Background Recent studies have suggested that a restrictive pattern assessed with a single spirometric test is associated with increased morbidity and mortality. This study was undertaken to determine demographic, clinical and mortality profiles of subjects with either a recurrent or an inconsistent restrictive spirometric pattern assessed prospectively.
Methods Data from 2048 adult participants in the population-based TESAOD study were analysed. Normal (forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC) ratio ≥70% and FVC ≥80% predicted), restrictive (FEV1/FVC ≥70% and FVC <80% predicted) and obstructive (FEV1/FVC <70%) patterns were assessed at the enrolment survey in 1972 and in 11 subsequent follow-up surveys up to 1996. Demographic and clinical characteristics were measured at enrolment and vital status and cause of death were assessed at January 2005.
Results Overall, 12% of participants had a restrictive spirometric pattern at enrolment. They were less likely to be male, to smoke and to have asthma, and had lower IgE levels than subjects in the obstructive group. Among subjects with a restrictive pattern at enrolment, 38% developed an obstructive pattern during follow-up. The remaining 62% had either a recurrent (restrictive pattern ≥50% of follow-up surveys) or inconsistent (restrictive pattern <50% of follow-up surveys) longitudinal restrictive pattern. The recurrent and inconsistent restrictive groups had increased mortality risk for all-cause (adjusted HR 1.7 (95% CI 1.3 to 2.3) and 1.9 (95% CI 1.4 to 2.6), respectively), heart disease (2.0 (95% CI 1.3 to 3.1) and 2.7 (95% CI 1.7 to 4.3)), stroke (2.4 (95% CI 0.9 to 6.3) and 3.5 (95% CI 1.2 to 9.8)) and diabetes (8.0 (95% CI 2.9 to 21.8) and 6.0 (95% CI 1.9 to 19.2)).
Conclusions The restrictive spirometric pattern identifies a pulmonary condition that is distinguishable from obstructive lung disease and is associated with an increased risk of life-threatening comorbidities.
- Spirometric restrictive pattern
- lung function
- clinical epidemiology
- COPD epidemiology
- lung physiology
- systemic disease and lungs
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Funding This study was funded by grants HL14136, HL085195 and HL095021 from the National Heart, Lung and Blood Institute, a grant award by the American Thoracic Society/Alpha1 Foundation, grant 0660059Z by the American Heart Association and an unrestricted grant from the Barry and Janet Lang Donor Advised Fund. SG was the recipient of a Parker B. Francis Fellowship.
Competing interests None.
Ethics approval This study was conducted with the approval of the Institutional Review Board of the University of Arizona.
Provenance and peer review Not commissioned; externally peer reviewed.
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