From Gartnavel General Hospital (Dr Maclay); and the University of Edinburgh, MRC Centre for Inflammation Research (Dr MacNee), The Edinburgh University.
Correspondence to: John D. Maclay, MBChB MD, University of Edinburgh, Centre for Inflammation Research, 47 Little France Crescent, Edinburgh EH16 4SB, Scotland; e-mail: firstname.lastname@example.org
Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts: Dr MacNee has acted in an advisory capacity for GlaxoSmithKline plc; Pfizer, Inc; Novartis AG; and Almirall, SA. He has received payment from GlaxoSmithKline plc and Pfizer, Inc for research programs and clinical activities and has also received payments from Boehringer-Ingelheim GmbH, GlaxoSmithKline, AstraZeneca, Novartis AG, and Janssen Pharmaceuticals to travel to meetings and/or present at conferences. Dr Maclay has reported 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.
We thank Drs Kheir and Salerno for their interest in our review.1 We agree that measuring N-terminal B-type natriuretic peptide (NT-proBNP) levels in COPD is of interest. Chang et al2 reported that in patients admitted with exacerbation of COPD, both plasma NT-proBNP and troponin T levels predicted mortality at 30 days, even after accounting for other markers of exacerbation severity. While these markers seem to reflect myocardial stretch and myocardial ischemia during acute exacerbation of COPD, it is less likely that NT-proBNP and troponin T are mediators of cardiovascular disease in COPD. In addition, it would be difficult to ascertain whether NT-proBNP release in exacerbation of COPD is due to right-sided heart dysfunction rather than left-sided heart dysfunction.3
Drs Kheir and Salerno comment that BNP is an independent predictor of endothelial dysfunction. BNP was shown to be an independent predictor of acetylcholine-mediated vasodilatation, a sensitive measure of systemic endothelial function.4 We have previously compared endothelial function using this gold standard method and showed no differences between patients with COPD and control subjects matched for age and cigarette smoke exposure.5
Thus, in summary, measuring NT-proBNP may have clinical relevance in exacerbation of COPD and may reflect myocardial strain in this circumstance. However, its contribution is likely to be as a marker rather than a mediator of cardiovascular dysfunction in COPD.
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