Ignite Creation Date:
2024-05-05 @ 10:23 AM
Last Modification Date:
2024-10-26 @ 9:01 AM
Study NCT ID:
NCT00000568
Status:
COMPLETED
Last Update Posted:
2016-04-14
First Post:
1999-10-27
Brief Title:
Lung Health Study LHS I and III
Sponsor:
National Heart Lung and Blood Institute NHLBI
Organization:
National Heart Lung and Blood Institute NHLBI
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2005-08
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
In the Lung Health Study I to determine the effects of Special Care compared to Usual Care on rate of decline in pulmonary function in a group of cigarette smokers identified as having mild abnormalities in pulmonary function
In the Lung Health Study III to determine the long-term effects of smoking cessation and continued smoking on cardiopulmonary morbidity mortality and the rate of decline in the one second forced expiratory volume FEV1 in men and women with early chronic obstructive lung disease who have been followed prospectively for 12 to 15 years
In the Lung Health Study III to determine the long-term effects of smoking cessation and continued smoking on cardiopulmonary morbidity mortality and the rate of decline in the one second forced expiratory volume FEV1 in men and women with early chronic obstructive lung disease who have been followed prospectively for 12 to 15 years
Detailed Description:
BACKGROUND
Chronic obstructive pulmonary disease COPD is a major cause of mortality and morbidity in the United States affecting nearly 10 million persons COPD accounts for 60000 deaths yearly and ranks as the fourth leading cause of death If current trends continue it may become the nations fourth or even third leading cause of death by the year 2000
Epidemiological studies consistently indicated that smoking was the over-whelming risk factor for accelerated decline in pulmonary function and subsequent development of COPD Furthermore evidence from several studies indicated that the rate of decline in pulmonary function approached a more normal rate of decline upon cessation of cigarette smoking
Another presumed risk factor for accelerated decline in pulmonary function was the presence of hyperreactive airways although it was not clear whether the mere presence of hyperreactive airways contributed to the accelerated decline or whether the decline resulted from the reaction of the airways to various irritants over a long period of time It is possible that if the hyperreactive airway was kept non-reactive by pharmacological means over a period of years the expected abnormal decline might be lessened This effect might be enhanced by the cessation of cigarette smoking
Although the evidence was strong that smoking and hyperreactive airways were risk factors for COPD it had not been demonstrated whether removal of risk factors at a stage when mild dysfunction had already occurred would effectively modify the course of COPD
DESIGN NARRATIVE
Lung Health Study I
Randomized and controlled Cigarette smokers with evidence of airways obstruction underwent baseline testing that included spirometric responses to isoproterenol and methacholine and were then randomly assigned to one of three groups a no intervention or usual care group a group receiving a smoking cessation program and bronchodilator therapy a group receiving a smoking cessation program and a placebo bronchodilator The placebobronchodilator therapy was double-blind The smoking intervention consisted of an intensive 12-session smoking cessation program combining behavior modification and use of nicotine gum with a continuing five-year maintenance program to minimize relapse The bronchodilator consisted of ipratropium bromide prescribed three times daily two puffs per time from a metered-dose inhaler All groups were followed yearly for five years The primary endpoint was the rate of change of FEV1 Respiratory morbidity was a secondary endpoint Recruitment began in November 1986 and was completed in January 1989 The clinical phase of the trial ended in April 1994 The study continues under contract N01-HR-46002 through September 2004 for data analysis and dissemination of research results
Lung Health Study III
Beginning in fiscal year 1998 all surviving participants of LHS I are invited to participate in the long-term followup The study will determine using an intent-to-treat analysis whether the LHS I smoking intervention significantly reduces the incidence of clinically important respiratory and cardiovascular disease over a 12- to 15-year period following study enrollment The study will also estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality after controlling for smoking history Studies will be conducted on the role of other factors such as gender airways reactivity weight gain and co-morbidities in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality A determination will also be made as to whether the improvement in lung function and reduction in respiratory symptoms associated with smoking cessation result in improved health-related quality of life HRQL and less depression over an extended follow-up period The LHS III an investigator initiated long-term follow-up study is not an NIH- defined clinical trial
Chronic obstructive pulmonary disease COPD is a major cause of mortality and morbidity in the United States affecting nearly 10 million persons COPD accounts for 60000 deaths yearly and ranks as the fourth leading cause of death If current trends continue it may become the nations fourth or even third leading cause of death by the year 2000
Epidemiological studies consistently indicated that smoking was the over-whelming risk factor for accelerated decline in pulmonary function and subsequent development of COPD Furthermore evidence from several studies indicated that the rate of decline in pulmonary function approached a more normal rate of decline upon cessation of cigarette smoking
Another presumed risk factor for accelerated decline in pulmonary function was the presence of hyperreactive airways although it was not clear whether the mere presence of hyperreactive airways contributed to the accelerated decline or whether the decline resulted from the reaction of the airways to various irritants over a long period of time It is possible that if the hyperreactive airway was kept non-reactive by pharmacological means over a period of years the expected abnormal decline might be lessened This effect might be enhanced by the cessation of cigarette smoking
Although the evidence was strong that smoking and hyperreactive airways were risk factors for COPD it had not been demonstrated whether removal of risk factors at a stage when mild dysfunction had already occurred would effectively modify the course of COPD
DESIGN NARRATIVE
Lung Health Study I
Randomized and controlled Cigarette smokers with evidence of airways obstruction underwent baseline testing that included spirometric responses to isoproterenol and methacholine and were then randomly assigned to one of three groups a no intervention or usual care group a group receiving a smoking cessation program and bronchodilator therapy a group receiving a smoking cessation program and a placebo bronchodilator The placebobronchodilator therapy was double-blind The smoking intervention consisted of an intensive 12-session smoking cessation program combining behavior modification and use of nicotine gum with a continuing five-year maintenance program to minimize relapse The bronchodilator consisted of ipratropium bromide prescribed three times daily two puffs per time from a metered-dose inhaler All groups were followed yearly for five years The primary endpoint was the rate of change of FEV1 Respiratory morbidity was a secondary endpoint Recruitment began in November 1986 and was completed in January 1989 The clinical phase of the trial ended in April 1994 The study continues under contract N01-HR-46002 through September 2004 for data analysis and dissemination of research results
Lung Health Study III
Beginning in fiscal year 1998 all surviving participants of LHS I are invited to participate in the long-term followup The study will determine using an intent-to-treat analysis whether the LHS I smoking intervention significantly reduces the incidence of clinically important respiratory and cardiovascular disease over a 12- to 15-year period following study enrollment The study will also estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality after controlling for smoking history Studies will be conducted on the role of other factors such as gender airways reactivity weight gain and co-morbidities in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality A determination will also be made as to whether the improvement in lung function and reduction in respiratory symptoms associated with smoking cessation result in improved health-related quality of life HRQL and less depression over an extended follow-up period The LHS III an investigator initiated long-term follow-up study is not an NIH- defined clinical trial
Study Oversight
Has Oversight DMC:
Is a FDA Regulated Drug?:
Is a FDA Regulated Device?:
Is an Unapproved Device?:
Is a PPSD?:
Is a US Export?:
Is an FDA AA801 Violation?: