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Chronic obstructive pulmonary disease (COPD) is characterized by poorly reversible airflow limitation, with an abnormal pulmonary and systemic inflammatory response to tobacco smoking. Systemic inflammation promotes atherosclerosis, to treat the complications of which beta-blockers are paramount. In the COPD setting, however, the use of beta-blockers has been limited by fears that they could adversely affect lung function. However, by controlling adrenergic drive and reducing the heart rate, beta-blockers could reduce the risk of arrhythmias and sudden death among COPD patients. Thus, beta-blocker use is strongly supported by evidence in COPD patients with history of myocardial infarction, but warrants consideration in other cardiovascular comorbidities. Studies specifically designed to ascertain the role of beta-blockers in patients with COPD with cardiovascular conditions are still needed, because the majority of the current evidence is based on retrospective observational studies.

Systemic sclerosis (SSc) is a connective tissue disorder of unknown etiology that is often complicated by pulmonary involvement, with pulmonary hypertension (PH) and interstitial lung disease (ILD) being the major causes of death. It has been suggested that the amount of nitric oxide (NO) in exhaled air may predict the onset of complications. The aim of the study was to measure exhaled NO in SSc patients and investigate its relationship with pulmonary involvement with and without PH.Fifty patients (5 men and 45 women; mean age, 59.1 +/- 11.7 years [+/- SD]) with a diagnosis of SSc based on the preliminary criteria of the American Rheumatism Association, and 40 healthy control subjects (5 men and 35 women; mean age, 58.3 +/- 12.2 years) underwent exhaled NO measurements by means of a chemiluminescence analyzer, pulmonary function tests, high-resolution thorax CT, and Doppler echocardiography.Exhaled NO concentrations were significantly higher in SSc patients than control subjects (p = 0.02), and significantly lower in the patients with ILD and/or PH than in those without PH (p0.01). There was a significant inverse correlation between pulmonary artery systolic pressure and exhaled NO concentration in all of the studied patients (r = - 0.5, p0.001).Our results indicate that exhaled air NO concentrations are lower in SSc patients with lung involvement than in those without, and that SSc patients without ILD or PH have higher exhaled NO values than healthy subjects.

The objective of this prospective, randomized, double-blind, placebo-controlled, multicenter parallel-group study was to evaluate the effect of long-term ambroxol treatment in preventing exacerbations of chronic obstructive pulmonary disease (COPD). Two hundred and forty-two outpatients with COPD defined by ATS criteria with value of FEV1 between > or =60 and 80% of predicted and history of one or more exacerbations in the previous year were recruited by 26 Respiratory Medicine Centers in Italy and treated for 1 year with one ambroxol retard capsule of 75 mg twice daily or placebo. The percentage of patients free from exacerbation at 6 months was 63% with ambroxol and 60% with placebo (p=0.366) and at 12 months 56% with ambroxol and 53% with placebo (p=0.363). In a subset of 45 patients with more severe baseline symptoms, ambroxol therapy was associated with a significant higher percentage of patients free from exacerbation compared to placebo: 63 vs. 38% (p=0.038). In conclusion, we did not find a significant difference between long-term ambroxol therapy and placebo, in preventing exacerbations in patients with COPD. In patients with more severe respiratory symptoms at baseline, however, we observed a significant difference in the cumulative exacerbation-free persistence between ambroxol and placebo, suggesting that long-term muco-regulatory therapy with ambroxol could be useful in highly symptomatic patients with COPD.

Study objectives: During a bronchial provocation test (BPT), the performance of maximal inspiratory-expiratory maneuvers, causing abrupt and marked shifts in intrathoracic pressure, may increase the risk of cardiac arrhythmias. Moreover, the inhalation of methacholine (MCh), a cholinergic agonist agent, could favor the development of unwelcome cardiovascular events, namely, cardiac arrhythmias. Subjects and methods: We studied the number and severity of cardiac arrhythmias by ECG-Holter monitoring before, during, and after BPTs with MCh challenge in a group of 46 consecutive nonselected subjects (28 men and 18 women) with clinical indications for BPT, without preexisting cardiovascular diseases, and not receiving arrhythmogenic drugs. The subjects performed a routine pulmonary function test (PFT), followed by BPT, during ECG-Holter monitoring. Determination of the serum potassium concentration, a baseline arterial blood gas analysis, and monitoring of oxyhemoglobin saturation also were performed. Results: We found no significant increase in the number of supraventricular and ventricular arrhythmias during the performance of PFTs and of BPTs with MCh in the subjects, either with or without bronchial hyperresponsiveness (BHR). However, during the performance of BPTs, we observed a significant reduction in mean heart rate. Conclusions: Our results indicate that the performance of PFTs and BPTs with MCh does not increase the cardiac arrhythmogenic risk in subjects without cardiovascular diseases, as well as in those with BHR, suggesting that these tests are safe to perform in most subjects.