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Overlap syndrome: Additive effects of COPD on the cardiovascular damages in patients with OSA

Publication year: 2012
Source:Respiratory Medicine

Kazuki Shiina, Hirofumi Tomiyama, Yoshifumi Takata, Masanobu Yoshida, Kota Kato, Yosuke Nishihata, Chisa Matsumoto, Mari Odaira, Hirokazu Saruhara, Yuki Hashimura, Yasuhiro Usui, Akira Yamashina

The chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) have been recently much focused as independent risks for cardiovascular disease. Furthermore, the complication of both has a worse prognosis compared with patients with only one of these diseases. However, the details of the underlying mechanisms of this worsened prognosis have not been clear. The cross-sectional study was conducted to examine whether the overlap of COPD augment the increase in arterial stiffness in subjects with OSA. If so, we examined the exaggeration of nocturnal hypoxemia and its related inflammation are related to this augmentation of increased arterial stiffness. In 524 male subjects with OSA diagnosed by polysomnography (apnea–hypopnea index >5/h) (52 ± 14 years old), the forced expiratory volume at 1 s/the forced vital capacity (FEV1/FVC) ratio, brachial-ankle pulse wave velocity (baPWV), blood C-reactive protein (CRP) and B-natriuretic peptide (BNP) levels were measured. The prevalence rate of COPD was 12% in this study subjects. Plasma BNP levels and the crude (median value, 17.2 vs. 14.1 m/s, p < 0.01) and adjusted value of baPWV were significantly higher in subjects with overlap syndrome than in those with OSA alone. However, parameters of nocturnal hypoxemia and serum CRP levels were similar between both groups. Thus, the overlap of COPD in patients with OSA augments increase in arterial stiffness without the exaggeration of nocturnal hypoxemia and inflammation. Even so, this augmentation may partially contribute to the increased cardiovascular risk in the overlap syndrome.




Effects of CPAP on systemic hypertension in OSAH: A monocentric, observational, cohort study

Publication year: 2012
Source:Respiratory Medicine

Paolo Bottini, Luigi Taranto-Montemurro, Mauro Novali, Michela Bettinzoli, Elisa Roca, Chiara Andreoli, Maurizio Bentivoglio, Luciano Corda, Claudio Tantucci

Background Obstructive sleep apnea-hypopnea (OSAH) is a risk factor for development of systemic arterial hypertension (SAH) and can worse the control of established SAH. We investigated the effects of long-term continuous positive airway pressure (CPAP) treatment in controlling and preventing SAH in a large cohort of subjects referred for sleep study for suspected OSAH. Methods In 495 subjects of whom 422 with OSAH and 73 without OSAH, the clinical history was obtained, arterial blood pressure was measured and the current anti-hypertensive drugs was recorded at diagnosis and/or at CPAP start. Subjects were interviewed after a follow-up period of (mean ± SD) 3.4 ± 2.2 yr (range 1–8 yr) and divided in patients with moderate-to-severe OSAH (n = 125) who referred to use CPAP regularly for at least 4 h every night (group 1), with moderate-to-severe OSAH (n = 70) who refused or abandoned the CPAP treatment after few weeks (group 2), with mild OSAH (n = 227) with no CPAP indication (group 3) and simple snorers or normals (n = 73) (group 4). For each group clinical status, BMI, and changes in SAH therapy and occurrence of SAH were assessed at the follow-up. Results At the follow-up, a higher risk of increasing treatment for SAH was found for group 2 and group 3 versus group 1 (OR = 5, 95%CI 1–20, p < 0.01 and OR = 3, 95%CI 1–10, p < 0.05), respectively. The occurrence of SAH was lower (p < 0.001) in the group 1 (1.9%), vs group 2 (35.9%), 3 (21.1%) and 4 (18.6%). Conclusions In moderate-to-severe OSAH patients, long-term CPAP treatment significantly reduces the development of SAH and, in those with SAH at baseline, the need of anti-hypertensive drugs.




Identifying patients at risk of late recovery (≥8 days) from acute exacerbation of chronic bronchitis and COPD

Publication year: 2012
Source:Respiratory Medicine

Antonio Anzueto, Marc Miravitlles, Santiago Ewig, Delfino Legnani, Stephanie Heldner, Kathrin Stauch

Objectives To identify factors associated with late recovery (≥8 days from exacerbation start) in patients with acute exacerbations of chronic bronchitis/COPD (AECB/AECOPD). Methods An international, observational, non-interventional study in outpatients with AECB/AECOPD who received treatment for their exacerbation with the antibiotic moxifloxacin. Factors analyzed for late recovery included patient demographic characteristics, geographic region and disease severity. Additionally, logistic regression analysis was undertaken to identify factors associated with late recovery. Results The analysis population was 40,435 patients aged ≥35 years, from Asia-Pacific, Europe, the Americas and Middle East/Africa. Most were male (63.1%), mean age 60.4 years and current or ex-smokers (60.6%) with history of ≥2 exacerbations in the previous year. Patients who underwent spirometry (n = 6408, 19.7%) had moderate airflow obstruction (mean FEV1 1.7 L). Both clinicians and patients reported that moxifloxacin provided clinical improvement in a mean of 3 days and recovery in 6 days. Clinical factors significantly associated with late recovery were: age ≥65 years, duration of chronic bronchitis >10 years, cardiac comorbidity, >3 exacerbations in the previous 12 months, current exacerbation type (Anthonisen I/II) and hospitalization in the last 12 months. Conclusions In a large cohort of patients, all treated with the same antibiotic for an exacerbation of chronic bronchitis or COPD, the main factors associated with late recovery (≥8 days) were: older age, history of frequent exacerbations, current exacerbation type of Anthonisen I/II, history of prior hospitalizations and cardiac comorbid conditions.




Smoking cessation and the risk of hospitalization for pneumonia

Publication year: 2012
Source:Respiratory Medicine, Volume 106, Issue 7

Laura M. Cecere, Emily C. Williams, Haili Sun, Chris L. Bryson, Brendan J. Clark, Katharine A. Bradley, David H. Au

Background Smoking increases the risk of hospitalization for pneumonia, yet it is unknown if smoking cessation changes this risk. We sought to determine if smoking cessation and the duration of abstinence from tobacco reduce the risk of pneumonia hospitalization. Methods We performed secondary analysis of data collected from male United States Veterans participating in a randomized trial. We used Cox proportional-hazard models to estimate risk of hospitalization for pneumonia within one year of enrollment. We adjusted for confounders, including: demographics, comorbidity, alcohol use, prior pneumonia, inhaled corticosteroid use, and intensity of tobacco exposure. Among a restricted cohort excluding never smokers, we assessed for effect modification by a diagnosis of chronic obstructive pulmonary disease (COPD). Results Of the 25,235 participants, we identified 6720 current, 13,625 former, and 4890 never smokers. Compared to current smokers, never smokers had a decreased (adjusted HR 0.48, 95% CI 0.31–0.74), while former smokers had no difference in (adjusted HR 0.83, 95% CI 0.63–1.09) risk of hospitalization for pneumonia. Among participants without COPD, former smokers had a lower risk of hospitalization (adjusted HR 0.65, 95% CI 0.45–0.95). However, this lower risk was isolated to those who quit tobacco more than 10 years previously (adjusted HR 0.62, 95% CI 0.41–0.93). Among those with COPD, there was no difference in risk with smoking cessation or duration of remaining tobacco-free. Conclusions Tobacco cessation is likely important in reducing hospital admissions for pneumonia, but its benefit depends on duration of smoking cessation and is likely attenuated in the presence of COPD.




Obstructive sleep apnea does not promote esophageal reflux in fibrosing interstitial lung disease

In patients with fibrosing interstitial lung disease (fILD), gastroesophageal reflux (GER) is highly prevalent, perhaps because of the effects of lung fibrosis on altering intrathoracic pressure, diaphragm morphology and lower esophageal sphincter (LES) function. For unclear reasons, obstructive sleep apnea (OSA) is also highly prevalent among patients with fILD.

We conducted this study to test our hypothesis that, in patients with fILD, OSA would exacerbate diaphragm/LES dysfunction and increase the propensity for—and severity of – GER.

Methods : We identified patients with fILD who underwent screening polysomnogram and pH or pH/impedence probe at our center during the same week. We examined the association between OSA and GER and used logistic regression to determine independent predictors of OSA or GER.

Results : In 54 included subjects, neither OSA (dichotomous) nor apnea hypopnea index (continuous) predicted the presence of GER. Regardless of body position (upright, recumbent), GER was no more frequent or severe among subjects with OSA vs. those without OSA. Subjects with idiopathic pulmonary fibrosis (IPF) had an odds of GER nearly seven-fold greater than subjects with other forms of fILD (odds ratio = 6.84, 95% confidence interval 1.36–34.43, p = 0.02). For the entire cohort and the subgroup with IPF, there was no correlation between pulmonary physiology and GER.

Conclusions : In fILD, OSA does not appear to promote GER. Research is needed to determine if compensatory mechanisms emanating from the crural diaphragm prevent GER in fILD patients with OSA and to sort out whether GER has a role in the pathogenesis of certain forms of fILD.

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