Daan W Loth1, Lies Lahousse2, Maarten J G Leening3, Bouwe P Krijthe1, Janine F Felix1, Henning Gall4, Albert Hofman5, H Ardeschir Ghofrani4, Oscar H Franco1, Bruno H Stricker6, Guy G Brusselle7. 1. Department of Epidemiology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands. 2. Department of Epidemiology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands; Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium. 3. Department of Epidemiology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands; Department of Cardiology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 4. Universities of Giessen and Marburg Lung Center (UGMLC) - Member of the German Center for Lung Research (DZL), Giessen, Germany. 5. Department of Epidemiology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 6. Department of Epidemiology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands; Inspectorate of Health Care, Utrecht, The Netherlands; Department of Internal Medicine, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands. 7. Department of Epidemiology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands; Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium; Department of Respiratory Medicine, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands. Electronic address: guy.brusselle@ugent.be.
Abstract
BACKGROUND: Pulmonary hypertension is a progressive heterogeneous syndrome, characterized by elevated pulmonary arterial pressure which can lead to right ventricular failure. Although the presence of elevated pulmonary arterial systolic pressure (PASP) in patients with a lung disease is a well-known occurrence, little is known about the association between pulmonary function and PASP in the general population. We hypothesized that pulmonary function and PASP are associated, irrespective of airflow limitation. METHODS: This study was performed within the Rotterdam Study, a prospective population-based cohort. We included 1660 participants with spirometry, performed and interpreted according to ATS/ERS-guidelines, and echocardiography performed according to the ASE/EAE/CSE-guidelines. We analyzed the association of Forced Expiratory Volume in 1 s (FEV1), Forced Vital Capacity (FVC), FEV1/FVC and diffusion capacity (DLCO) with estimated PASP (ePASP). Furthermore, we investigated the association between spirometry measures, COPD, and echocardiographic pulmonary hypertension. RESULTS: A 10% absolute decrease in FEV1 was associated with an ePASP increase of 0.46 mmHg (95%CI: 0.31; 0.61). Similarly, per absolute 10% decrease, FVC was significantly associated with an increased ePASP of 0.42 mmHg (95%CI: 0.25; 0.59). FEV1/FVC showed an association of 1.01 mmHg (95%CI: 0.58; 1.45) increase in ePASP per 10% absolute decrease. A decrease in DLCO (in mL/min/kPa) was associated with an increased ePASP (0.46 mmHg, 95%CI: 0.17; 0.76). We found significant associations for FEV1 and FVC with echocardiographic pulmonary hypertension. Importantly, an increased ePASP was significantly associated with mortality (Hazard Ratio: 1.042 per mmHg [95%CI: 1.023-1.062; p < 0.001]). CONCLUSION: We observed a clearly graded association between pulmonary function and ePASP and pulmonary hypertension, even in individuals without airflow limitation.
BACKGROUND:Pulmonary hypertension is a progressive heterogeneous syndrome, characterized by elevated pulmonary arterial pressure which can lead to right ventricular failure. Although the presence of elevated pulmonary arterial systolic pressure (PASP) in patients with a lung disease is a well-known occurrence, little is known about the association between pulmonary function and PASP in the general population. We hypothesized that pulmonary function and PASP are associated, irrespective of airflow limitation. METHODS: This study was performed within the Rotterdam Study, a prospective population-based cohort. We included 1660 participants with spirometry, performed and interpreted according to ATS/ERS-guidelines, and echocardiography performed according to the ASE/EAE/CSE-guidelines. We analyzed the association of Forced Expiratory Volume in 1 s (FEV1), Forced Vital Capacity (FVC), FEV1/FVC and diffusion capacity (DLCO) with estimated PASP (ePASP). Furthermore, we investigated the association between spirometry measures, COPD, and echocardiographic pulmonary hypertension. RESULTS: A 10% absolute decrease in FEV1 was associated with an ePASP increase of 0.46 mmHg (95%CI: 0.31; 0.61). Similarly, per absolute 10% decrease, FVC was significantly associated with an increased ePASP of 0.42 mmHg (95%CI: 0.25; 0.59). FEV1/FVC showed an association of 1.01 mmHg (95%CI: 0.58; 1.45) increase in ePASP per 10% absolute decrease. A decrease in DLCO (in mL/min/kPa) was associated with an increased ePASP (0.46 mmHg, 95%CI: 0.17; 0.76). We found significant associations for FEV1 and FVC with echocardiographic pulmonary hypertension. Importantly, an increased ePASP was significantly associated with mortality (Hazard Ratio: 1.042 per mmHg [95%CI: 1.023-1.062; p < 0.001]). CONCLUSION: We observed a clearly graded association between pulmonary function and ePASP and pulmonary hypertension, even in individuals without airflow limitation.
Authors: Matthew Jankowich; Beth Elston; Qing Liu; Siddique Abbasi; Wen-Chih Wu; Chad Blackshear; Mark Godfrey; Gaurav Choudhary Journal: Ann Am Thorac Soc Date: 2018-10