The 2004 American Thoracic Society/European Respiratory Society task force position paper (1) presented the first set of guidelines that defined chronic obstructive pulmonary disease (COPD) as a lung disease that also produces significant systemic consequences. In the revised 2006 version of the GOLD (Global Initiative for Chronic Obstructive Lung Disease) guidelines, weight loss, nutritional abnormalities, and skeletal muscle dysfunction are mentioned as well-recognized extrapulmonary effects. In addition, it is stated that patients with COPD are at increased risk for—among others—depression, diabetes, sleep disorders, anemia, glaucoma, osteoporosis, and myocardial infarction (2). From epidemiologic studies, it is known that a large percentage of deaths in patients with COPD arise from cardiovascular diseases (3). In addition, COPD is one of the most important comorbidities in patients with myocardial infarction (4). Moreover, patients with myocardial infarction and COPD have a higher mortality than those without lung disease (5). We do not know for sure how cardiovascular diseases are related to COPD: Are they just a consequence of the same bad habit (ie, cigarette smoking), or is there a cause–effect relationship in the sense that COPD induces the development of cardiovascular disorders? The article by Sabit and colleagues (6) in this issue of the Journal (pp. 1259–1265) gives important and new information concerning this issue. The authors assumed that COPD leads to alterations in vascular structure. To evaluate this hypothesis, they analyzed arterial stiffness by measuring aortic pulse wave velocity. Increased arterial stiffness has been shown to predict cardiovascular outcomes in various populations (7). Aortic pulse wave velocity is considered the most clinically relevant measure of arterial stiffness and independently predicts cardiovascular risk (8). Sabit and colleagues included patients with stable COPD representing GOLD stages I–IV. Healthy smokers and ex-smokers were used as control subjects. Mean aortic pulse wave velocity was greater in patients than in control subjects. Furthermore, pulse wave velocity was correlated to the GOLD stage—the more severe the flow limitation, the higher the pulse wave velocity values. Thus, COPD may induce increased arterial stiffness, which in turn may promote vascular remodeling, thickening of arterial walls, and plaque formation. This process may start in the early stages of COPD and worsen with decline of lung function. These results are supported by data from Eickhoff and coworkers (9) who analyzed endothelial function in the brachial artery of patients with COPD by measuring endothelium-dependent flowmediated dilution. In that study, this parameter was lower in patients with COPD compared with healthy smokers and much lower compared with nonsmokers, suggesting the presence of significant endothelial dysfunction in COPD. The second focus of the article by Sabit and colleagues was osteoporosis. The authors found that bone mineral density was lower in patients with COPD than in control subjects. Among the patients with COPD, 32% had osteoporosis and this was not