© 2008 American Thoracic Society
Arterial Stiffness and Chronic Obstructive Pulmonary DiseaseFrom the Authors:We thank Drs. Boussuges and Gouitaa for their interest in our article (1). While we accept that heart rate (HR) was higher in patients with COPD compared with control subjects, we do not believe that this explains the difference in augmentation index (AIx) and aortic pulse wave velocity (PWV) between groups. We have previously shown that HR influences AIx (2), which is why in our study all values of AIx were corrected to 75 beats per minute. Additionally, HR was included as an independent variable in all stepwise regression models. The influence of HR on aortic PWV remains controversial, with a number of studies demonstrating no association (2, 3). We read with interest the authors' reference to their article demonstrating reduced total arterial and brachial artery compliance in patients with COPD. While we welcome further support for our finding of increased arterial stiffness in patients with COPD, we caution against the use of brachial PWV. Unlike aortic PWV, which is widely regarded as the gold standard measure of central arterial stiffness (4), brachial PWV to date has not been shown to be predictive of cardiovascular outcome (5). The article by Zureik and coworkers to which the authors refer was the first study to demonstrate a relationship between impaired pulmonary function and aortic stiffness (6). However, when considering the relationship between arterial stiffness and COPD, the results of this study must be interpreted with caution since impaired pulmonary function was not characterized into obstructive and restrictive defects. Moreover, this study had only male subjects and included patients with diabetes mellitus, hypertension, and hypercholesterolemia, known confounders for arterial stiffness. Finally, we agree with the authors that increased vascular smooth muscle tone is a contributor to increased arterial stiffness in COPD and that a number of factors influence vascular smooth muscle tone, including sympathetic activation and endothelium-derived nitric oxide (NO) (7). This suggests that elements of arterial stiffness may be modifiable in patients with COPD and that drugs which increase the bioavailability of endothelium-derived NO may be of benefit (7).
Cardiff University, Academic Centre
Cardiff University, Wales Heart Research Institute
Cardiff University, Academic Centre FOOTNOTES Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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