COPD
Course of Disease
Syndrome rather than disease
COPD is not a single disease; rather, it is a syndrome. Thus, there is no single COPD natural history. What we call “COPD” today is the end result of a complex set of gene–environment interactions. They start during pregnancy, and continue after birth during infancy, adolescence, adulthood and old age.1
After attaining a maximum in young adulthood, in most individuals, lung function remains constant for about 10 years, after which it slowly declines at about 20 mL·year-1 in the healthy never-smoking individual. Healthy females have a less steep rate of lung function decline through life than males.1
In cigarette smokers, the duration of the “plateau phase” can be reduced and the decline begin earlier, whereas some nonsmokers can also experience a shortened plateau phase that could result in compromised lung function at an earlier age and increased risk of COPD.1
Fletcher and Peto model of COPD
The traditional Fletcher and Peto model of COPD proposes that in “susceptible” smokers, this plateau phase is followed by progressive clinical worsening of symptoms, particularly dyspnea and more limitation of airflow, until the disease becomes more severe and limiting (Figure 1). This “progressive” model of COPD may not be so, since data from clinical trials and observational studies suggest that FEV1 decline trajectories may be set at a younger age and follow parallel paths.1
Figure 1. Fletcher and Peto model of COPD2
EASI model
Understanding the dynamic nature of COPD offers new windows of opportunity for prevention and treatment, provided that appropriate research is done. All these findings have to be incorporated into any new model(s) describing the natural history (or histories) of COPD, since each of these features is likely to have a natural history that may be quite independent of that of airflow limitation.1
An integrative computational approximation was proposed to the natural history of COPD (the EASI model; Figure 2) that seeks to facilitate the investigation of the variability and determinants of different “individual natural histories” of COPD.1
Figure 2. EASI model
The EASI model integrates dynamically and represents graphically the relationships between exposure (E) to inhaled particles and gases (e.g. smoking), the biological activity (e.g. inflammatory response) of the disease (A), the severity (S) of airflow limitation (FEV1) and the impact (I) of the disease (breathlessness) in different clinical scenarios.1
References
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Agustí A, Celli B. ERJ Open Res 2017;3(4):00117-2017.
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Bednarek M, et al. Thorax 2006;61(10):869-73.