The STAMPEDE subjects (11 18, 21, & 23) with the group 1 miRNA expression profile have provisional diagnoses of chronic obstructive pulmonary disease, fixed obstruction, airway hyperreactivity, air trapping, asthma, low DLCO (2 subjects), and constrictive bronchiolitis.
Increased pulmonary blood flow can be detrimental in case of obstructed pulmonary venous flow, by causing worsening pulmonary edema in the face of a fixed obstruction [6].
Subjects with severe established fixed obstruction were excluded.
Nevertheless, the flow-volume curve typically displayed localized fixed obstruction of central airways.
Previous work has shown that in patients with similar levels of fixed obstruction, history can distinguish asthma and COPD as separate airway pathologies [ 25, 26].
Thus there was bias against the inclusion of asthmatic smokers destined to develop fixed obstruction rapidly, so we do not present any analyses confined to smokers.
Notwithstanding differences in study methodology, this discrepancy may reflect gene-environment differences, where varying thresholds of amount smoked lead to the development of fixed obstruction.
In individuals who already have asthma, endotoxin may also contribute to airway remodeling and fixed obstruction in the airways (Reed and Milton 2001).
More recently, air trapping as a radiological finding has been reported as a significant determinant of fixed obstruction in asthma [ 39, 43].
The most likely inference is that the subjects with PostBDFEV1 < 70% are asthma patients who have developed fixed obstruction in association with smoking.
