The aim of the study is to demonstrate a basic mechanism that supports our hypothesis: Does increased respiratory function after administration of a bronchodilator in patients with COPD lead to elevated pulmonary retention of the harmful compounds…
ID
Source
Brief title
Condition
- Cardiac disorders, signs and symptoms NEC
- Bronchial disorders (excl neoplasms)
- Arteriosclerosis, stenosis, vascular insufficiency and necrosis
Synonym
Research involving
Sponsors and support
Intervention
Outcome measures
Primary outcome
1. The fraction of cigarette smoke particles and constituents retained in the
lungs related to the (changed) lungfunction.
2. The concentration of certain biomarkers associated with cardiovascular
dysfunction and risk, related to the (changed) lungfunction.
Secondary outcome
not applicable
Background summary
COPD currently is one of the most frequent diseases. In more than 90% of COPD
patients, the disease is caused by smoking. About half of the COPD patients are
active smokers, although smoking is also the most important prognostic factor.
Also, smoking is an important cause as well as an important prognostic factor
in cardiovascular disease. The corner stone of medical treatment in COPD is
bronchodilation; more than half of the patients use a long-acting
bronchodilator. Recently, several studies suspect a possible relation between
these long-acting agents and cardiovascular disease. Surprising however, no
studies are done to investigate the interaction between the most important
prognostic factor (smoking) and the most important treatment (bronchodilation).
An increase of the pathogenic effect of smoking by an increased longfunction
after bronchodilation is likely though, since more pathogenic particles would
penetrate the lung parenchym. This mechanism would thereby negatively affect
smoking-related morbidity, especially cardiovascular disease. Therefore, our
hypothesis is that long-acting bronchodilators increase cardiovascular disease
in COPD patients who smoke.
Study objective
The aim of the study is to demonstrate a basic mechanism that supports our
hypothesis: Does increased respiratory function after administration of a
bronchodilator in patients with COPD lead to elevated pulmonary retention of
the harmful compounds in inhaled cigarette smoke and to short-term biological
effects associated with cardiovascular disease?
Study design
A randomised doubleblinde crossover intervention study of a cohort in a
laboratory setting.
Intervention
Patients recieve whether a bronchodilator or a placebo twice, preceded and
followed by repeatedly inhaling cigarette smoke during two hours as by a strict
time schedule.
Study burden and risks
The interventions of the experiment do not essentially differ from the home
situation. The burden of the experiment is mainly based on spended time of the
patient and possibly on an experienced nuisance by the venapuncture.
Venapuncture is a wide accepted and applied action. The risk is reasonably
neglectable since it is only caused by the relative harmless risks of
venapuncture, that may cause a hematoma or slight bleeding.
Postbus 9101
6500 HB Nijmegen
Nederland
Postbus 9101
6500 HB Nijmegen
Nederland
Listed location countries
Age
Inclusion criteria
active cigarette smoker
COPD gold klasse II-III
Exclusion criteria
not mastering the Dutch language
not capable of following technical instructions
not willing to withheld from smoking and bronchodilation for a certain time before the study
recent exacerbation within the last 2 weeks before the experiment
asthmatic component
Design
Recruitment
Medical products/devices used
Followed up by the following (possibly more current) registration
No registrations found.
Other (possibly less up-to-date) registrations in this register
No registrations found.
In other registers
| Register | ID |
|---|---|
| CCMO | NL25227.091.09 |