| Institution: | 1. Manchester University NHS Foundation Trust, Wythenshawe Hospital, Manchester, United Kingdom;2. Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom;3. Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA;4. Cardiovascular Magnetic Resonance Center, Heart and Vascular Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA;5. Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, Pennsylvania, USA;6. Division of Infection, Immunity, and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom;7. Stepping Hill Hospital, Stockport NHS Foundation Trust, Hazel Grove, Stockport, United Kingdom;8. Royal Bolton Hospital, Bolton NHS Foundation Trust, Farnworth, Bolton, United Kingdom;9. Royal Albert Edward Infirmary, Wrightington, Wigan and Leigh NHS Foundation Trust, Wigan, United Kingdom;10. Tameside Hospital, Tameside and Glossop Integrated Care NHS Foundation Trust, Ashton-under-Lyne, United Kingdom;11. Trafford General Hospital, Manchester University NHS Foundation Trust, Davyhulme, Manchester, United Kingdom;12. Fairfield General Hospital, Pennine Acute Hospitals NHS Trust, Oldham, United Kingdom;13. Macclesfield District General Hospital, East Cheshire NHS Trust, Macclesfield, Cheshire, United Kingdom;14. Liverpool School of Tropical Medicine, Liverpool, United Kingdom;15. National Heart and Lung Institute, Imperial College London, London, United Kingdom;p. Division of Cell-Matrix Biology and Regenerative Medicine, Wellcome Centre for Cell-Matrix Research, School of Biology, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom |
| Abstract: | ObjectivesThe purposes of this study were to determine why chronic obstructive pulmonary disease (COPD) is associated with heart failure (HF). Specific objectives included whether COPD is associated with myocardial fibrosis, whether myocardial fibrosis is associated with hospitalization for HF and death in COPD, and whether COPD and smoking are associated with myocardial inflammation.BackgroundCOPD is associated with HF independent of shared risk factors. The underlying pathophysiological mechanism is unknown.MethodsA prospective, multicenter, longitudinal cohort study of 572 patients undergoing cardiac magnetic resonance (CMR), including 450 patients with COPD and 122 age- and sex-matched patients with a median: 726 days (interquartile range: 492 to 1,160 days) follow-up. Multivariate analysis was used to examine the relationship between COPD and myocardial fibrosis, measured using cardiac magnetic resonance (CMR). Cox regression analysis was used to examine the relationship between myocardial fibrosis and outcomes; the primary endpoint was composite of hospitalizations for HF or all-cause mortality; secondary endpoints included hospitalizations for HF and all-cause mortality. Fifteen patients with COPD, 15 current smokers, and 15 healthy volunteers underwent evaluation for myocardial inflammation, including ultrasmall superparamagnetic particles of iron oxide CMR.ResultsCOPD was independently associated with myocardial fibrosis (p < 0.001). Myocardial fibrosis was independently associated with the primary outcome (hazard ratio HR]: 1.14; 95% confidence interval CI]: 1.08 to 1.20; p < 0.001), hospitalization for HF (HR: 1.25 95% CI: 1.14 to 1.36]); p < 0.001), and all-cause mortality. Myocardial fibrosis was associated with outcome measurements more strongly than any other variable. Acute and stable COPD were associated with myocardial inflammation.ConclusionsThe associations between COPD, myocardial inflammation and myocardial fibrosis, and the independent prognostic value of myocardial fibrosis elucidate a potential pathophysiological link between COPD and HF. |
