Heart rate response to cortical arousals in patients with isolated obstructive sleep apnea and with comorbid insomnia (COMISA).

PURPOSE: Comorbid insomnia often occurs in patients with obstructive sleep apnea (OSA), referred to as COMISA. Cortical arousals manifest as a common feature in both OSA and insomnia, often accompanied by elevated heart rate (HR). Our objective was to evaluate the heart rate response to nocturnal cortical arousals in patients with COMISA and patients with OSA alone. METHODS: We analyzed data from patients with COMISA and from patients with OSA matched for apnea-hypopnea index. Sleep staging and analysis of respiratory events and cortical arousals were performed using the Philips Somnolyzer automatic scoring system. Beat-by-beat HR was analyzed from the onset of the cortical arousal to 30 heartbeats afterwards. HR responses were divided into peak and recovery phases. Cortical arousals were separately evaluated according to subtype (related to respiratory events and spontaneous) and duration (3-6 s, 6-10 s, 10-15 s). RESULTS: A total of 72 patients with COMISA and 72 patients with OSA were included in this study. There were no overall group differences in the number of cortical arousals with and without autonomic activation. No significant differences were found for spontaneous cortical arousals. The OSA group had more cortical arousals related to respiratory events (21.0 [14.8-30.0] vs 16.0 [9.0-27.0], p = 0.016). However, the COMISA group had longer cortical arousals (7.2 [6.4-7.8] vs 6.7 [6.2-7.7] s, p = 0.024) and the HR recovery phase was prolonged (52.5 [30.8-82.5] vs 40.0 [21.8-55.5] beats/min, p = 0.017). Both the peak and the recovery phase for longer cortical arousals with a duration of 10-15 s were significantly higher in patients with COMISA compared to patients with OSA (47.0 [27.0-97.5] vs 34.0 [21.0-71.0] beats/min, p = 0.032 and 87.0 [47.0-132.0] vs 71.0 [43.0-103.5] beats/min, p = 0.049, respectively). CONCLUSIONS: The HR recovery phase after cortical arousals related to respiratory events is prolonged in patients with COMISA compared to patients with OSA alone. This response could be indicative of the insomnia component in COMISA.

Long term survival after admission for COPD exacerbation: A comparison with the general population.

BACKGROUND AND OBJECTIVE: Life expectancy data of COPD patients in comparison to the general population are primarily based upon long-term population cohort studies. These studies are limited by a poor definition of clinically significant COPD. The key element in the course of COPD is a clinical exacerbation. Therefore, this study investigated 15-year survival following hospitalization for an exacerbation of COPD in comparison to the general population. METHODS: A number of 4229 subjects was studied, including 845 hospitalized COPD patients and 3384 age and sex matched controls. Mortality risks were assessed using Kaplan-Meier survival curves, and hazard rate ratios for death were estimated using Cox proportional hazards regression models, for each Gold Class separately. RESULTS: Overall 15-year survival was 7.3% in the COPD group and 40.6% in the general population. Survival was 24%, 11.1%, 5.3% and 0% for COPD GOLD I-IV. The mean life expectancy following hospitalization was 9.7, 7.1, 6.1 and 3.4 years for stage GOLD I-IV and 10.2 years for the general population. Overall, negative prognostic factors were age, male gender, low FEV1, low TLCO, respiratory insufficiency, Charlson comorbidity class, ICU-admission and exacerbation frequency. Factors differed among GOLD stages. CONCLUSIONS: The 15-year survival for hospitalized COPD patients is reduced by 82% in comparison to the general population. This indicates a more deleterious course of clinically significant COPD in comparison to population cohorts. As such, every possible effort should be taken to reduce exacerbations in a personalized way.

F-18 FDG PET/CT scanning in Charcot disease: a brief report.

PURPOSE: because of the increasing prevalence of diabetes, complications of diabetes will also become more prevalent. The pathophysiology of Charcot neuro-osteoarthropathy (Charcot disease) as a complication of diabetes is still enigmatic. As a consequence, the optimal diagnostic, follow-up, and therapeutic strategies are unclear. To obtain more insight into the relation between bony abnormalities and the (concurrent) inflammatory response in acute Charcot disease, thereby creating more insight into the pathophysiology of this disease, we performed F-18 FDG PET/CT scanning. RESEARCH DESIGN AND METHODS: We performed F-18 FDG PET/CT and Tc-99m bone scintigraphy in 10 patients with Charcot disease. Bony abnormalities on CT-scan and areas of increased uptake on F-18 FDG PET and Tc-99m bone scintigraphy were assessed independently. Subsequently, fused PET/CT images were evaluated for number and location of PET lesions. RESULTS: nine patients had increased uptake of F-18 FDG, indicating inflammation, in 25 areas of soft tissue and/or bone without concurrent bony abnormalities on CT. CONCLUSIONS: presented F-18 FDG PET/CT data may indicate an inflammatory origin of Charcot disease, with secondary bone resorption, possibly due to decreased inhibitory neurogenic inflammatory responses as a result of small fiber neuropathy. If these findings can be confirmed in future studies, F-18 FDG PET/CT scanning may be added to the diagnostic arsenal in Charcot disease, and anti-inflammatory drugs may be added to the therapeutic arsenal.

[Sweet syndrome in underlying malignancy]. / Syndroom van Sweet bij onderliggende maligniteit.

Sweet syndrome, also known as acute febrile neutrophilic dermatosis, was diagnosed in two patients. Patient A, a 68-year-old man, had had chronic lymphatic leukaemia for four years, with a recent relapse. Patient B, a 58-year-old man, had been diagnosed with renal cell carcinoma four years earlier. Both patients presented with general discomfort, high fever, neutrophilic leukocytosis and diffuse, non-tender maculopapular exanthema, partly blanching on applied pressure, and vesicles spread over the body. Patient A had clinical signs of a septic shock. In both patients, histological examination confirmed clinical suspicion of Sweet syndrome and both had a good response on prednisone. In patient B, progression of renal cell carcinoma was found more than a half year later. It is important to recognise the varied clinical picture of the rare disorder that is Sweet syndrome because it can lead to severe clinical illness, especially in patients with an underlying malignancy.