TY - JOUR T1 - COPD: CardiOPulmonary Disease? JF - European Respiratory Journal JO - Eur Respir J SP - 1241 LP - 1243 DO - 10.1183/09031936.00009413 VL - 41 IS - 6 AU - Steven M. Kawut Y1 - 2013/06/01 UR - http://erj.ersjournals.com/content/41/6/1241.abstract N2 - Chronic obstructive pulmonary disease (COPD) is defined by the presence of airflow limitation which is not fully reversible, but COPD encompasses numerous phenotypes [1]. Phenotypes are the products of genetic and environmental interactions, with “environment” being broadly defined. The systematic measurement and analysis of clinical and other qualitative and quantitative traits may refine COPD phenotypes, features of which may be shared between different disease states [2, 3]. Han et al. [4] have defined clinical phenotypes in COPD as “a single or combination of disease attributes that describe differences between individuals with COPD as they relate to clinically meaningful outcomes (symptoms, exacerbations, response to therapy, rate of disease progression, or death).” Identification of such phenotypes would not only facilitate outcome prediction and “personalised” treatment, but also improve the understanding of critical biological and mechanistic disease pathways. The systemic impact of COPD has led to consideration of extrapulmonary disease manifestations in recent efforts to construct these phenotypes.This issue of the European Respiratory Journal contains one of two recent studies that focus on cardiovascular phenotyping in COPD [5, 6]. Hurdman et al. [5] have carefully evaluated the phenotype of severe pulmonary hypertension (PH) (mean pulmonary artery pressure ≥40 mmHg) in COPD (PH-COPD) in comparison to the mild–moderate PH phenotype in a prospective cohort of patients referred to a specialty centre over almost a decade [7]. Echocardiography, spirometry and lung computed tomography (CT) imaging were performed with standardised interpretation. 59 patients with severe PH-COPD were compared to 42 patients with mild–moderate PH-COPD, with complete follow-up in all. Patients with severe PH-COPD had worse oxygenation and a lower diffusing capacity for carbon monoxide (DLCO), but higher forced expiratory volume in 1 s (FEV1), forced vital capacity … ER -