Sleep architecture in patients with interstitial lung disease with and without pulmonary hypertension.

PURPOSE: Sleep disturbance is common in patients with advanced interstitial lung disease (ILD) often complicated by pulmonary hypertension (PH) and may contribute to poor quality of life. The etiology of sleep disturbance and the relationship between PH and sleep architecture in patients with ILD remains unknown. METHODS: We performed a retrospective cohort study comparing sleep architecture on polysomnography in patients with ILD with and without PH, defined as mean pulmonary artery pressure on right heart catheterization ≥ 20 mmHg. We tested the hypothesis that patients with ILD and PH would have increased wake time after sleep onset (WASO) compared to patients with ILD without PH using univariate analysis and multivariable linear regression. RESULTS: In our cohort of patients with ILD who underwent polysomnography (N = 49), patients with PH had lower total diffusion capacity for carbon monoxide (DLCO) (9.28 vs. 12.87 ml/min/mmHg, P = 0.04) and percent DLCO (39% vs. 53%, P = 0.03). On polysomnography, patients with PH had increased percentage of total sleep time with saturation < 90% (T90) (17% vs. 6%, P = 0.03), decreased N2 sleep (181 vs. 233 min, P = 0.03), decreased %N2 sleep (59% vs. 66%, P = 0.04), increased %N1 sleep (22% vs. 14%, P = 0.02), decreased sleep efficiency (62% vs. 72%, P = 0.03), and increased WASO (133 vs. 84 min, P = 0.01). In multivariable analysis, PH was associated with a 43-min increase in WASO (95% CI 6.2-80.2, P = 0.02). CONCLUSION: Patients with ILD and PH have decreased total and %N2 sleep, increased %N1 sleep, decreased sleep efficiency, and increased WASO, likely indicating increased sleep fragmentation.

Respiratory effort-related arousals contribute to sympathetic modulation of heart rate variability.

PURPOSE: Sympathetic activation induced by sleep-disordered breathing may contribute to cardiovascular morbidity. However, the apnea-hypopnea index (AHI) excludes respiratory effort-related arousals (RERAs) associated with inspiratory flow limitation without oxygen desaturation. We sought to determine whether RERAs are associated with sympathetic activation. METHODS: Twenty-five adults (12 males, 13 females) with AHI < 10/h and RERA index >5/h were included in this study. Power spectral density analysis was performed on two non-contiguous 10-min segments containing inspiratory flow limitation and arrhythmia-free electrocardiogram during N2 sleep. One segment contained RERA; the other did not, NO-RERA. Spectral power was described in a low-frequency domain (LF; 0.04-0.15 Hz), primarily sympathetic modulation, and a high frequency domain (HF; 0.15-0.4 Hz), parasympathetic modulation. RESULTS: Analyses of LF and HF powers were made using normalized and absolute values. LF power was greater during RERA compared to NO-RERA (50.3 vs. 30.1 %, p < 0.001) whereas HF power was greater during NO-RERA compared to RERA (69.9 vs. 49.7 %, p < 0.001). The LF/HF ratio was greater during RERA than NO-RERA (1.01 vs. 0.43, p < 0.001). Gender differences emerged using absolute values of power: The percentage increase in LF power during RERA relative to NO-RERA was significantly greater for females than males, 247.6 vs. 31.9 %, respectively (p < 0.02). CONCLUSIONS: RERAs are associated with a marked increase in cardiac sympathetic modulation, especially in females. Patients with a high RERA index, even in the setting of a low or normal AHI, may be exposed to elevated sympathetic tone during sleep.

Comparison of obstructive sleep apnoea prevalence and severity across WHO pulmonary hypertension groups.

INTRODUCTION: Pulmonary hypertension is classified into five groups in the WHO classification system. Patients with pulmonary hypertension often have comorbid obstructive sleep apnoea (OSA), yet the prevalence and severity of OSA in each of the WHO pulmonary hypertension groups have not been well established. METHODS: To compare the prevalence and severity of OSA between WHO pulmonary hypertension groups, we performed a retrospective cohort study, including patients who had polysomnography or a home sleep study and confirmed pulmonary hypertension on right heart catheterisation. The primary outcomes of OSA prevalence and severity were measured by median apnoea hypopnea index (AHI) or respiratory event index (REI) and were compared by WHO pulmonary hypertension group. Multivariable negative binomial regression was used to evaluate the association between the outcome of OSA severity by AHI or REI and WHO group. RESULTS: Among the cohort of 132 patients, OSA was common in all WHO pulmonary hypertension groups but was most common and most severe in WHO group II pulmonary hypertension. Median AHI or REI in WHO group II was 12.0 events/hour compared with 2.8 in group I, 3.7 in group III, 10.0 in group IV and 6.4 in group V. Multivariable negative binomial regression showed about a twofold increase in AHI or REI in WHO group II compared with WHO group I pulmonary hypertension. DISCUSSION: Our findings demonstrate that OSA deserves greater consideration as a treatable comorbidity that may affect pulmonary haemodynamics and quality of life in patients with pulmonary hypertension across all WHO groups.

Corticosteroid responsive fludarabine pulmonary toxicity.

Fludarabine monophosphate is a purine nucleoside antimetabolite with efficacy in the treatment of lymphoproliferative disorders and chronic lymphocytic leukemia. It is the 2-fluoro, 5' phosphate derivative of 9-beta-D-arabinofuranosyl adenine (ara-A, vidarabine) and the mechanism of action is through inhibition of DNA synthesis and the cytolytic effects through the induction of endonuclease-independent apoptosis.

Transtornos del sueño no respiratorios

Una adecuada higiene del sueño y el empleo cuidadoso de agentes farmacológicos permiten por lo general controlar los insomnios de corto plazo. Otras causas de sueño no reparador y de somnolencia excesiva durante el día necesita una evaluación más a fondo