interventions to reduce symptom burden in this vulnerable population. Clinical Relevance: Careful consideration of symptom management options should be done with patients to select options that are effective and potentially target multiple symptoms

Sleep-Disordered Breathing and Cardiac Arrhythmias in Adults: Mechanistic Insights and Clinical Implications: A Scientific Statement From the American Heart Association

Sleep-disordered breathing (SDB), characterized by specific underlying physiological mechanisms, comprises obstructive and central pathophysiology, affects nearly 1 billion individuals worldwide, and is associated with excessive cardiopulmonary morbidity. Strong evidence implicates SDB in cardiac arrhythmogenesis. Immediate consequences of SDB include autonomic nervous system fluctuations, recurrent hypoxia, alterations in carbon dioxide/acid-base status, disrupted sleep architecture, and accompanying increases in negative intrathoracic pressures directly affecting cardiac function. Day-night patterning and circadian biology of SDB-induced pathophysiological sequelae collectively influence the structural and electrophysiological cardiac substrate, thereby creating an ideal milieu for arrhythmogenic propensity. Cohort studies support strong associations of SDB and cardiac arrhythmia, with evidence that discrete respiratory events trigger atrial and ventricular arrhythmic events. Observational studies suggest that SDB treatment reduces atrial fibrillation recurrence after rhythm control interventions. However, high-level evidence from clinical trials that supports a role for SDB intervention on rhythm control is not available. The goals of this scientific statement are to increase knowledge and awareness of the existing science relating SDB to cardiac arrhythmias (atrial fibrillation, ventricular tachyarrhythmias, sudden cardiac death, and bradyarrhythmias), synthesizing data relevant for clinical practice and identifying current knowledge gaps, presenting best practice consensus statements, and prioritizing future scientific directions. Key opportunities identified that are specific to cardiac arrhythmia include optimizing SDB screening, characterizing SDB predictive metrics and underlying pathophysiology, elucidating sex-specific and background-related influences in SDB, assessing the role of mobile health innovations, and prioritizing the conduct of rigorous and adequately powered clinical trials

Sleep-Disordered Breathing and Cardiac Arrhythmias in Adults: Mechanistic Insights and Clinical Implications: A Scientific Statement From the American Heart Association

Sleep-disordered breathing (SDB), characterized by specific underlying physiological mechanisms, comprises obstructive and central pathophysiology, affects nearly 1 billion individuals worldwide, and is associated with excessive cardiopulmonary morbidity. Strong evidence implicates SDB in cardiac arrhythmogenesis. Immediate consequences of SDB include autonomic nervous system fluctuations, recurrent hypoxia, alterations in carbon dioxide/acid-base status, disrupted sleep architecture, and accompanying increases in negative intrathoracic pressures directly affecting cardiac function. Day-night patterning and circadian biology of SDB-induced pathophysiological sequelae collectively influence the structural and electrophysiological cardiac substrate, thereby creating an ideal milieu for arrhythmogenic propensity. Cohort studies support strong associations of SDB and cardiac arrhythmia, with evidence that discrete respiratory events trigger atrial and ventricular arrhythmic events. Observational studies suggest that SDB treatment reduces atrial fibrillation recurrence after rhythm control interventions. However, high-level evidence from clinical trials that supports a role for SDB intervention on rhythm control is not available. The goals of this scientific statement are to increase knowledge and awareness of the existing science relating SDB to cardiac arrhythmias (atrial fibrillation, ventricular tachyarrhythmias, sudden cardiac death, and bradyarrhythmias), synthesizing data relevant for clinical practice and identifying current knowledge gaps, presenting best practice consensus statements, and prioritizing future scientific directions. Key opportunities identified that are specific to cardiac arrhythmia include optimizing SDB screening, characterizing SDB predictive metrics and underlying pathophysiology, elucidating sex-specific and background-related influences in SDB, assessing the role of mobile health innovations, and prioritizing the conduct of rigorous and adequately powered clinical trials

Risk factors for chronic insomnia following hospitalisation

Aim. This paper reports a study whose purpose was to determine whether there is an increase in the incidence of chronic insomnia following hospitalization and, if so, to identify patients at risk.Background. The consequences of difficulty sleeping in hospital have received scant attention from clinicians or researchers. Implicit in this lack of interest is the assumption that difficulty in sleeping is a transient reaction to hospitalization that will resolve on discharge, an assumption not empirically supported. It has been argued that in susceptible people this type of temporary disruption to sleep can be the catalyst for the development of chronic insomnia.Method. Established sleep and depression rating instruments were used to monitor the sleep of 57 cardiac and 29 orthopaedic patients after elective surgery (n = 86), recruited through a hospital preadmission clinic.Results. Preadmission chronic insomnia of 10% was consistent with general population prevalence estimates of 6&ndash;12%. Three months after discharge the incidence had almost doubled to 19%. Sixty-one per cent of this variance could be explained by hyperarousal, sleep hygiene issues, and dysfunctional cognitions about sleep. Depression was found to be a salient predictor but not an independent risk factor. Age, sex, and hospital-related data, such as score for difficulty sleeping in hospital, proved to be statistically insignificant.Conclusions. The results support the role of hyperarousal and dysfunctional sleep attitudes and behaviours as stronger predictors of chronic insomnia than patient demographics or environmental issues. Given that most of the patients were ambivalent about how they slept in hospital, with high satisfaction (71%) in the presence of significant disruption (63%), preadmission sleep education given to these patients prior to admission potentially contributed to the development of more realistic expectations of the quality of in-hospital sleep.<br /