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The COPDGene Study1 is providing important new information about the natural history of several chronic obstructive pulmonary disease (COPD) phenotypes.2 This multicentre study enrolled a large number of current and former smokers with a wide range of spirometry results (from normal to very severe airflow obstruction), carefully characterised them during their baseline examination, and has been following them for several important outcome measures. The key phenotypes include (1) chronic airflow obstruction (CAO) defined by a low post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC), (2) high-resolution CT (HRCT)-defined emphysema (low attenuation at maximal inhalation, total lung capacity), (3) hyperinflation or gas trapping on HRCT, defined as low attenuation of the lungs at low lung volume (around functional residual capacity), and (4) airway inflammation (defined by bronchial wall thickening on HRCT, also known as bronchiectasis). A comparison of two of these phenotypes—CAO versus emphysema—has been described.3 Not surprisingly, the analyses showed ‘striking disagreement’ between spirometric CAO (regardless of how mild airway obstruction was defined) and HRCT-defined emphysema. Only 13% of smokers with CAO had emphysema, while 39% had air trapping.
The authors then compared the prevalence of HRCT-defined emphysema in smokers with borderline to mild CAO defined by the faulty fixed ratio versus the lower limit of the normal range (LLN) for FEV1/FVC. About 7% of the adult smokers in the cohort had an FEV1/FVC below 0.70 but above the LLN (a discordant CAO classification). This ‘fixed-only’ subgroup of …