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Boston, MA
Dr. Celli is Professor of Medicine, Tufts University.
Correspondence to: Bartolome R. Celli, MD, FCCP, Caritas-St. Elizabeth’s Medical Center, Pulmonary Critical Care Division, 736 Cambridge St, Boston. MA, 02135; e-mail: bcelli{at}copdnet.org
Since the studies of Fletcher and colleagues,1 the natural history of COPD has been associated with the accelerated progressive decline of FEV1. FEV1 became the defining feature of the disease, and because it predicted mortality, health costs, and exacerbations,234 it constituted the logical target for disease-modifying interventions. Unfortunately, the diagnosis of COPD mandates that there be minimal FEV1 response to bronchodilators, thus making changes in FEV1 very difficult to achieve.
It is time to change the way in which we define disease modification in COPD. Indeed, COPD is associated with clinical manifestations not closely related to the FEV1, such as worsened dyspnea, reduction in exercise capacity, pulmonary hypertension, peripheral muscle weakness, and malnutrition.5 Furthermore, all of these factors appear to be more important predictors of mortality than FEV1.6789 Therefore, defining disease modification solely on the improvement on the FEV1 does not reflect the clinical manifestations of the disease and its ultimate prognosis.
Borrowing from the experience of other medical fields, disease modification in COPD can be defined as any of the changes in a patient with COPD that are caused by an intervention. The changes should be maintained over time. If we accept certain patient-centered outcomes as important, changes in any of them should be conceived as disease modifying. One such intervention, lung volume reduction surgery (LVRS), was popularized by Cooper et al10 as a therapy for COPD patients with primarily upper-lobe emphysema. Although the National Emphysema Treatment Trial11 did not confer survival advantage to the surgical group as a whole, it resulted in differences in health status and exercise capacity in favor of LVRS and, at least in patients with upper-lobe emphysema and poor exercise capacity, a difference in survival after 3 years. It would be extremely useful if there were "surrogate" markers that could detect changes in a relatively short period of time, and that were accurate in predicting patient outcome. In this sense that marker could become a tool in monitoring disease modification. The multidimensional index BODE that includes the body mass index (B), percentage of predicted FEV1 (O), dyspnea (D), and the 6-min walk distance (E) is such a tool,12 as it predicts mortality better than FEV1. Furthermore, the variables that contribute to the index are amenable to change by interventions and thus make the BODE a potential tool to use in the evaluation of disease-modifying interventions.
In this issue of CHEST (see page 873), Imfeld and coworkers13 evaluated the power of short-term (3 months) changes in the BODE index in predicting survival in 186 patients undergoing LVRS. Using C statistics, the postoperative BODE index was a better predictor of survival than FEV1, dyspnea score, or 6-min walk distance. These results are in line with those reported by Cote and Celli,14 who showed that the BODE index can improve after pulmonary rehabilitation and that the magnitude of the change was predictive of survival.
In the last few years, there have been important changes in the way we view COPD. Unfortunately, the regulatory agencies, the medical public at large, and many in our midst still cling to the old concept that it is only by changing FEV1 that we modify the course of the disease. Imfeld and coworkers are to be praised for helping show that there are disease-modifying interventions and that tools such as the BODE index can be used as markers defining ulterior outcome.
References
This article has been cited by other articles:
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  B. R. Celli Update on the Management of COPD Chest, June 1, 2008; 133(6): 1451 - 1462. [Abstract] [Full Text] [PDF]
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C. G. Cote, L. J. Dordelly, and B. R. Celli Impact of COPD Exacerbations on Patient-Centered Outcomes Chest, March 1, 2007; 131(3): 696 - 704. [Abstract] [Full Text] [PDF]
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