Convergence of the epidemiology and pathology of COPD

The epidemiology of chronic obstructive pulmonary disease (COPD) has been dominated by one hypothesis stating that cigarette smoking and chronic bronchitis were the key to pathogenesis and another that asthma, chronic bronchitis, and even emphysema are related to different expressions of a primary airway abnormality. The first hypothesis was rejected in the late 1960s based on a longitudinal study of working men where only a fraction of smokers developed COPD and where development of COPD was independent of the absence or presence of chronic bronchitis. Chronic bronchitis in more advanced COPD was subsequently associated with a more rapid decline in lung function and more frequent exacerbations. The second hypothesis is more difficult to test but longitudinal studies have shown that the presence of bronchial hyperresponsiveness may predict the subjects who go on to develop COPD. This brief review attempts to reconcile these findings with the pathology found in the lung.     

Chronic lung disease in the Papua New Guinea Highlands.

In the Eastern Highlands of Papua New Guinea 46 men and 24 women with chronic lung disease underwent clinical and lung function investigations. In all cases the sole or predominant abnormality was irreversible airways obstruction, probably from chronic bronchitis with variable amounts of acompanying emphysema. There were close similarities to chronic obstructife lung disease in European populations in terms of symptoms, airways obstruction, transfer factor, and radiographic emphysema and inflammatory changes. Bronchiectasis and local fibrosis were present in a few subjects, but previous reports that pulmonary and pleural fibrosis are features of the disease were not confirmed. Possibly environmental and genetic factors may increase the associated blood gas disturbances leading to pulmonary hypertension. Unlike chronic obstructive lung disease in European populations, tobacco smoking is not an important aetiological factor. Although there is no direct evidence, the most likely possibilities are domestic wood smoke and acute chest infections.     

Relation of ventilatory impairment and of chronic mucus hypersecretion to mortality from obstructive lung disease and from all causes.

The relation of ventilatory impairment and chronic mucus hypersecretion to death from all causes and death from obstructive lung disease (chronic bronchitis, emphysema and asthma) was studied in 13,756 men and women randomly selected from the general population of the City of Copenhagen. During the 10 year follow up 2288 subjects died. In 164 subjects obstructive lung disease was considered to be an underlying or a contributory cause of death (obstructive lung disease related death); in 73 subjects it was considered to be the underlying cause of death (obstructive lung disease death). Forced expiratory volume in one second, expressed as a percentage of the predicted value (FEV1% pred), and the presence of chronic phlegm were used to characterise ventilatory function and chronic mucus hypersecretion respectively. For mortality analysis the proportional hazards regression model of Cox was used; it included age, sex, pack years, inhalation habit, body mass index, alcohol consumption, and the presence or absence of asthma, heart disease, and diabetes mellitus as confounding factors. By comparison with subjects with an FEV1 of 80% pred or more, subjects with an FEV1 below 40% pred had increased risk of dying from all causes (relative risk (RR) = 5.0 for women, 2.7 for men), a higher risk of obstructive lung disease related death (RR = 57 for women, 34 for men), and a higher risk of obstructive lung disease death (RR = 101 for women, 77 for men). Chronic mucus hypersecretion was associated with only a slightly higher risk of death from all causes (RR = 1.1 for women, 1.3 for men). The association between chronic mucus hypersecretion and obstructive lung disease death varied with the level of ventilatory function, being weak in subjects with normal ventilatory function (for an FEV1 of 80% pred the RR was 1.2), but more pronounced in subjects with reduced ventilatory function (for an FEV1 of 40% pred the RR was 4.2). A similar though statistically non-significant trend was observed with regard to obstructive lung disease related death. This study shows that impaired lung function is very strongly related to total mortality, obstructive lung disease related mortality, and obstructive lung disease mortality and suggests that chronic mucus hypersecretion, in those with impaired ventilatory function, is also a significant risk factor for death from obstructive lung disease.     

Mortality of adults with asthma: a prospective cohort study

BACKGROUND: Few studies have been published on the overall survival of adult patients with asthma. A cohort study was performed to assess the mortality from all causes, from chronic obstructive pulmonary disease, and from lung cancer among adult asthmatic subjects. METHODS: A population of 31,110 Finnish adult women and men, mostly twins, was studied to compare the 16 year mortality rates among asthmatic (n = 471) and non-asthmatic persons. A further 293 twin pairs, discordant for asthma, were also studied to determine whether the mortality of patients with asthma differs from that of their age matched siblings. RESULTS: Mortality from all causes was increased among asthmatic adults (age adjusted hazard ratios 1.49, 95% CI 1.09 to 2.05 for men and 1.53, 95% CI 1.10 to 2.13 for women), and mortality due to chronic obstructive pulmonary diseases was also significantly increased in asthmatic subjects. The risk of death due to lung cancer was increased in men with asthma (hazard ratio adjusted for smoking 3.19, 95% CI 1.39 to 7.31). The risk ratios found among twins discordant for asthma corresponded to those found in the whole cohort. CONCLUSIONS: Survival in adults with asthma is worse than in those without asthma. The excess deaths due to chronic obstructive pulmonary disease may explain some part of the increased mortality rates, but not all of it.


     

Unilateral lung transplantation as an effective therapy in primary lung emphysema

Unilateral lung transplantation is the treatment of choice for terminal restrictive lung disease. We report about three patients with end-stage pulmonary emphysema treated by single lung transplantation. All patients are alive 3, 6 and 7 months after the operation with good quality of life. Blood gases have normalized and lung function parameters have markedly improved. We conclude, that single lung transplantation can be an effective treatment for selected patients with end-stage obstructive lung diseases in the absence of chronic infections.     

Prevalence of chronic bronchitis in a rural community of the Hill Region of Nepal.

A house to house survey of everyone aged 20 years and above living in a rural community in the Hill Region of Nepal, situated about 16 km outside Kathmandu city, was conducted to determine the prevalence of chronic bronchitis and cor pulmonale. Of the total eligible population, 2826 (95.5%) were interviewed. Chronic bronchitis was diagnosed according to the British Medical Research Council criteria, and emphysema and cor pulmonale according to the World Health Organisation expert committee criteria. The crude prevalence of chronic bronchitis was found to be 18.3%. The prevalence rate of chronic bronchitis was similar in men and women, whereas in most parts of the world much lower rates have been recorded in women. Study of a random sample of 85 individuals with chronic bronchitis showed that 57.4% had evidence of airways obstruction, whereas 15.8% of a representative sample (n = 111) of the surveyed population (excluding those with chronic bronchitis) showed evidence of airway obstruction. Of 516 subjects diagnosed as having chronic bronchitis, 382 were subsequently investigated in hospital, 134 having declined further investigation. The diagnosis was confirmed in most of the patients (93.2%) who were investigated. Other diseases played an insignificant part in the production of the observed high prevalence rates of chronic bronchitis. Of the 382 patients studied in hospital, 87 had emphysema and 42 had cor pulmonale, yielding overall prevalence rates for these two conditions of at least 3.1% and at least 1.5% respectively.     

Childhood smoking is an independent risk factor for obstructive airways disease in women

OBJECTIVE: To assess whether starting to smoke in childhood increases the risk of obstructive airways disease (OAD) in adult life. METHODS: A retrospective cohort analysis was undertaken of 12 504 current and ex-smokers in the EPIC-Norfolk cohort. The main exposure was starting to smoke during childhood (age <16 years). Three definitions of OAD were used: doctor diagnosed asthma, doctor diagnosed bronchitis/emphysema, and "any OAD" (doctor diagnosed asthma or bronchitis/emphysema, or taking medication used in the treatment of OAD). RESULTS: Childhood smokers had significantly more pack years of exposure and poorer lung function than subjects who started to smoke in adulthood (>/=16 years). Compared with starting in adulthood, starting to smoke in childhood was associated with a greater risk of bronchitis/emphysema in female smokers (OR 1.79, 95% CI 1.25 to 2.56) and ex-smokers of both sexes (OR 1.29, 95% CI 1.07 to 1.55 in men and OR 1.40, 95% CI 1.05 to 1.85 in women), and of "any OAD" in female smokers (OR 1.72, 95% CI 1.24 to 2.38) and male and female ex-smokers (OR 1.20, 95% CI 1.03 to 1.40 in men and 1.34, 95% CI 1.07 to 1.57 in women). After adjustment for pack years, childhood smoking was associated with poorer lung function (FEV(1) 92.3% predicted in adult smokers and 89.5% in childhood smokers, p = 0.03) and a greater risk of bronchitis/emphysema (adjusted OR 1.55, 95% CI 1.08 to 2.24) and for "any OAD" (OR 1.54, 95% CI 1.10 to 2.13) in female smokers but not in male and female ex-smokers. CONCLUSION: Starting to smoke in childhood is associated with an increased risk of airways disease because of the extra pack years smoked. In women, childhood smoking is itself an independent risk factor for the development of airways disease.     

Management of the patient with emphysema,coronary artery disease,and lung cancer

Coronary artery disease, emphysema, and lung cancer often occur together and have cigarette smoking as a common etiologic contributor. The management of the patient with lung cancer, coronary artery disease, and emphysema is complex. The patient with significant coronary artery disease should undergo coronary artery bypass before or concurrently with pulmonary resection. Only proven carcinomas should be resected at the time of coronary artery bypass grafting because immunosuppression secondary to cardiopulmonary bypass can result in the life-threatening spread of fungal or other infections if biopsy is performed at the time of cardiopulmonary bypass. The risk of pulmonary resection is increased in the patient with emphysema because of decreased efficiency of the lungs and chest wall. Likewise, emphysema results in greater risk in the patient with coronary artery disease because of increased demands on the heart.     

Obstructive airways disease in surgical practice

Asthma and chronic obstructive pulmonary disease (COPD), i.e. chronic bronchitis and emphysema are common. The pathological and clinical features of these diseases are described. Ventilatory function, lung volumes and 6-min walking tests are used to assess respiratory function while blood gas estimations are essential when managing respiratory failure. The causal mechanisms of respiratory failure are described. In COPD careful assessment with maximization of respiratory function is essential preoperatively. Continued smoking increases postoperative complications sixfold. Bronchial irritability, common in asthma and COPD, increases the anaesthetic risks while many anaesthetic agents adversely affect respiratory function. Postoperative pulmonary complications remain common particularly in COPD. The hypoxia occurring in the first 2 hours post-surgery is usually more pronounced in COPD. Careful postoperative monitoring with aggressive treatment of any complications is essential in these patients. Surgical treatment may significantly improve respiratory function in some patients with bullous emphysema.     

Serum studies of leucocyte elastase in acute and chronic lung diseases.

Immunoreactive leucocyte elastase was measured in the serum of patients with chronic obstructive bronchitis. No evidence was found to demonstrate the release of this enzyme in the pulmonary circulation. However the average serum concentrations (573 . 0 micrograms/l; SD +/- 261 . 0) were higher (2p less than 0 . 001) in this group of patients than in age matched control subjects (355 . 2 micrograms/l; SD +/- 274 . 8). Further studies confirmed this finding but patients with other active lung diseases had similarly increased leucocyte elastase concentration in the serum. This suggests that a raised serum leucocyte elastase concentration is a feature of active lung diseases and not a feature of obstructive bronchitis alone.     

Computer analysis of ventilation-perfusion scans for detection and assessment of lung disease.

A previously reported computer analysis has been used to provide numerical ventilation-perfusion lung scan data, for comparison with tests of airways function and results of arterial blood gas analysis in 11 patients with pulmonary embolism, 18 with asthma, and 37 with chronic obstructive lung disease. In pulmonary embolism an index of underperfusion showed high sensitivity, and an index of ventilation-perfusion mismatching correlated well with severity (hypoxaemia). In asthma an index of underventilation was sensitive and correlated well with severity of airways obstruction. In chronic obstructive lung disease the same index was sensitive but correlated poorly with severity. This was attributed to heterogeneity of the lung disease (airways obstruction plus emphysema) in chronic obstructive lung disease. Ventilation-perfusion mismatching was frequently present in airways disease, and was often of great severity in chronic obstructive lung disease. Discrimination between pulmonary embolism and either type of airways disease was possible by using a combination of underfusion and underventilation indices. The technique offers the prospect of increasing the information derived from lung scans and of automating the reporting of scans.     

Determinants of airflow obstruction in severe alpha-1-antitrypsin deficiency

BACKGROUND: Severe alpha(1)-antitrypsin (AAT) deficiency is an autosomal recessive genetic condition associated with an increased but variable risk for chronic obstructive pulmonary disease (COPD). A study was undertaken to assess the impact of chronic bronchitis, pneumonia, asthma and sex on the development of COPD in individuals with severe AAT deficiency. METHODS: The AAT Genetic Modifier Study is a multicentre family-based cohort study designed to study the genetic and epidemiological determinants of COPD in AAT deficiency. 378 individuals (age range 33-80 years), confirmed to be homozygous for the SERPINA1 Z mutation, were included in the analyses. The primary outcomes of interest were a quantitative outcome, forced expiratory volume in 1 s (FEV(1)) percentage predicted, and a qualitative outcome, severe airflow obstruction (FEV(1) <50% predicted). RESULTS: In multivariate analysis of the overall cohort, cigarette smoking, sex, asthma, chronic bronchitis and pneumonia were risk factors for reduced FEV(1 )percentage predicted and severe airflow obstruction (p<0.01). Index cases had lower FEV(1) values, higher smoking histories and more reports of adult asthma, pneumonia and asthma before age 16 than non-index cases (p<0.01). Men had lower pre- and post-bronchodilator FEV(1) percentage predicted than women (p<0.0001); the lowest FEV(1) values were observed in men reporting a history of childhood asthma (26.9%). This trend for more severe obstruction in men remained when index and non-index groups were examined separately, with men representing the majority of non-index individuals with airflow obstruction (71%). Chronic bronchitis (OR 3.8, CI 1.8 to 12.0) and a physician's report of asthma (OR 4.2, CI 1.4 to 13.1) were predictors of severe airflow obstruction in multivariate analysis of non-index men but not women. CONCLUSION: In individuals with severe AAT deficiency, sex, asthma, chronic bronchitis and pneumonia are risk factors for severe COPD, in addition to cigarette smoking. These results suggest that, in subjects severely deficient in AAT, men, individuals with symptoms of chronic bronchitis and/or a past diagnosis of asthma or pneumonia may benefit from closer monitoring and potentially earlier treatment.     

Impaired lung function and lung cancer incidence in a cohort of Swedish construction workers

BACKGROUND: Although impaired lung function in general has been associated with an increased risk of lung cancer, past studies typically have not attempted to investigate separately the obstructive and restrictive components of respiratory impairment. To deal with this question further, data from a large (n = 176 997) cohort of male Swedish construction workers, for whom spirometry measurements before follow-up were available, were analysed. METHODS: Cancer incidence for 1971-2001 was obtained through linkage with the national cancer registry. Using a modification of the Global Initiative for Chronic Obstructive Lung Disease criteria for chronic obstructive pulmonary disease (COPD), subjects were classified into five categories of lung function: normal, mild COPD, moderate COPD, severe COPD and restrictive lung disease (RLD). Rate ratios (RR) and 95% confidence intervals (CI) for lung cancer across lung function categories were calculated using Poisson regression, adjusted for age and smoking. Other end points (histological types of lung cancer, non-lung tobacco-related cancers, other cancers, total mortality) were also investigated. RESULTS: 834 incident cases of lung cancer were identified. Increased rates of lung cancer were observed for both COPD (mild: RR 1.5, 95% CI 1.2 to 1.9; moderate/severe: RR 2.2, 95% CI 1.8 to 2.7) and RLD (RR 2.0, 95% CI 1.6 to 2.5) relative to normal lung function. These associations did not meaningfully change on applying follow-up lag times of 5, 10 and 15 years after spirometry. When analysed by histological type, associations with both COPD and RLD were stronger for squamous cell carcinoma and small cell carcinoma, and weaker for adenocarcinoma. Both COPD and RLD were associated with increased rates of total mortality. CONCLUSIONS: Obstructive and restrictive impairments in lung function are associated with increased lung cancer risk.     

Chronic non-specific respiratory disease with reference to 926 cases]

This study has been compiled from the hospital records of 926 patients with chronic non-specific respiratory disease, i.e. asthma, chronic bronchitis and emphysema. The aims of the study were to ascertain the role of age, allergy, family history, cigarette smoking, social class and occupation in the genesis of these diseases, and to investigate aggravating factors and the morbidity associated with these diseases. Asthma was found to occur in the younger age groups, allergy and family history being the outstanding aetiological factors in this disease. In chronic bronchitis the age factor is not decisive, and the influence of allergy, family history and the smoking of cigarettes is evenly distributed. Emphysema occurs mainly in later life, although 2 cases of younger onset with alpha1-antitrypsin deficiency were noted. In this disease, allergy and family history appear to be of lesser aetiological importance than the smoking of cigarettes. The majority of patients in all diagnostic categories fell into social group III (skilled workers) and most did work not associated with dust. In each diagnostic category, a certain number of patients were found in whom the factors of allergy, family history, cigarette smoking and general atmospheric pollution did not play a part. In these patients the possible role of the microclimate at the place of work is emphasised and warrants further study. The high prevalence, especially of asthma and chronic bronchitis, among housewives is stressed. Aggravating factors, i.e. humidity, irritating substances, temperature variations, dust, and type and locality of work, are shown to influence the symptomatology of asthma, bronchitis and emphysema. These diseases have a high associated morbidity, resulting in the loss of working days and in early retirement for the sufferers.     

Preoperative pulmonary rehabilitation in patients undergoing lung resection for non-small cell lung cancer.

BACKGROUND: The impact of short-term preoperative pulmonary rehabilitation on exercise capacity of patients with chronic obstructive pulmonary disease undergoing lobectomy for non-small cell lung cancer is evaluated. METHODS: A prospective observational study was designed. Inclusion criteria consisted of an indication to lung resection because of a clinical stage I or II non-small cell lung cancer and a chronic obstructive disease on preoperative pulmonary function test. In such conditions, maximal oxygen consumption by a cardio-pulmonary exercise test was evaluated; when this resulted as being < or =15 ml/kg/min a pulmonary rehabilitation programme lasting 4 weeks was considered. Twelve patients fulfilled inclusion criteria, completed the preoperative rehabilitation programme and underwent a new functional evaluation prior to surgery. The postoperative record of these patients was collected. RESULTS: On completion of pulmonary rehabilitation, the resting pulmonary function test and diffuse lung capacity of patients was unchanged, whereas the exercise performance was found to have significantly improved; the mean increase in maximal oxygen consumption proved to be at 2.8 ml/kg/min (p<0.01). Eleven patients underwent lobectomy; no postoperative mortality was noted and mean hospital stay was 17 days. Postoperative pulmonary complication was recorded in 8 patients. CONCLUSIONS: Short-term preoperative pulmonary rehabilitation could improve the exercise capacity of patients with chronic obstructive pulmonary disease who are candidates for lung resection for non-small cell lung cancer.     

Association of silicosis, lung dysfunction, and emphysema in gold miners.

BACKGROUND--In an earlier study of gold miners men with silicosis were found to have abnormal lung function, including airflow obstruction and reduced diffusing capacity. In a follow up study a sample of these men was examined by computed tomography to determine whether emphysema accounted for these abnormalities, which are associated with silicosis in this working population. METHODS--A sample of 70 men from a cohort of older gold miners with and without silicosis who had worked underground for a mean period of 29 years was examined by computed tomography to determine whether each man had emphysema. In addition, each man had lung function tests and routine chest radiography (125 kV). RESULTS--A total of 48 men had emphysema on examination by computed tomography. On the basis of the results in a chest radiograph 55 of the men had silicosis. Emphysema was related to silicosis, being present in five of the 15 men without silicosis and in 43 of the 55 with silicosis. Diffuse emphysema was apparent in two men without silicosis (14%) and in 25 men with silicosis (45%). The proportion of men with diffuse emphysema increased from 14% in those with International Labour Organisation category 0 nodule profusion to 46% in those with category 1, 48% in those with category 2, and 67% in those with category 3. Emphysema was also related to smoking: eight of the 18 who had never smoked and 40 of the 52 smokers had emphysema. All of those who had never smoked and had emphysema had silicosis with category 2/2 or greater nodule profusion. Lung function tests showed changes associated with silicosis that could be explained by the associated emphysema. CONCLUSIONS--In this population emphysema occurred in association with silicosis and accounted for the abnormalities in lung function associated with silicosis.     

Effect of cigarette smoking, pulmonary inflammation, and lung disease on concentrations of carcinoembryonic antigen in serum and secretions.

A specific radioimmunoassay for carcinoembryonic antigen was used to investigate aspects of its measurement in lung disease. The results confirm that serum carcinoembryonic antigen concentrations are higher in healthy smokers and patients with chronic obstructive bronchitis than in healthy non smokers (p less than 0.01). Corticosteroid treatment reduced the concentration in nine patients with bronchitis (p less than 0.05). Other inflammatory lung diseases (bronchiectasis, pneumonia, fibrosing alveolitis) are not associated with a raised serum carcinoembryonic antigen concentration. The sputum concentrations were about 100 times those found in serum and there was a positive correlation (r = 0.611 2p less than 0.01) between the concentrations in sputum and serum in patients with bronchitis. No preferential rise in sputum concentration was found in current smokers or patients with lung carcinoma (n = 16). A higher ratio of carcinoembryonic antigen to albumin concentration (p less than 0.05) was, however, found in lavage fluid obtained from the tumour site than in fluid from "normal" lung in the same patients, suggesting an increase in carcinoembryonic antigen secretion in the vicinity of the tumour. Despite this "local" effect the sputum concentration does not, however, appear to be a useful marker of lung carcinoma and the measurement could not be used as a screening test.     

Thyroid function and endocrine abnormalities in elderly patients with severe chronic obstructive lung disease.

Serum pituitary and thyroid hormones, testosterone, and the response of pituitary hormones to thyrotrophin releasing hormone were measured in 20 inpatients (mean age 68, range 42-81 years) with severe chronic obstructive lung disease and in 15 control convalescent inpatients (mean age 73, range 57-83 years) who had normal respiratory function. No significant differences were found in total and free thyroid hormone concentrations and basal concentrations of thyrotrophin, growth hormone, and prolactin; and their increments after injection of thyrotrophin releasing hormone were similar in patients with chronic obstructive lung disease, and control patients. Three patients with chronic obstructive lung disease, however, had no thyrotrophin responses to thyrotrophin releasing hormone. In men, low testosterone concentrations were found both in patients with chronic obstructive lung disease and in controls. Luteinising hormone concentrations were higher in men with chronic obstructive lung disease (p less than 0.02), whereas concentrations of follicle stimulating hormone in the two groups were not significantly different. There was no significant correlation between arterial blood gas tensions and these hormone measurements. General effects of age and illness may be more important than direct effects of hypoxia in determining hypothalamic-pituitary function in elderly patients with chronic obstructive lung disease.     

HIV associated pulmonary emphysema: a review of the literature and inquiry into its mechanism

Chronic lung diseases are increasingly recognised complications of the human immunodeficiency virus (HIV) infection and acquired immune deficiency syndrome (AIDS). Of these, pulmonary emphysema, characterised by permanent destruction of the lung parenchyma distal to the terminal bronchioles accompanied by various degrees of inflammation, is emerging as a distinct source of morbidity for patients infected with HIV. Similarly, HIV is now frequently cited as a susceptibility factor for the development of emphysema, independent of cigarette smoking status. The presence of common coexistent confounding factors that may predispose patients to chronic lung injury such as drugs, opportunistic infections and malnutrition, limits the scope of studies of direct mechanisms involved in HIV associated emphysematous lung disease. We review the clinical studies supporting a direct association between HIV infection and emphysema. Recent developments in the basic understanding of HIV infection and emphysema are also reviewed, since they may aid in understanding the pathobiology of HIV associated emphysema. The authors emphasise how HIV infection may affect cytotoxic lymphocyte activation, lung capillary endothelial cell injury and apoptosis, sphingolipid imbalance and oxidative stress in the lung. A better understanding of the pathogenesis of HIV associated pulmonary emphysema may provide clues and therapeutic targets that have broader application in this disease, including cigarette smoke induced emphysema.     

Is there an association between chronic lung disease and abdominal aortic aneurysm expansion?

Background: Although there is evidence demonstrating an association between chronic obstructive pulmonary disease (COPD) and abdominal aortic aneurysm (AAA), it is not clear whether COPD predicts greater rates of expansion of established aneurysms. We sought such an association in a cohort of men with aneurysms detected in a population‐based study of screening for aneurysms. Methods: In addition to regular aortic ultrasound scans, 179 men with AAA underwent full lung function testing in order to identify the presence of COPD and its subgroups, emphysema and other obstructive ventilatory defects (OVD). The rate of expansion of each aneurysm was calculated and the men were divided into ‘rapid expanders’ (3 mm or more per year) and ‘slow expanders’ (less than 3 mm per year). Any association with the presence of COPD or smoking was tested using a multivariate model. Results: Over a median follow‐up period of 36 months the mean rate of aortic expansion for the cohort of 179 men was 2.1 mm/year. There was no significant difference in prevalence of COPD (68% overall) or having ever been a smoker (87% overall) between the rapid expanders and the slow expanders. Conclusions: Although there was a high prevalence of COPD among men with an AAA, there was no association between the rate of expansion of AAA and the presence of any form of this disease.