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Firdaus A. A. Mohamed Hoesein, MD, PhD; Pieter Zanen, MD, PhD
Author and Funding Information

From the Division of Heart & Lungs, Department of Respiratory Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.

Correspondence to: Pieter Zanen, MD, PhD, Division of Heart & Lungs, Department of Respiratory Medicine, University Medical Center Utrecht, HP F.02.333, PO Box 85500, 3508 GA, Utrecht, The Netherlands; e-mail: p.zanen@umcutrecht.nl


Funding/Support: Funding was received from European Union FP7 [Grant 201379 COPACETIC (COPD Pathology: Addressing Critical Gaps, Early Treatment and Innovative Concepts)].

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(1):277. doi:10.1378/chest.12-2192
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To the Editor:

We appreciate the correspondence of Dr van Dijk on our study in CHEST,1 in which we examined lung function decline in three groups of heavy smokers classified by their baseline prebronchodilator FEV1/FVC: >70%, ≤70%, and less than the lower limit of normal. We believe that Dr van Dijk misinterpreted the outcomes reported in Table 4. As can be found in the “Materials and Methods” section,1 the decline was analyzed by multiple linear regression with the follow-up FEV1 as the dependent variable and the baseline FEV1, among others, as an independent variable. In our Table 4, the regression coefficients (β) of the significant independent variables are listed. Classically, in linear regression analysis, the independent variables are multiplied with their regression coefficient (βx), in this case, baseline FEV1 × 0.94. From this it can be easily concluded that a higher baseline FEV1 results in a lower follow-up FEV1, and not, as implied by Dr van Dijk, in preserving airflow.

We corrected for smoking status and pack-years smoked, and, therefore, do not find it likely that our results can be explained by differences in smoking status. Moreover, in the patients with an FEV1/FVC <70% and less than lower limit of normal, pack-years smoked and number of current smokers was highest. Nonetheless, at the end, we agree with Dr van Dijk that lung function decline in our cohort of heavy smokers was substantial and that smoking cessation is one of the major interventions to address this.

Acknowledgments

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscript.

Mohamed Hoesein FAA, Zanen P, Boezen HM, et al. Lung function decline in male heavy smokers relates to baseline airflow obstruction severity. Chest. 2012;142(6):1530-1538. [CrossRef]
 

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References

Mohamed Hoesein FAA, Zanen P, Boezen HM, et al. Lung function decline in male heavy smokers relates to baseline airflow obstruction severity. Chest. 2012;142(6):1530-1538. [CrossRef]
 
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