Long-term effectiveness of CPAP in patients with severe obesity-hypoventilation syndrome.

PURPOSE: The optimal mode of long-term positive airway pressure (PAP) treatment for obesity-hypoventilation syndrome (OHS) is not clear. The objectives of this study were to analyze whether or not patients with severe OHS treated with continuous positive airway pressure (CPAP) remained controlled with this therapy over the long term and to investigate which variables were associated with CPAP failure and the need to switch to non-invasive ventilation (NIV). METHODS: In a retrospective single-center study, patients admitted to the hospital because of severe OHS between 1996 and 2015 were analyzed. A multiple regression analysis was performed in order to determine which variables were associated with either CPAP success or failure to maintain long-term control. RESULTS: Of 126 consecutive patients, 115 accepted long-term PAP treatment. CPAP or NIV treatment was prescribed according to a protocol that included overnight polysomnographic PAP titration. Follow-up time was 8.0 ± 4.8 years. At the end of this period, 29% of CPAP-treated patients had been re-assigned to NIV because of recurrence of global respiratory failure. High levels of obesity, weight gain, lower FEV1/FVC values and the need for nocturnal supplementary oxygen independently predicted CPAP failure. CONCLUSION: CPAP therapy for severe OHS in patients who have these risk factors should be closely monitored in the long-term for possible treatment failure.

Pronóstico del síndrome de hipoventilación-obesidad con y sin síndrome de apnea obstructiva asociado / Prognosis of Obesity Hypoventilation Syndrome With and Without Concomitant Obstructive Sleep Apnea Syndrome

No disponible

Obesity-hypoventilation syndrome: increased risk of death over sleep apnea syndrome.

AIM: To study whether mortality and cardiovascular morbidity differ in non-invasive ventilation (NIV)-treated patients with severe obesity-hypoventilation syndrome (OHS) as compared with CPAP-treated patients with obstructive sleep apnea syndrome (OSAS), and to identify independent predictors of mortality in OHS. MATERIAL AND METHODS: Two retrospective cohorts of OHS and OSAS were matched 1:2 according to sex, age (± 10 year) and length of time since initiation of CPAP/NIV therapy (± 6 months). RESULTS: Three hundred and thirty subjects (110 patients with OHS and 220 patients with OSAS) were studied. Mean follow-up time was 7 ± 4 years. The five year mortality rates were 15.5% in OHS cohort and 4.5% in OSAS cohort (p< 0.05). Patients with OHS had a 2-fold increase (OR 2; 95% CI: 1.11-3.60) in the risk of mortality and 1.86 fold (OR 1.86; 95% CI: 1.14-3.04) increased risk of having a cardiovascular event. Diabetes, baseline diurnal SaO2 < 83%, EPAP < 7 cmH2O after titration and adherence to NIV < 4 hours independently predicted mortality in OHS. CONCLUSION: Mortality of severe OHS is high and substantially worse than that of OSAS. Severe OHS should be considered a systemic disease that encompasses respiratory, metabolic and cardiovascular components that require a multimodal therapeutic approach.

Prognostic value of walk distance, work, oxygen saturation, and dyspnea during 6-minute walk test in COPD patients.

BACKGROUND: Distance walked during the 6-min walk test (6MWT) predicts mortality in COPD. The body weight of the patient affects the work required to walk. Calculated work during the 6MWT (6MWT work) may account for differences in walk distance resulting from change in body weight. Thus, 6MWT work might be a better predictor of mortality than distance walked. This study was designed to test this hypothesis and to assess if other variables measured during the 6MWT, like continuous oximetry recording, offered additional prognostic information. METHODS: This was a retrospective analysis of prospectively collected data; 104 COPD patients were studied. 6MWT was performed in all cases. 6MWT work was calculated as body weight (in kg) × distance walked (in m). Receiver operating characteristic curves were used to assess the value of variables to predict mortality. Additional analysis was performed using Kaplan-Meier survival plots and Cox proportional hazards regression models. RESULTS: Mean follow-up was 590 ± 472 d. Eleven subjects (10.6%) died. 6MWT work was not better than distance walked to predict mortality (area under the curve 0.77 for 6MWT work vs 0.80 for distance; difference 0.03, 95% CI -0.05 to 0.12, P = .45). Subjects who died had more dyspnea (measured using the Borg scale) after the 6MWT (8.5 vs 4.0, P < .001), lower baseline SpO2 (85% vs 93%, P = .001), worse oxygen saturation during the 6MWT (mean SpO2 while walking 74.0% vs 86.6%, P = .02) and walked less distance (255 m vs 480 m, P = .001). On multivariate analysis, only 6MWT distance and dyspnea after the test correlated independently with mortality (P = .005 for both variables). CONCLUSIONS: 6MWT work was not more useful than 6MWT distance to predict mortality. The study confirms that 6MWT distance and dyspnea on exertion are key elements in prognostic evaluation in COPD, while the value of exercise oxygen desaturation is less clear.

Electrocardiogram score predicts severity of pulmonary embolism in hemodynamically stable patients.

BACKGROUND: Risk stratification of patients with pulmonary embolism (PE) is essential to guide therapy. The presence of right ventricle dysfunction (RVD) and the anatomic extent of PE have been suggested to predict clinical course. The aim of this study was to assess the ability of an electrocardiogram (ECG) scoring system to predict RVD or the clot load score in normotensive patients with PE. METHODS: Consecutive patients presenting to the emergency room with PE and hemodynamic stability were prospectively included. ECG, echocardiography and computed tomography pulmonary angiography (CTPA) were performed on all patients. RESULTS: A total of 103 patients were studied. ECG score correlated significantly with the clot load score (r = 0.41, 95% confidence interval [CI]: 0.22-0.57, P < 0.001), systolic pulmonary artery pressure (r= 0.31, 95% CI: 0.09-0.49, P = 0.006), pulmonary artery diameter (r = 0.28, 95% CI: 0.07-0.47, P = 0.011) and right ventricle to left ventricle ratio, both measured with echocardiography (r = 0.42, 95% CI: 0.22-0.57, P < 0.001) and with CTPA (r= 0.36, 95% CI: 0.13-0.56, P = 0.004). Area under the receiver operating characteristic curve for detecting RVD was 0.82 (95% CI: 0.72-0.89). Interobserver agreement regarding ECG score was substantial (κ = 0.80). CONCLUSIONS: ECG score correlates with the severity of PE in hemodynamically stable patients. It is potentially useful for risk-stratification strategies in this setting.

Comparison of tinzaparin and acenocoumarol for the secondary prevention of venous thromboembolism: a multicentre, randomized study.

The objective of the present study was to evaluate the efficacy, safety and healthcare resource utilization of long-term treatment with tinzaparin in symptomatic patients with acute pulmonary embolism as compared to standard therapy. In this open-label trial, 102 patients with objectively confirmed pulmonary embolism were randomized to receive, after initial treatment with tinzaparin, either tinzaparin (175 IU/kg/day) or international normalized ratio-adjusted acenocoumarol for 6 months. Clinical endpoints were assessed during the 6 months of treatment. A pharmacoeconomic analysis was carried out to evaluate the cost of the long-term treatment with tinzaparin in comparison with the standard one. In an intention-to-treat analysis, one of 52 patients developed recurrent venous thromboembolism in the tinzaparin group compared with none of the 50 patients in the acenocoumarol group. One patient in each group had a major haemorrhagic complication. Six patients in the acenocoumarol group had minor bleeding compared with none in the tinzaparin group (P = 0.027). Median hospital length of stay was shorter in the tinzaparin group compared to the acenocoumarol group (7 versus 9 days; P = 0.014). When all the direct and indirect cost components were combined for the entire population, we found a slight, nonstatistically significant (mean difference €345; 95% CI 1382-2071; P = 0.69) reduction in total cost with tinzaparin. Symptomatic acute pulmonary embolism treatment with full therapeutic doses of tinzaparin for 6 months is a feasible alternative to conventional treatment with vitamin K antagonists.