Exercise as a diagnostic and therapeutic tool for the prevention of cardiovascular dysfunction in breast cancer patients

Author:

Howden Erin J1,Bigaran Ashley12,Beaudry Rhys3,Fraser Steve45,Selig Steve5,Foulkes Steve145,Antill Yoland6,Nightingale Sophie7,Loi Sherene8,Haykowsky Mark J13,La Gerche André19

Affiliation:

1. Department of Sports Cardiology, Baker Heart and Diabetes Institute, Australia

2. Exercise and Nutrition Research Program, Mary MacKillop Institute for Health Research, Australian Catholic University, Australia

3. Integrated Cardiovascular Exercise Physiology and Rehabilitation Laboratory, College of Nursing & Health Innovation, University of Texas Arlington, USA

4. Institute for Physical Activity and Nutrition, Deakin University, Australia

5. School of Exercise and Nutrition Sciences, Deakin University, Australia

6. Oncology Care Victoria, Cabrini Health, Australia

7. Surgical Oncology Department, Peter MacCallum Cancer Centre, Australia

8. Translational Breast Cancer Genomics Laboratory, Peter MacCallum Cancer Centre, Australia

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 ([Formula: see text] peak). We sought to determine (a) whether a structured exercise training program would attenuate reductions in [Formula: see text] 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 [Formula: see text] peak and functional disability ([Formula: see text] 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 [Formula: see text] 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.

Publisher

Oxford University Press (OUP)

Subject

Cardiology and Cardiovascular Medicine,Epidemiology

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