Assessment of Right Ventricular Afterload in COPD.

BACKGROUND: We aimed to study whether pulmonary hypertension (PH) and elevated pulmonary vascular resistance (PVR) could be predicted by conventional echo Doppler and novel tissue Doppler imaging (TDI) in a population of chronic obstructive pulmonary disease (COPD) free of LV disease and co-morbidities. METHODS: Echocardiography and right heart catheterization was performed in 100 outpatients with COPD. By echocardiography the time-integral of the TDI index, right ventricular systolic velocity (RVSmVTI) and pulmonary acceleration-time (PAAcT) were measured and adjusted for heart rate. The COPD patients were randomly divided in a derivation (n = 50) and a validation cohort (n = 50). RESULTS: PH (mean pulmonary artery pressure (mPAP) ≥ 25mmHg) and elevated PVR ≥ 2Wood unit (WU) were predicted by satisfactory area under the curve for RVSmVTI of 0.93 and 0.93 and for PAAcT of 0.96 and 0.96, respectively. Both echo indices were 100% feasible, contrasting 84% feasibility for parameters relying on contrast enhanced tricuspid-regurgitation. RVSmVTI and PAAcT showed best correlations to invasive measured mPAP, but less so to PVR. PAAcT was accurate in 90- and 78% and RVSmVTI in 90- and 84% in the calculation of mPAP and PVR, respectively. CONCLUSIONS: Heart rate adjusted-PAAcT and RVSmVTI are simple and reproducible methods that correlate well with pulmonary artery pressure and PVR and showed high accuracy in detecting PH and increased PVR in patients with COPD. Taken into account the high feasibility of these two echo indices, they should be considered in the echocardiographic assessment of COPD patients.

Validity of the European short list of respiratory diseases: a 40-year autopsy study.

The predictors of autopsy and the accuracy of European short list (E) codes of respiratory diseases lack recent knowledge. A 10% random sample (n=6811) of inhabitants of Bergen, Norway, aged 20-70 years, was invited to participate in a survey in 1965-1971 (participation rate 83%). By December 31, 2005, 4387 (64%) participants had died and 1163 (27% of the deceased) had been given an autopsy. Causes of death were tuberculosis (E02, 0.2%), lung malignancy (E15, 3.5%), influenza (E38, 0.2%), pneumonia (E39, 6.5%) and chronic lower respiratory diseases (E40, 3.2%). Male sex, early deaths in the surveillance period and E15 were positive predictors of an autopsy examination, whereas old age and E39 were strong negative predictors. Among those referred for a post mortem examination, the cause of death was verified as tuberculosis in 0.3%, lung cancer in 8.1%, acute pneumonia in 2.0% and chronic obstructive lung diseases in 4.9%. Cohen's kappa coefficients (E codes versus autopsy) were 0.91 (95% CI 0.86-0.96) for E15, 0.37 (95% CI 0.20-0.54) for E39 and 0.65 (95% CI 0.54-0.76) for E40. These findings matter when deaths from respiratory diseases are used as end-points in epidemiological association studies and clinical trials.

Haemodynamic responses to exercise in patients with COPD.

The present study aimed to explore the prevalence of pre-capillary pulmonary hypertension (PH) and characterise haemodynamic vascular responses to physical exercise in chronic obstructive pulmonary disease (COPD) outpatients, where left ventricular dysfunction and comorbidities were excluded. 98 patients with COPD underwent right heart catheterisation at rest and during supine exercise. Mean pulmonary artery pressure (Ppa), pulmonary capillary wedge pressure (Ppcw) and cardiac output (CO) were measured at rest and during exercise. Exercise-induced increase in mean Ppa was interpreted relative to increase in blood flow, mean Ppa/CO, workload (W) and mean Ppa/W. Pulmonary vascular resistance (PVR) and pulmonary artery compliance (PAC) were calculated. PH at rest was defined as mean Ppa at rest ≥25 mmHg and Ppcw at rest <15 mmHg. Prevalence of PH was 5%, 27% and 53% in Global Initiative for Chronic Obstructive Lung Disease stages II, III and IV, respectively. The absolute exercise-induced rise in mean Ppa did not differ between subjects with and without PH. Patients without PH showed similar abnormal haemodynamic responses to exercise as the PH group, with increased PVR, reduced PAC and steeper slopes for mean Ppa/CO and mean Ppa/W. Exercise revealed abnormal physiological haemodynamic responses in the majority of the COPD patients. The future definition of PH on exercise in COPD should rely on the slope of mean Ppa related to cardiac output and workload rather than the absolute values of mean Ppa.

Left ventricular dysfunction in COPD without pulmonary hypertension.

OBJECTIVES: We aimed to assess prevalence of left ventricular (LV) systolic and diastolic function in stable cohort of COPD patients, where LV disease had been thoroughly excluded in advance. METHODS: 100 COPD outpatients in GOLD II-IV and 34 controls were included. Patients were divided by invasive mean pulmonary artery pressure (mPAP) in COPD-PH (≥25 mmHg) and COPD-non-PH (<25 mmHg), which was subdivided in mPAP ≤20 mmHg and 21-24 mmHg. LV myocardial performance index (LV MPI) and strain by tissue Doppler imaging (TDI) were used for evaluation of LV global and systolic function, respectively. LV MPI ≥0.51 and strain ≤-15.8% were considered abnormal. LV diastolic function was assessed by the ratio between peak early (E) and late (A) velocity, early TDI E´, E/E´, isovolumic relaxation time, and left atrium volume. RESULTS: LV MPI ≥0.51 was found in 64.9% and 88.5% and LV strain ≤-15.8% in 62.2.% and 76.9% in the COPD-non-PH and COPD-PH patients, respectively. Similarly, LV MPI and LV strain were impaired even in patients with mPAP <20 mmHg. In multiple regression analyses, residual volume and stroke volume were best associated to LV MPI and LV strain, respectively. Except for isovolumic relaxation time, standard diastolic echo indices as E/A, E´, E/E´ and left atrium volume did not change from normal individuals to COPD-non-PH. CONCLUSIONS: Subclinical LV systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure. Evidence of LV diastolic dysfunction was hardly present as measured by conventional echo indices.

Exercise capacity in COPD patients with exercise-induced pulmonary hypertension.

BACKGROUND: Pulmonary hypertension (PH) in patients with COPD is associated with reduced exercise capacity. A subgroup of COPD patients has normal mean pulmonary artery pressure (mPAP) at rest, but develops high mPAP relative to cardiac output (CO) during exercise, a condition we refer to as exercise-induced pulmonary hypertension (EIPH). We hypothesized that COPD patients with EIPH could be identified by cardiopulmonary exercise test (CPET) and that these patients have lower exercise capacity and more abnormal CPET parameters compared to COPD patients with normal hemodynamic exercise response. METHODS: Ninety-three stable outpatients with COPD underwent right heart catheterization with the measurement of mPAP, CO, and capillary wedge pressure at rest and during supine exercise. Resting mPAP <25 mmHg with ΔmPAP/ΔCO slope above or below 3 mmHg/L/min were defined as COPD-EIPH and COPD-normal, respectively. Pulmonary function tests and CPET with arterial blood gases were performed. Linear mixed models were fitted to estimate differences between the groups with adjustment for gender, age, and airflow obstruction. RESULTS: EIPH was observed in 45% of the study population. Maximal workload was lower in COPD-EIPH compared to COPD-normal, whereas other CPET measurements at peak exercise in % predicted values were similar between the two groups. After adjustment for gender, age, and airflow obstruction, patients with COPD-EIPH showed significantly greater increase in oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate with increasing work load, as well as more reduction in pH compared to those with normal hemodynamic responses. CONCLUSION: COPD-EIPH could not be discriminated from COPD-normal by CPET. However, COPD-EIPH experienced a higher cost of exercise in terms of higher oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate for a given increase in workload compared to COPD-normal.

Cardiopulmonary exercise test and PaO2 in evaluation of pulmonary hypertension in COPD.

Background: Exercise tolerance decreases as COPD progresses. Pulmonary hypertension (PH) is common in COPD and may reduce performance further. COPD patients with and without PH could potentially be identified by cardiopulmonary exercise test (CPET). However, results from previous studies are diverging, and a unified conclusion is missing. We hypothesized that CPET combined with arterial blood gases is useful to discriminate between COPD outpatients with and without PH. Methods: In total, 93 COPD patients were prospectively included. Pulmonary function tests, right heart catheterization, and CPET with blood gases were performed. The patients were divided, by mean pulmonary artery pressure, into COPD-noPH (<25 mmHg) and COPD-PH (≥25 mmHg) groups. Linear mixed models (LMMs) were fitted to estimate differences when repeated measurements during the course of exercise were considered and adjusted for gender, age, and airway obstruction. Results: Ventilatory and/or hypoxemic limitation was the dominant cause of exercise termination. In LMM analyses, significant differences between COPD-noPH and COPD-PH were observed for PaO2, SaO2, PaCO2, ventilation, respiratory frequency, and heart rate. PaO2 <61 mmHg (8.1 kPa) during unloaded pedaling, the only load level achieved by all the patients, predicted PH with a sensitivity of 86% and a specificity of 78%. Conclusion: During CPET, low exercise performance and PaO2 strongly indicated PH in COPD patients.

Symptoms and quality of life in patients with chronic obstructive pulmonary disease treated with aclidinium in a real-life setting.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is a progressive disease with symptoms that can have a major impact on patients' physical health. The aim of this study was to evaluate quality of life (QoL), symptom severity and dyspnoea in COPD patients treated with aclidinium up to 24 weeks. METHODS: In this prospective non-interventional multicentre study (198 centres in Sweden, Denmark, and Norway), COPD patients (age ≥40 years) who started treatment with aclidinium (initial therapy, change of treatment, or add-on therapy) could be included. Health-related QoL was obtained by COPD assessment test (CAT). Symptoms were evaluated on a 6-point Likert scale. The modified Medical Research Council (mMRC) Dyspnoea Scale was used as a simple grading system to assess the level of dyspnoea/shortness of breath from0 to 4. Patients on treatment with aclidinium who completed baseline and at least one follow-up visit (week 12 or 24) were included in the study population. RESULTS: Overall, 1,093 patients were enrolled (mean 69 years, 54% females), one-third had ≥1 exacerbation the year prior to baseline. At enrolment, 48% were LAMA naïve. Mean (standard deviation, SD) CAT score decreased from 16.9 (7.7) at baseline to 14.3 (7.3) at week 24 (p<0.01) with a decrease in all individual CAT items (p<0.05). Mean difference in morning and night-time symptoms from baseline to week 24 was -0.60 (SD 2.51) and -0.44 (SD 2.48), respectively (both p<0.001). Mean (SD) mMRC Dyspnoea Scale changed from 1.6 (1.0) at baseline to 1.5 (1.0) at week 24 (p<0.001). CONCLUSION: In this observational study of a Nordic real-life COPD population, treatment with aclidinium was associated with a clinically important improvement in QoL and morning and night-time symptoms, most pronounced in the LAMA naïve group. However, there is still room for improvement in the management of symptomatic COPD patients.

[Clinical pharmacist improves the use of drugs in hospital]. / Klinisk farmasøyt forbedrer legemiddelbruken i sykehus.

BACKGROUND: We investigated how a clinical pharmacist can contribute to quality assurance of the use of drugs for inpatients in a respiratory ward. MATERIAL AND METHODS: Up to twice a week over two periods (43 meetings, 31 in the first and 12 in the second period), a clinical pharmacist sat in on the morning meetings regarding patients. Various drug-related problems were identified and discussed. RESULTS: The clinical pharmacist took part in discussions of 232 (70%) of a total of 332 patients. On average, 0.71 drug-related problems per patient resulting in a prescription change were identified. This included 239 drug-related problems: lack of use of drugs (25), unnecessary use (18) or wrong use (1); too low dose (16), too high dose (30); adverse effects (29); compliance (10) and miscellaneous problems (110). The average number of prescription changes suggested by the clinical pharmacist went down from 0.81 per patient in the first period to 0.57 in the second (p < 0.001). INTERPRETATION: We conclude that many drug-related problems were identified and the quality of drug use was improved by including a clinical pharmacist in the medical team.

Factors associated with a prolonged length of stay after acute exacerbation of chronic obstructive pulmonary disease (AECOPD).

BACKGROUND: Early identification of patients with a prolonged stay due to acute exacerbation of chronic obstructive pulmonary disease (COPD) may reduce risk of adverse event and treatment costs. This study aimed to identify predictors of prolonged stay after acute exacerbation of COPD based on variables on admission; the study also looked to establish a prediction model for length of stay (LOS). METHODS: We extracted demographic and clinical data from the medical records of 599 patients discharged after an acute exacerbation of COPD between March 2006 and December 2008 at Oslo University Hospital, Aker. We used logistic regression analyses to assess predictors of a length of stay above the 75th percentile and assessed the area under the receiving operating characteristic curve to evaluate the model's performance. RESULTS: We included 590 patients (54% women) aged 73.2±10.8 years (mean ± standard deviation) in the analyses. Median LOS was 6.0 days (interquartile range [IQR] 3.5-11.0). In multivariate analysis, admission between Thursday and Saturday (odds ratio [OR] 2.24 [95% CI 1.60-3.51], P<0.001), heart failure (OR 2.26, 95% CI 1.34-3.80), diabetes (OR 1.90, 95% CI 1.07-3.37), stroke (OR 1.83, 95% CI 1.04-3.21), high arterial PCO2 (OR 1.26 [95% CI 1.13-1.41], P<0.001), and low serum albumin level (OR 0.92 [95% CI 0.87-0.97], P=0.001) were associated with a LOS >11 days. The statistical model had an area under the receiver operating characteristic curve of 0.73. CONCLUSION: Admission between Thursday and Saturday, heart failure, diabetes, stroke, high arterial PCO2, and low serum albumin level were associated with a prolonged LOS. These findings may help physicians to identify patients that will need a prolonged LOS in the early stages of admission. However, the predictive model exhibited suboptimal performance and hence is not ready for clinical use.

Long-term improvements in pulmonary function 5 years after bariatric surgery.

BACKGROUND: Obesity is associated with reduced pulmonary function. We evaluated pulmonary function and status of asthma and obstructive sleep apnoea syndrome (OSAS) before and 5 years after bariatric surgery. METHODS: Spirometry was performed at baseline and 5 years postoperatively. Information of asthma and OSAS were recorded. Of 113 patients included, 101 had undergone gastric bypass, 10 duodenal switch and 2 sleeve gastrectomy. RESULTS: Eighty (71%) patients were women, mean preoperative age was 40 years and preoperative weight was 133 kg in women and 158 kg in men. Five years postoperatively, weight reduction was 31% (42 kg; p < 0.001) in women and 24% (38 kg; p < 0.001) in men. Forced expiratory volume in 1 s (FEV1) increased 4.1% (116 ml; p < 0.001) in women and 6.7% (238 ml; p = 0.003) in men. Forced vital capacity (FVC) increased 5.8% (209 ml; p < 0.001) in women and 7.6% (349 ml; p < 0.001) in men. Gender and weight loss were independently associated with the improvements in FEV1 and FVC. At follow-up, FEV1 had increased 36% of the difference towards the estimated normal FEV1, and there was a corresponding 70% recovery of FVC. These improvements occurred despite an expected decline in pulmonary function by age during the study period. Of the asthmatics and OSAS patients, 48 and 80%, respectively, were without symptoms 5 years postoperatively. CONCLUSIONS: Pulmonary function measured with spirometry was significantly improved 5 years after bariatric surgery, despite an expected age-related decline during this period. Symptoms of asthma and OSAS also improved.

Readmissions for COPD: propensity case-matched comparison between pulmonary and non-pulmonary departments.

INTRODUCTION: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is a common cause of hospitalisation, and the readmission rate is high. We aimed to determine whether patients discharged from a pulmonary department (PD) after an AECOPD episode had a lower COPD-related readmission rate during the next 12 months than comparable patients discharged from other internal medicine departments (ODs). METHODS: The medical records of 566 patients discharged after an episode of AECOPD between March 2006 and December 2008 at Oslo University Hospital, Aker, were reviewed retrospectively. Demographic and medical data, together with number of readmissions because of AECOPD during 12 months following the index admission were extracted. We matched patients discharged from the PD and the ODs using a propensity score and used the paired t-test to compare COPD-related readmission rates between the matched patients. RESULTS: In total, 481 patients were included in the analysis, 247 patients discharged from the PD and 234 from ODs. The propensity score matching process resulted in 155 well-matched pairs. The mean (standard deviation) number of readmissions within 1 year was 0.8 (1.3) for the PD versus 1.1 (1.9) for ODs (P = 0.09). After adjusting for exposure time, the corresponding readmission rates were 1.1 (2.3) and 1.6 (4.0) per year, respectively (P = 0.17). CONCLUSION: There was little difference in COPD-related readmission rates between comparable patients discharged from the PD and the ODs after an AECOPD during 1 year following the index admission.

Pulmonary artery pressure and PaO2 in chronic obstructive pulmonary disease.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is a common cause of pre-capillary pulmonary hypertension (PH). This complication may be overlooked in patients with COPD, as symptoms frequently are attributed to ventilatory limitation. Predictors of PH may identify patients with increased risk of morbidity and mortality. OBJECTIVE: The aims of this COPD study were to (i) evaluate the relationship between mean pulmonary artery pressure (mPAP) and PaO2, (ii) identify significant predictors of mPAP and PaO2 and (iii) use PaO2 as a marker of PH. METHODS: Altogether 95 COPD patients with mild to very severe airway obstruction and without left ventricular (LV) dysfunction were included. Pulmonary function tests, right heart catheterizations and exercise tests with blood gases were performed. RESULTS: Multivariate regression analyses showed that only PaO2 was a significant predictor of mPAP. FEV1 and mPAP were significant predictors of PaO2 both at rest and at peak exercise. PaO2 at peak exercise was better to identify pulmonary hypertension than PaO2 at rest. By combining PaO2 at rest and peak exercise, it was possible to predict PH with a detection rate of 76% and a false-positive rate of 24%. CONCLUSION: In an outpatient COPD population where LV disease was thoroughly excluded, we observed that only PaO2 was a significant predictor of mPAP. PaO2 at rest and peak exercise below 9.5 kPa (71 mmHg) and 8.5 kPa (64 mmHg), respectively, indicates the need for further evaluation of coexisting PH.

Acetazolamide improves oxygenation in patients with respiratory failure and metabolic alkalosis.

INTRODUCTION: Coexistent respiratory failure and metabolic alkalosis is a common finding. Acidotic diuretics cause a fall in pH that may stimulate respiration. OBJECTIVE: The purpose of the study was to evaluate the effectiveness of short-term treatment with acetazolamide for combined respiratory failure and metabolic alkalosis. METHODS: A randomised, placebo-controlled and double-blind parallel group trial where oral acetazolamide 250 mg three times a day for 5 days were administered to patients hospitalised for respiratory failure because of a pulmonary disease (Pa O2 ≤ 8 kPa and/or Pa CO2 ≥ 7 kPa) who had concurrent metabolic alkalosis [base excess (BE) ≥ 8 mmol/L]. Pa O2 after 5 days was the primary effect variable. Secondary effect variables were Pa CO2 , BE and pH on day 5, and the total number of days in hospital. RESULTS: Of 70 patients enrolled (35 in each group), data from 54 were analysed per protocol, while last observation carried forward was used for the remaining 16. During the 5-day treatment, Pa O2 increased on average 0.81 kPa in the placebo group and 1.41 kPa in the acetazolamide group. After adjustment for baseline skewness, the difference was statistically significant (adjusted mean difference 0.55 kPa, 95% confidence interval 0.03-1.06). Pa CO2 decreased in both groups, but the difference was not statistically significant. As expected, pH and BE decreased markedly in the acetazolamide group. CONCLUSION: Acetazolamide may constitute a useful adjuvant treatment mainly to be considered in selected patients with respiratory failure combined with prominent metabolic alkalosis or where non-invasive ventilation is insufficient or infeasible.

Right ventricular dysfunction and remodeling in chronic obstructive pulmonary disease without pulmonary hypertension.

OBJECTIVES: The aim of the present study was to elucidate right ventricular (RV) function and structure in patients with chronic obstructive pulmonary disease (COPD) without pulmonary hypertension (PH). BACKGROUND: There is little knowledge of RV function and remodeling in COPD without PH. METHODS: Thirty-four controls and 98 patients with COPD were included. The study patients were divided into 2 groups by right heart catheterization: no PH (mean pulmonary artery pressure [mPAP] <25 mm Hg) and PH (mPAP ≥25 mm Hg). The echocardiographic tissue Doppler imaging variables of RV isovolumic acceleration, peak systolic strain, and RV myocardial performance index were measured at the basal free wall, and RV wall thickness and RV internal dimension were measured in the RV outflow tract. RESULTS: The increases in RV wall thickness and RV dimension were more evident when comparing controls with the no PH group (3.5 ± 0.5 mm to 5.5 ± 1.0 mm [p < 0.01] and 1.5 cm ± 0.2 to 2.0 ± 0.5 cm [p < 0.01]) than comparing the no PH group with the PH group (5.5 ± 1.0 mm to 6.6 ± 1.1 mm [p < 0.01] and 2.0 cm ± 0.5 to 2.1 ± 0.3 cm [p = NS]), respectively. Similarly, RV isovolumic acceleration, performance index, and strain deteriorated significantly when comparing controls with the no PH group and comparing the no PH group with the PH group (p < 0.01). Significant correlations were observed between mPAP and RV isovolumic acceleration, performance index, strain, and RV wall thickness (p < 0.01). RV impairment and increased RV wall thickness and RV dimensions were present even at slight elevations of mPAP (18 ± 3 mm Hg) in the no PH group. CONCLUSIONS: The present study showed that impaired RV systolic function, hypertrophy, and dilation were present even at a slight increase of mPAP, which indicates an early impact on RV function and structure in patients with COPD. RV isovolumic acceleration, performance index, and strain could detect subclinical disease and separate controls from those with no PH.

The association between lung function and fatal stroke in a community followed for 4 decades.

BACKGROUND: Previous studies, all of <20 years of follow-up, have suggested an association between lung function and the risk of fatal stroke. This study investigates the stability of this association in a cohort followed for 4 decades. METHODS: The Bergen Clinical Blood Pressure Survey was conducted in Norway in 1964-1971. The risk of fatal stroke associated with forced expiratory volume after one second (FEV(1)) was estimated with Cox proportional hazards regression, making progressive adjustment for potential confounders. RESULTS: Of 5617 (84%) participants with recorded baseline FEV(1), 462 died from stroke over 152 786 subsequent person-years of follow-up according to mortality statistics of 2005; mean (SD) follow-up was 27 (12) years. An association between baseline FEV(1) (L) and fatal stroke was observed; HR=1.38 (95% CI 1.11 to 1.71) and HR=1.62 (95% CI 1.22 to 2.15) for men and women, respectively (adjusted for age and height). The findings were not explained by smoking, hypertension, diabetes, atherosclerosis, socioeconomic status, obstructive lung disease, physical inactivity, cholesterol or body mass index and persisted in subgroups of never-smokers, subgroups without respiratory symptoms and survivors of the first 20 years of follow-up. For male survivors with a valid FEV(1) at follow-up (1988-1990) (n=953), baseline FEV(1) (L) indicated a possible strong and independent association to the risk of fatal stroke after adjustments for individual changes in FEV(1) (ml/year) (HR 1.95 (95% CI 0.98 to 3.86)). CONCLUSION: There is a consistent, independent and long-lasting association between lung function and fatal stroke, probably irrespective of changes during adult life.

Rheumatic mitral valve stenosis mimicking advanced lung cancer.

This report describes a patient with a perihilar mass and mediastinal lymphadenopathy mimicking advanced lung cancer. The patient, a 45-year old regular smoker, was admitted to hospital for dyspnea and tachyarrhythmia, and during hospitalization he was diagnosed with severe rheumatic mitral valve stenosis (MVS) and aortic regurgitation as well as pulmonary venous hypertension. Surgical valve replacement and removal of an atrial thrombus was delayed considerably by diagnostic work-up for suspected malignancy. After cardiac surgery had been performed, recovery was uneventful. On follow-up 1 year later, echocardiography showed well-functioning prosthetic mitral and aortic valves, and normal findings on chest X-ray. Perihilar masses and mediastinal lymphadenopathy presented in this case constitute infrequent yet established findings in MVS, resulting from pulmonary venous congestion and hypertension, and focal lymphedema.

Bronchodilator reversibility testing in an adult general population; the importance of smoking and anthropometrical variables on the response to a beta2-agonist.

Normative cut-off values for the bronchodilator reversibility test are published neglecting factors that may influence the test result other than disease. The objective of this cross-sectional study of a general population was to examine how a salbutamol reversibility test response is depending on anthropometrical variables and smoking. An age and gender stratified random sample of all adults aged 47-48 and 71-73 years living in Bergen, Norway, was invited. The 3506 attendants (69%) filled in a questionnaire and performed spirometry before and after inhalation of 400 microg salbutamol. The mean (SD) absolute FEV(1) bronchodilator response, the change in % predicted, and the change in % initial among middle-aged were 71 (122) ml, 2.0 (3.3)%, and 2.4 (4.1)%, and in the elderly 64 (113) ml, 2.4 (4.3)% and 3.3 (5.9)%, respectively. In a multiple linear regression analysis including adjustment for the initial FEV1 in % predicted, smoking and pack-years were negatively correlated to all indices. Current smoking was considerably more important than past smoking. Female gender, old age, and BMI were positively correlated with the percentage change indices, but the correlation with BMI decreased with increasing heights. These trends were unchanged after excluding subjects with obstructive lung disease or coronary heart disease. This study demonstrates that smoking habits predict all indices expressing the salbutamol bronchodilator response among middle-aged and elderly from a general population. Also, the change in % predicted and the change in % initial indices are dependent on anthropometrical variables. However, although smoking and anthropometrical variables, as well as level of lung function predict the response to inhaled beta2-agonists, these factors explain only 7-16% of the total variation of the measurement indices, and seem therefore of minor importance to the interpretation of the test result.