Pulmonary vascular involvement in COPD.
Alterations in pulmonary vessel structure and function are highly prevalent in patients with COPD. Vascular abnormalities impair gas exchange and may result in pulmonary hypertension, which is one of the principal factors associated with reduced survival in COPD patients. Changes in pulmonary circulation have been identified at initial disease stages, providing new insight into their pathogenesis. Endothelial cell damage and dysfunction produced by the effects of cigarette smoke products or inflammatory elements is now considered to be the primary alteration that initiates the sequence of events resulting in pulmonary hypertension. Cellular and molecular mechanisms involved in this process are being extensively investigated. Progress in the understanding of the pathobiology of pulmonary hypertension associated with COPD may provide the basis for a new therapeutic approach addressed to correct the imbalance between endothelium-derived vasoactive agents. The safety and efficacy of endothelium-targeted therapy in COPD-associated pulmonary hypertension warrants further investigation in randomized clinical trials.
Department of Pulmonary Medicine, Hospital Clínic, Universitat de Barcelona, Barcelona, Spain; Institut d' Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Ciber de Enfermedades Respiratorias, Barcelona, Spain.
Víctor I
VI
Peinado
Department of Pulmonary Medicine, Hospital Clínic, Universitat de Barcelona, Barcelona, Spain; Institut d' Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Ciber de Enfermedades Respiratorias, Barcelona, Spain.
Sandra
S
Pizarro
Department of Pulmonary Medicine, Hospital Clínic, Universitat de Barcelona, Barcelona, Spain; Institut d' Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Ciber de Enfermedades Respiratorias, Barcelona, Spain. Electronic address: jbarbera@clinic.ub.es.
Joan Albert
JA
Barberà
D004730:Endothelium, Vascular / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D008168:Lung / Q000098:blood supply*; D011652:Pulmonary Circulation / Q000502:physiology; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology