Thibaud Soumagne1, Nicolas Roche2, Alicia Guillien3, Malika Bouhaddi4, Steffi Rocchi5, Sophie Hue6, Frédéric Claudé7, Lucie Bizard8, Pascal Andujar9, Jean-Charles Dalphin10, Bruno Degano11. 1. Service de Physiologie-Explorations Fonctionnelles, Centre Hospitalier Universitaire Besançon, Besançon, France; Service de Pneumologie, Centre Hospitalier Universitaire Besançon, Besançon, France. Electronic address: thibaud_soumagne@live.fr. 2. Service de Pneumologie et Soins Intensifs Respiratoires, Groupe Hospitalier Cochin, Site Val de Grâce, AP-HP, and Université Paris Descartes (EA2511), Sorbonne-Paris-Cité, Paris, France. 3. Equipe d'Epidémiologie Environnementale, Institute for Advanced Biosciences, Centre de Recherche UGA, INSERM U1209, CNRS UMR 5309, Grenoble, France. 4. Service de Physiologie-Explorations Fonctionnelles, Centre Hospitalier Universitaire Besançon, Besançon, France. 5. Service de Parasitologie-Mycologie, Centre Hospitalier Universitaire Besançon, Besancon, France. 6. Immunologie-Biologie, Hôpital Henri-Mondor, AP-HP, Paris, France; INSERM Unité U955, Equipe 4, Créteil, France. 7. Service de Pneumologie, Centre Hospitalier Universitaire Besançon, Besançon, France. 8. INSERM Unité U955, Equipe 4, Créteil, France. 9. INSERM Unité U955, Equipe 4, Créteil, France; Faculté de Médecine, Université Paris-Est Créteil, Créteil, France; Service de Pathologie Professionnelle et de l'Environnement, Centre Hospitalier Intercommunal de Créteil, Créteil, France. 10. Service de Pneumologie, Centre Hospitalier Universitaire Besançon, Besançon, France; UMR CNRS Chrono Environnement, Université de Franche-Comté, Besançon, France. 11. Service Hospitalier Universitaire Pneumologie Physiologie, Pôle Thorax et Vaisseaux, Centre Hospitalier Universitaire Grenoble-Alpes, Grenoble, France; Université Grenoble Alpes, Grenoble, France.
Abstract
BACKGROUND: The observation that COPD is an independent risk factor for cardiovascular disease (CVDs) comes from comparisons between smokers with COPD and smokers without COPD. The mechanisms that explain increased risk of CVD in patients with COPD are still unclear. OBJECTIVES: The goal of this study was to assess systemic arterial stiffness (a predictor of CVD mortality) and to evaluate its determinants in a group of patients with mild to moderate COPD secondary to organic dust exposure, tobacco smoking, or both. METHODS: Systemic arterial stiffness was assessed by using aortic pulse wave velocity (aPWV). Measurements were made in 142 patients with COPD and 155 healthy control subjects matched for age, sex, BMI, and tobacco smoking, exposed to tobacco smoking (n = 56/70 for COPD/control subjects, respectively), organic dusts (n = 44/48), or both (n = 42/37). RESULTS: aPWV was higher in COPD than in healthy controls in subjects exposed to tobacco smoking and to both organic dusts and tobacco smoking. By contrast, among never smokers exposed to organic dusts, patients with COPD and matched control subjects had similar aPWV. Multivariate analysis of the 142 patients with COPD (exposed to tobacco smoking and/or to organic dusts) showed that tobacco smoking was associated with high aPWV. Moreover, soluble suppression of tumorigenicity 2, a marker of major cardiovascular events, was correlated with aPWV in these patients. CONCLUSIONS: Analysis of an unselected group of patients with COPD with different causes suggests that: (1) COPD by itself is not sufficient to explain increased aPWV; and (2) tobacco smoking is a risk factor for elevated aPWV in COPD.
BACKGROUND: The observation that COPD is an independent risk factor for cardiovascular disease (CVDs) comes from comparisons between smokers with COPD and smokers without COPD. The mechanisms that explain increased risk of CVD in patients with COPD are still unclear. OBJECTIVES: The goal of this study was to assess systemic arterial stiffness (a predictor of CVD mortality) and to evaluate its determinants in a group of patients with mild to moderate COPD secondary to organic dust exposure, tobacco smoking, or both. METHODS: Systemic arterial stiffness was assessed by using aortic pulse wave velocity (aPWV). Measurements were made in 142 patients with COPD and 155 healthy control subjects matched for age, sex, BMI, and tobacco smoking, exposed to tobacco smoking (n = 56/70 for COPD/control subjects, respectively), organic dusts (n = 44/48), or both (n = 42/37). RESULTS: aPWV was higher in COPD than in healthy controls in subjects exposed to tobacco smoking and to both organic dusts and tobacco smoking. By contrast, among never smokers exposed to organic dusts, patients with COPD and matched control subjects had similar aPWV. Multivariate analysis of the 142 patients with COPD (exposed to tobacco smoking and/or to organic dusts) showed that tobacco smoking was associated with high aPWV. Moreover, soluble suppression of tumorigenicity 2, a marker of major cardiovascular events, was correlated with aPWV in these patients. CONCLUSIONS: Analysis of an unselected group of patients with COPD with different causes suggests that: (1) COPD by itself is not sufficient to explain increased aPWV; and (2) tobacco smoking is a risk factor for elevated aPWV in COPD.