Acute Effect of Pulmonary Desufflation on Cardiac Performance in COPD Patients

Summary

Chronic Obstructive Pulmonary disease (COPD) is one of the major clinical entities that causes thousands of deaths every year all over the world and weights a lot on the health care system of every country in terms of direct and indirect costs. The physiopathological modifications that characterise COPD are represented by irreversible (sometimes partially reversible) airflow obstruction, and bronchiolar inflammation. Lungs that develop emphysema lack of elastic recoil and imply increased resistances and airflow obstruction due to loss of lung parenchyma and supporting elastic structures. All these modifications produce air trapping and so lung hyperinflation. The latter is precisely the cause of the symptoms and particularly dyspnoea which is often heavily perceived by COPD patients and that drives to the limitation of daily activities. Lung hyperinflation and the other alterations that occur in COPD imply gas retention and increase in pulmonary vascular resistances. Considering that the rib cage has limited elastic properties, the effects of gas trapping and lung parenchymal damage on mediastinum and particularly on heart mechanics is indisputable. Together with alveolar hypoxia, lung hyperinflation is responsible for the development, as the disease progresses, of the cor pulmonale. Tha latter causes pulmonary hypertension and increased mechanic load during right heart chambers contraction and relaxation. Those alterations may effect left heart chambers too.

Airflow obstruction in COPD is usually treated by inhaled bronchodilators and corticosteroids. The main and most used bronchodilators are represented by beta 2 agonists (short, long and ultra-long acting) and anticholinergic inhalatory drugs, which can be also short, long and ultra long acting. Among ultra long acting beta 2 agonists, indacaterol is characterised by quick onset of action (5 minutes), and guarantees an effective bronchodilation duration of 24 hours. It is also known that it has an important effect on reducing lung hyperinflation decreasing residual volume and consequently allowing an increase of inspiratory capacity. The purpose of our study is to evaluate the effects of indacaterol on lung hyperinflation in COPD subjects of any stage and with lung air trapping, and the consequent potential effects on heart performance evaluated by cardiac trans thoracic echo color doppler.

Conditions

• COPD
• Hyperinflation
• Right Cardiac Failure

Interventions

DRUG

Indacaterol Fumarate

150 mcg inhalation powder, hard capsules, once daily

DRUG

Placebo

Fructose, dry inhalation powder, hard capsules via breezhaler

Sponsors & Collaborators

• Fondazione Salvatore Maugeri

  collaborator OTHER

• University of Milan

  lead OTHER

Principal Investigators

• Pierachille Santus, Md, PhD · Università degli Studi di Milano-Pneumologia Riabilitativa-Fondazione Salvatore Maugeri-MILANO

Study Design

Allocation

RANDOMIZED

Purpose

BASIC_SCIENCE

Masking

DOUBLE

Model

PARALLEL

Eligibility

Min Age

50 Years

Max Age

85 Years

Sex

ALL

Healthy Volunteers

No

Timeline & Regulatory

Start

2013-11-30

Primary Completion

2014-10-31

Completion

2014-10-31

Countries

• Italy

Study Locations