Erin J Howden1, Ashley Bigaran1,2, Rhys Beaudry3, Steve Fraser4,5, Steve Selig5, Steve Foulkes1,4,5, Yoland Antill6, Sophie Nightingale7, Sherene Loi8, Mark J Haykowsky1,3, André La Gerche1,9. 1. 1 Department of Sports Cardiology, Baker Heart and Diabetes Institute, Australia. 2. 2 Exercise and Nutrition Research Program, Mary MacKillop Institute for Health Research, Australian Catholic University, Australia. 3. 3 Integrated Cardiovascular Exercise Physiology and Rehabilitation Laboratory, College of Nursing & Health Innovation, University of Texas Arlington, USA. 4. 4 Institute for Physical Activity and Nutrition, Deakin University, Australia. 5. 5 School of Exercise and Nutrition Sciences, Deakin University, Australia. 6. 6 Oncology Care Victoria, Cabrini Health, Australia. 7. 7 Surgical Oncology Department, Peter MacCallum Cancer Centre, Australia. 8. 8 Translational Breast Cancer Genomics Laboratory, Peter MacCallum Cancer Centre, Australia. 9. 9 Cardiology Department, St Vincent's Hospital Melbourne, Melbourne VIC, Australia.
Abstract
BACKGROUND: Anthracycline chemotherapy may be associated with decreased cardiac function and functional capacity measured as the peak oxygen uptake during exercise ( V·O2 peak). We sought to determine (a) whether a structured exercise training program would attenuate reductions in V·O2 peak and (b) whether exercise cardiac imaging is a more sensitive marker of cardiac injury than the current standard of care resting left ventricular ejection fraction (LVEF). METHODS: Twenty-eight patients with early stage breast cancer undergoing anthracycline chemotherapy were able to choose between exercise training (mean ± SD age 47 ± 9 years, n = 14) or usual care (mean ± SD age 53 ± 9 years, n = 14). Measurements performed before and after anthracycline chemotherapy included cardiopulmonary exercise testing to determine V·O2 peak and functional disability ( V·O2 peak < 18 ml/min/kg), resting echocardiography (LVEF and global longitudinal strain), cardiac biomarkers (troponin and B-type natriuretic peptide) and exercise cardiac magnetic resonance imaging to determine stroke volume and peak cardiac output. The exercise training group completed 2 × 60 minute supervised exercise sessions per week. RESULTS: Decreases in V·O2 peak during chemotherapy were attenuated with exercise training (15 vs. 4% reduction, P = 0.010) and fewer participants in the exercise training group met the functional disability criteria after anthracycline chemotherapy compared with those in the usual care group (7 vs. 50%, P = 0.01). Compared with the baseline, the peak exercise heart rate was higher and the stroke volume was lower after chemotherapy ( P = 0.003 and P = 0.06, respectively). There was a reduction in resting LVEF (from 63 ± 5 to 60 ± 5%, P = 0.002) and an increase in troponin (from 2.9 ± 1.3 to 28.5 ± 22.4 ng/mL, P < 0.0001), but no difference was observed between the usual care and exercise training group. The baseline peak cardiac output was the strongest predictor of functional capacity after anthracycline chemotherapy in a model containing age and resting cardiac function (LVEF and global longitudinal strain). CONCLUSIONS: The peak exercise cardiac output can identify patients at risk of chemotherapy-induced functional disability, whereas current clinical standards are unhelpful. Functional disability can be prevented with exercise training.
BACKGROUND:Anthracycline chemotherapy may be associated with decreased cardiac function and functional capacity measured as the peak oxygen uptake during exercise ( V·O2 peak). We sought to determine (a) whether a structured exercise training program would attenuate reductions in V·O2 peak and (b) whether exercise cardiac imaging is a more sensitive marker of cardiac injury than the current standard of care resting left ventricular ejection fraction (LVEF). METHODS: Twenty-eight patients with early stage breast cancer undergoing anthracycline chemotherapy were able to choose between exercise training (mean ± SD age 47 ± 9 years, n = 14) or usual care (mean ± SD age 53 ± 9 years, n = 14). Measurements performed before and after anthracycline chemotherapy included cardiopulmonary exercise testing to determine V·O2 peak and functional disability ( V·O2 peak < 18 ml/min/kg), resting echocardiography (LVEF and global longitudinal strain), cardiac biomarkers (troponin and B-type natriuretic peptide) and exercise cardiac magnetic resonance imaging to determine stroke volume and peak cardiac output. The exercise training group completed 2 × 60 minute supervised exercise sessions per week. RESULTS: Decreases in V·O2 peak during chemotherapy were attenuated with exercise training (15 vs. 4% reduction, P = 0.010) and fewer participants in the exercise training group met the functional disability criteria after anthracycline chemotherapy compared with those in the usual care group (7 vs. 50%, P = 0.01). Compared with the baseline, the peak exercise heart rate was higher and the stroke volume was lower after chemotherapy ( P = 0.003 and P = 0.06, respectively). There was a reduction in resting LVEF (from 63 ± 5 to 60 ± 5%, P = 0.002) and an increase in troponin (from 2.9 ± 1.3 to 28.5 ± 22.4 ng/mL, P < 0.0001), but no difference was observed between the usual care and exercise training group. The baseline peak cardiac output was the strongest predictor of functional capacity after anthracycline chemotherapy in a model containing age and resting cardiac function (LVEF and global longitudinal strain). CONCLUSIONS: The peak exercise cardiac output can identify patients at risk of chemotherapy-induced functional disability, whereas current clinical standards are unhelpful. Functional disability can be prevented with exercise training.
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