Marc W Heidorn1, Stefanie Steck1, Felix Müller1, Sven-Oliver Tröbs1, Gregor Buch2, Andreas Schulz3, Sören Schwuchow-Thonke4, Alexander Schuch1, Konstantin Strauch5, Irene Schmidtmann5, Karl J Lackner6, Tommaso Gori4, Thomas Münzel4, Philipp S Wild7, Jürgen H Prochaska8. 1. Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany; German Center for Cardiovascular Research, partner site Rhine Main, Mainz, Germany. 2. Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany; Institute of Medical Biostatistics, Epidemiology and Informatics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. 3. Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. 4. German Center for Cardiovascular Research, partner site Rhine Main, Mainz, Germany; Department of Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. 5. Institute of Medical Biostatistics, Epidemiology and Informatics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. 6. German Center for Cardiovascular Research, partner site Rhine Main, Mainz, Germany; Institute for Clinical Chemistry and Laboratory Medicine, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. 7. Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany; German Center for Cardiovascular Research, partner site Rhine Main, Mainz, Germany; Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. 8. Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany; German Center for Cardiovascular Research, partner site Rhine Main, Mainz, Germany; Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Electronic address: juergen.prochaska@unimedizin-mainz.de.
Abstract
BACKGROUND: COPD is an established predictor of clinical outcome in patients with chronic heart failure (HF). However, little evidence is available about the predictive value of FEV1 in chronic HF. RESEARCH QUESTION: Is pulmonary function related to the progression of chronic HF? STUDY DESIGN AND METHODS: The MyoVasc study (ClinicalTrials.gov Identifier: NCT04064450) is a prospective cohort study of HF. Information on pulmonary and cardiac functional and structural status was obtained by body plethysmography and echocardiography. The primary study end point was worsening of HF. RESULTS: Overall 2,998 participants (age range, 35-84 years) with available FEV1 data were eligible for analysis. Linear multivariate regression analysis revealed an independent relationship of FEV1 (per -1 SD) with deteriorated systolic and diastolic left ventricle (LV) function as well as LV hypertrophy under adjustment of age, sex, height, cardiovascular risk factors (CVRFs), and clinical profile (LV ejection fraction: β-estimate, -1.63% [95% CI, -2.00% to -1.26%]; E/E' ratio: β-estimate, 0.82 [95% CI, 0.64-0.99]; and LV mass/height2.7: β-estimate, 1.58 [95% CI, 1.07-2.10]; P < .001 for all). During a median time to follow-up of 2.6 years (interquartile range, 1.1-4.1 years), worsening of HF occurred in 235 individuals. In Cox regression model adjusted for age, sex, height, CVRF, and clinical profile, pulmonary function (FEV1 per -1 SD) was an independent predictor of worsening of HF (hazard ratio [HR], 1.44 [95% CI, 1.27-1.63]; P < .001). Additional adjustment for obstructive airway pattern and C-reactive protein mitigated, but did not substantially alter, the results underlining the robustness of the observed effect (HRFEV1, 1.39 [95% CI, 1.20-1.61]; P < .001). The predictive value of FEV1 was consistent across subgroups, including individuals without obstruction (HR, 1.55 [95% CI, 1.34-1.77]; P < .001) and nonsmokers (HR, 1.72 [95% CI, 1.39-1.96]; P < .001). INTERPRETATION: FEV1 represents a strong candidate to improve future risk stratification and prevention strategies in individuals with chronic, stable HF. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT04064450; URL: www.clinicaltrials.gov.
BACKGROUND: COPD is an established predictor of clinical outcome in patients with chronic heart failure (HF). However, little evidence is available about the predictive value of FEV1 in chronic HF. RESEARCH QUESTION: Is pulmonary function related to the progression of chronic HF? STUDY DESIGN AND METHODS: The MyoVasc study (ClinicalTrials.gov Identifier: NCT04064450) is a prospective cohort study of HF. Information on pulmonary and cardiac functional and structural status was obtained by body plethysmography and echocardiography. The primary study end point was worsening of HF. RESULTS: Overall 2,998 participants (age range, 35-84 years) with available FEV1 data were eligible for analysis. Linear multivariate regression analysis revealed an independent relationship of FEV1 (per -1 SD) with deteriorated systolic and diastolic left ventricle (LV) function as well as LV hypertrophy under adjustment of age, sex, height, cardiovascular risk factors (CVRFs), and clinical profile (LV ejection fraction: β-estimate, -1.63% [95% CI, -2.00% to -1.26%]; E/E' ratio: β-estimate, 0.82 [95% CI, 0.64-0.99]; and LV mass/height2.7: β-estimate, 1.58 [95% CI, 1.07-2.10]; P < .001 for all). During a median time to follow-up of 2.6 years (interquartile range, 1.1-4.1 years), worsening of HF occurred in 235 individuals. In Cox regression model adjusted for age, sex, height, CVRF, and clinical profile, pulmonary function (FEV1 per -1 SD) was an independent predictor of worsening of HF (hazard ratio [HR], 1.44 [95% CI, 1.27-1.63]; P < .001). Additional adjustment for obstructive airway pattern and C-reactive protein mitigated, but did not substantially alter, the results underlining the robustness of the observed effect (HRFEV1, 1.39 [95% CI, 1.20-1.61]; P < .001). The predictive value of FEV1 was consistent across subgroups, including individuals without obstruction (HR, 1.55 [95% CI, 1.34-1.77]; P < .001) and nonsmokers (HR, 1.72 [95% CI, 1.39-1.96]; P < .001). INTERPRETATION: FEV1 represents a strong candidate to improve future risk stratification and prevention strategies in individuals with chronic, stable HF. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT04064450; URL: www.clinicaltrials.gov.