ECG-based risk factors for adverse cardiopulmonary events and treatment outcomes in COPD

R Chad Wade; Fernando J Martinez; Gerard J Criner; Lee Tombs; David A Lipson; David M G Halpin; MeiLan K Han; Dave Singh; Robert A Wise; Ravi Kalhan; Mark T Dransfield

doi:10.1183/13993003.00171-2024

ECG-based risk factors for adverse cardiopulmonary events and treatment outcomes in COPD

Eur Respir J. 2024 Nov 21:2400171. doi: 10.1183/13993003.00171-2024. Online ahead of print.

Authors

R Chad Wade¹, Fernando J Martinez², Gerard J Criner³, Lee Tombs⁴, David A Lipson^{5

6}, David M G Halpin⁷, MeiLan K Han⁸, Dave Singh⁹, Robert A Wise¹⁰, Ravi Kalhan¹¹, Mark T Dransfield¹²

Affiliations

¹ Division of Pulmonary, Allergy, and Critical Care Medicine, Lung Health Center, University of Alabama at Birmingham, Birmingham, AL, USA.
² Division of Pulmonology and Critical Care Medicine, Weill Cornell Medicine, New York, NY, USA.
³ Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
⁴ Precise Approach Ltd, London, UK.
⁵ GSK, Collegeville, PA, USA.
⁶ Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
⁷ University of Exeter Medical School, University of Exeter, Exeter, UK.
⁸ Univeristy of Michigan, Ann Arbor, MI, USA.
⁹ Centre for Respiratory Medicine and Allergy, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, University of Manchester, Manchester University NHS Foundation Trust, Manchester, UK.
¹⁰ Johns Hopkins University School of Medicine, Baltimore, MD, USA.
¹¹ Department of Preventive Medicine and Division of Pulmonary and Critical Care Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
¹² Division of Pulmonary, Allergy, and Critical Care Medicine, Lung Health Center, University of Alabama at Birmingham, Birmingham, AL, USA [email protected].

PMID: 39467609
DOI: 10.1183/13993003.00171-2024

Abstract

Background: COPD has high mortality, compounded by comorbid cardiovascular disease. We investigated two electrocardiogram (ECG) markers, Cardiac Infarction Injury Score (CIIS) and P pulmonale, as prognostic tools for adverse cardiopulmonary events in COPD.

Methods: Post hoc analysis of the IMPACT trial. Outcomes included odds (odds ratio [95% confidence intervals]) of adverse cardiopulmonary events stratified by CIIS threshold (<20/≥20) and P pulmonale (baseline). Events included all-cause death, hospitalisation/death, cardiovascular adverse event of special interest (CVAESI), severe COPD exacerbations, and moderate/severe COPD exacerbations. Effects of fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI) versus FF/VI or UMEC/VI based on CIIS and P pulmonale were also assessed.

Results: We included 9448 patients. Patients with CIIS ≥20 had greater odds of all-cause death (1.73[1.27-2.37]; p<0.001), hospitalisation/death (1.33[1.17-1.50]; p<0.001), CVAESI (1.27[1.08-1.48]; p<0.005), severe COPD exacerbations (1.41[1.21-1.64]; p<0.001) and moderate/severe COPD exacerbations (1.25[1.13-1.40]; p<0.001) versus CIIS <20. Patients with P pulmonale (versus without) had greater odds of all-cause death (2.25[1.54-3.29]; p<0.001), hospitalisation/death (1.51[1.28-1.79]; p<0.001), severe COPD exacerbations (2.00[1.65-2.41]; p<0.001) and moderate/severe COPD exacerbations (1.25[1.08-1.46]; p<0.001). A combined model demonstrated patients with CIIS ≥20 and P pulmonale had increased risk of all-cause death (3.38[1.23-9.30]; p=0.019), hospitalisation/death (1.61[1.14-2.22]; p=0.004), and rate of severe COPD exacerbations (1.89[1.22-2.91]; p=0.004) and moderate/severe COPD exacerbations (1.25[1.00-1.56]; p=0.046). The risk of all-cause death and CVAESI was reduced with FF/UMEC/VI versus UMEC/VI in patients with CIIS ≥20, but not CIIS <20.

Conclusions: These findings suggest potential clinical relevance of CIIS and P pulmonale as risk indicators for adverse cardiopulmonary events in COPD.