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Association between lung function, hypertension and blood pressure medication

Several studies showed an association between lung function and hypertension. However, it must be considered that antihypertensive treatment might have an effect on lung function, too. So far, this potential effect of antihypertensive medication on lung function has been investigated mainly in patients with already existing pulmonary diseases. Thus, the aim of this analysis was to determine whether hypertension and its medical treatment are associated with lung function impairment in a general adult population.

Methods : Within the cross-sectional study ECRHS-I Erfurt 1158 adults aged between 20 and 65 years performed lung function tests and blood pressure measurements. Additionally, information on anthropometric measurements, sociodemographic characteristics and medical history was available. Multivariate regression models were applied to study the association between lung function, blood pressure and antihypertensive treatment.

Results : The combination of high blood pressure and the use of antihypertensive medication had the strongest negative effect on lung function. Thus, it was associated with a deterioration in FEV1 of −150ml (p=0.01) and in FVC of −190ml (p<0.01). When using both high blood pressure and antihypertensive medication as individual variables in one regression model, only medication decreased FEV1 and FVC significantly (each p<0.01).

Conclusions : We speculate that high blood pressure in combination with antihypertensive treatment and not HBP itself might be associated with reduced lung function in a general adult population. Nevertheless, it must be considered that antihypertensive medication might just be an indicator for very high blood pressure.

Indacaterol once-daily provides superior efficacy to salmeterol twice-daily in COPD: A 12-week study

 

Indacaterol is a novel, inhaled once-daily ultra-long-acting β2-agonist for the treatment of COPD.

Methods

This 12-week randomised, parallel-group study compared the efficacy of indacaterol 150 μg once-daily to salmeterol 50 μg twice-daily in patients with moderate-to-severe COPD. Assessments included FEV1 standardised area under curve (AUC) from 5 min to 11 h 45 min at Week 12 (primary endpoint), 24-h trough FEV1 (mean of 23 h 10 min and 23 h 45 min post-dose) at Week 12 (key secondary endpoint), FEV1 and FVC measured over 24-h, transition dyspnoea index (TDI) and rescue medication use.

Results

Of 1123 patients randomised 92.1% completed. Mean ± SD age was 62.8 ± 8.78 years, post-bronchodilator FEV1 51.8 ± 12.32% predicted, FEV1/FVC 50.6 ± 9.54%. At Week 12, FEV1 AUC5 min–11 h 45 min for indacaterol was statistically superior (p < 0.001) to salmeterol (adjusted mean difference [95% CI] 57 [35, 79] mL), as was 24-h trough FEV1 (60 [37, 83] mL, p < 0.001). Indacaterol also showed statistical superiority over salmeterol in terms of FEV1 and FVC measured over 24-h at Week 12. For TDI at Week 12, the mean total score was statistically superior for indacaterol versus salmeterol (difference 0.63 [0.30, 0.97], p < 0.001), as was the percentage of patients with a clinically relevant (i.e., ≥1 point) change from baseline (69.4% vs 62.7%, p < 0.05). For rescue medication, patients on indacaterol used fewer puffs/day (difference −0.18 [–0.36, 0.00] puffs/day, p < 0.05) and had a greater percentage of days with no rescue use (difference 4.4 [0.6, 8.2], p < 0.05).

Conclusion

Once-daily indacaterol provided statistically superior bronchodilation with an improvement in breathlessness and rescue use compared with twice-daily salmeterol.

 

Lung volumes and emphysema in smokers with interstitial lung abnormalities.

Cigarette smoking is associated with emphysema and radiographic interstitial lung abnormalities. The degree to which interstitial lung abnormalities are associated with reduced total lung capacity and the extent of emphysema is not known.

Smoking and subclinical interstitial lung disease.

The relationships between cigarette smoking and heart disease, lung cancer, and chronic obstructive pulmonary disease (COPD) are well known; in contrast, the topic of the relationship between smoking and interstitial lung disease is almost obscure. Despite its lack of a public persona, this relationship is important, since smoking plays a key role in the pathobiology of several interstitial lung diseases — respiratory bronchiolitis, desquamative interstitial pneumonia, pulmonary Langerhans'-cell histiocytosis, and perhaps idiopathic pulmonary fibrosis ...

Dietary sodium manipulation and asthma.

Background : There is a wide geographical variation in the prevalence of asthma and observational studies have suggested that dietary sodium may play a role.
Objectives To assess the effect of dietary sodium manipulation on asthma control.

Search strategy : We carried out a search using the Cochrane Airways Group asthma register. We searched the bibliographies of included randomised controlled trials (RCTs) for additional studies. We carried out the most recent search in November 2010.

Selection criteria : We considered only RCTs that involved dietary sodium reduction or increased sodium intake in patients with asthma.

Data collection and analysis : Both review authors assessed study and extracted data. We conducted data analyses in RevMan 5 using mean differences and random effects.

Main results : We identified a total of nine studies in relation to sodium manipulation and asthma, of which five were in people with asthma (318 participants), and four in people with exercise-induced asthma (63 participants). There were no significant benefits of salt restriction on the control of asthma. There was some evidence from the exercise-induced asthma studies that a low sodium diet may improve lung function after exercise and possibly baseline lung function, but this is based on findings from a very small numbers of participants.

Conclusions : This review did not find any evidence that dietary sodium reduction significantly improves asthma control. Although dietary sodium reduction may result in improvements in lung function in exercise-induced asthma, the clinical significance of this effect is unclear.

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