Clinically Significant and Comorbid Anxiety and Depression Symptoms Predict Severe Respiratory Exacerbations in Smokers: A Post Hoc Analysis of the COPDGene and SPIROMICS Cohorts

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To the Editor: Anxiety and depression are important comorbidities in smokers, especially those with chronic obstructive pulmonary disease (COPD) (1, 2). Although the individual effect of anxiety or depression symptoms on respiratory exacerbations in COPD has been previously investigated, studies have not examined the impact of having clinically significant and comorbid anxiety and depression symptoms together in a broader population of smokers (3, 4). This complex clinical state of having combined anxiety and depression symptoms as opposed to having each condition individually occurs in approximately two-thirds of people with mental illness in the general population, is difficult to recognize and treat, and has been associated with an increased risk for mortality in cardiovascular disease (5, 6). The goal of this study was to examine the impact of having clinically significant and comorbid anxiety and depression symptoms on severe respiratory exacerbations in smokers. We conducted a post hoc analysis of data from two multicenter and prospective cohort studies: 1) COPDGene (Genetic Epidemiology of COPD study) (March 2019 dataset) and 2) SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study) (Core 6) (7, 8). We categorized clinically significant anxiety and depression symptoms by using the Hospital Anxiety and Depression Scale (HADS), which has subscales for anxiety and depression that range from 0–21, with higher scores being associated with more severe symptoms (9). We generated the following HADS categories for clinically significant anxiety and depression symptoms: 1) no clinically significant anxiety or depression symptoms (HADS–Anxiety [HADS-A] score < 8 and HADS–Depression [HADS-D] score < 8), 2) clinically significant anxiety symptoms only (HADS-A score ⩾ 8 and HADS-D score < 8), 3) clinically significant depression symptoms only (HADS-A score < 8 and HADS-D score ⩾ 8), and 4) clinically significant and comorbid anxiety and depression symptoms (HADS-A score ⩾ 8 and HADS-D score ⩾ 8) (2). In both cohorts, we included adult participants who were current and former smokers with and without airflow obstruction in available post-bronchodilator spirometry results. We excluded nonsmokers and those without spirometry data and other missing clinical data. In COPDGene, the HADS score was collected at the “phase 2 visit” or 5 years after the initial phase 1 study visit and served as the baseline time point in COPDGene. In SPIROMICS, HADS was collected at the baseline visit (“visit 1”). In both cohorts, the primary outcome of prospective, patient-reported, and adjudicated severe respiratory exacerbations (i.e., those requiring an emergency room visit or hospitalization) was recorded by phone as cumulative exacerbations up to approximately 12 months after the HADS measurement.

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