0
Correspondence |

Response FREE TO VIEW

Ari Chaouat, MD; Laurent Savale, MD; Serge Adnot, MD
Author and Funding Information

From the Centre Hospitalier Régional Universitaire Nancy (Dr Chaouat), Hôpital de Brabois, Service des Maladies Respiratoires et Réanimation Respiratoire; the Assistance Publique - Hôpitaux de Paris (Drs Savale and Adnot), Hôpital Henri Mondor, Service de Physiologie Explorations Fonctionnelles; and INSERM U841 (Drs Savale and Adnot), Faculté de Médecine de Créteil.

Correspondence to: Ari Chaouat, MD, Centre Hospitalier Régional Universitaire de Nancy, Service des Maladies Respiratoires et Réanimation Respiratoire, Hôpital d'adultes de Brabois, Allée du Morvan, 54511 Vandoeuvre-lés-Nancy Cedex, France; e-mail: a.chaouat@chu-nancy.fr


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 (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(5):1251. doi:10.1378/chest.10-0025
Text Size: A A A
Published online

To the Editor:

We thank Young and Hopkins for their interesting comments on our article (September 2009).1 They suggest that low-grade systemic inflammation mediated by interleukin-6 (IL-6) may act concomitantly on the skeletal muscles and pulmonary vasculature to impair exercise capacity in patients with COPD. It has been shown that IL-6 is increased in the plasma of patients with COPD2 and induces the release of acute-phase proteins; furthermore, IL-6 probably has other systemic effects that have not yet been fully elucidated. The hypothesis put forward by Young and Hopkins is partly supported by our results. Our study1 did not establish a link between systemic inflammation and exercise capacity, because it focused on the mechanism of pulmonary hypertension in patients with COPD. However, we found a weak but significant correlation between the 6-min walk distance and plasma IL-6 level (r = −0.329, P =.04). However, as stated in our article, the 6-min walk distance did not correlate with mean pulmonary artery pressure. Only very few studies found that mean pulmonary artery pressure determined the severity of exercise limitation in COPD.3 We fully agree with Young and Hopkins that any drugs designed to improve exercise capacity in COPD must have several targets, as shown in their Figure 1. Indeed, in our opinion, a drug that only lowers mean pulmonary artery pressure is likely to improve neither the dyspnea nor the exercise capacity and is probably not worth pursuing. It is also important to emphasize that smoke exposure in genetically susceptible individuals promotes the development of COPD4 and may also promote the development of comorbidities through systemic inflammation.

Regarding pulmonary hypertension complicating COPD, we already know that the Rho A/Rho-kinase pathway, a target of statins, has an important role in pulmonary artery endothelial dysfunction and remodeling.5 Therefore, current knowledge suggests that statin therapy in patients with COPD may improve the pulmonary hypertension and skeletal muscle dysfunction6 and may, therefore, increase exercise capacity. To confirm these hypotheses, further pathophysiologic studies of the relationships linking low-grade systemic inflammation to comorbidities in COPD are needed. Finally, large randomized controlled studies investigating the effects and safety of statins in COPD are mandatory to determine whether these drugs should be routinely added to the current long-term pharmacologic regimens.

Chaouat A, Savale L, Chouaid C, et al. Role for interleukin-6 in COPD-related pulmonary hypertension. Chest. 2009;1363:678-687. [CrossRef] [PubMed]
 
Bhowmik A, Seemungal TA, Sapsford RJ, Wedzicha JA. Relation of sputum inflammatory markers to symptoms and lung function changes in COPD exacerbations. Thorax. 2000;552:114-120. [CrossRef] [PubMed]
 
Leuchte HH, Neurohr C, Baumgartner R, et al. Brain natriuretic peptide and exercise capacity in lung fibrosis and pulmonary hypertension. Am J Respir Crit Care Med. 2004;1704:360-365. [CrossRef] [PubMed]
 
Hunninghake GM, Cho MH, Tesfaigzi Y, et al. MMP12, lung function, and COPD in high-risk populations. N Engl J Med. 2009;36127:2599-2608. [CrossRef] [PubMed]
 
Duong-Quy S, Dao P, Hua-Huy T, et al. Role of Rho-kinase pathway in ET-1-induced vasoconstriction in pulmonary artery of chronic obstructive pulmonary disease (COPD).Accessed February 19, 2010 Abstract presented at: European Respiratory Society Annual Congress; September 12-16 2009; Vienna, Austria.http://www.ersnet.org/learning_resources_player/abstract_print_09/main_frameset.htm.
 
Yende S, Waterer GW, Tolley EA, et al. Inflammatory markers are associated with ventilatory limitation and muscle dysfunction in obstructive lung disease in well functioning elderly subjects. Thorax. 2006;611:10-16. [CrossRef] [PubMed]
 

Figures

Tables

References

Chaouat A, Savale L, Chouaid C, et al. Role for interleukin-6 in COPD-related pulmonary hypertension. Chest. 2009;1363:678-687. [CrossRef] [PubMed]
 
Bhowmik A, Seemungal TA, Sapsford RJ, Wedzicha JA. Relation of sputum inflammatory markers to symptoms and lung function changes in COPD exacerbations. Thorax. 2000;552:114-120. [CrossRef] [PubMed]
 
Leuchte HH, Neurohr C, Baumgartner R, et al. Brain natriuretic peptide and exercise capacity in lung fibrosis and pulmonary hypertension. Am J Respir Crit Care Med. 2004;1704:360-365. [CrossRef] [PubMed]
 
Hunninghake GM, Cho MH, Tesfaigzi Y, et al. MMP12, lung function, and COPD in high-risk populations. N Engl J Med. 2009;36127:2599-2608. [CrossRef] [PubMed]
 
Duong-Quy S, Dao P, Hua-Huy T, et al. Role of Rho-kinase pathway in ET-1-induced vasoconstriction in pulmonary artery of chronic obstructive pulmonary disease (COPD).Accessed February 19, 2010 Abstract presented at: European Respiratory Society Annual Congress; September 12-16 2009; Vienna, Austria.http://www.ersnet.org/learning_resources_player/abstract_print_09/main_frameset.htm.
 
Yende S, Waterer GW, Tolley EA, et al. Inflammatory markers are associated with ventilatory limitation and muscle dysfunction in obstructive lung disease in well functioning elderly subjects. Thorax. 2006;611:10-16. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543