Why the study?
The study aimed to characterize peak exercise cardiac function and thigh muscle fatty infiltration and determine their relationships with VO2peak among anthracycline-treated breast cancer survivors.
Does prior anthracycline chemotherapy impair cardiorespiratory fitness through cardiac and skeletal muscle changes in breast cancer survivors?
Does prior anthracycline chemotherapy impair cardiorespiratory fitness through cardiac and skeletal muscle changes in breast cancer survivors?
Answers are grounded in this paper and cite their sources.
Impaired cardiorespiratory fitness in breast cancer survivors ~1 year post-anthracycline therapy is driven by both myocardial fibrosis limiting cardiac reserve and thigh muscle fatty infiltration limiting oxygen extraction.
This study aimed to characterize peak exercise cardiac function and thigh muscle fatty infiltration and their relationships with VO₂peak among anthracycline-treated breast cancer survivors (BCS). BCS who received anthracycline chemotherapy ~ 1 year earlier (n = 16) and matched controls (matched-CON, n = 16) were enrolled. Resting and peak exercise cardiac function, myocardial T₁ mapping (marker of fibrosis), and thigh muscle fat infiltration were assessed by magnetic resonance imaging, and VO₂peak by cycle test. Compared to matched-CON, BCS had lower peak SV (64 ± 9 vs 57 ± 10 mL/m², p = 0.038), GLS (- 30.4 ± 2.2 vs - 28.0 ± 2.5%, p = 0.008), and arteriovenous oxygen difference (16.4 ± 3.6 vs 15.2 ± 3.9 mL/100 mL, p = 0.054). Mediation analysis showed: (1) greater myocardial T₁ time (fibrosis) is inversely related to cardiac output and end-systolic volume exercise reserve; (2) greater thigh muscle fatty infiltration is inversely related to arteriovenous oxygen difference; both of which negatively influence VO₂peak. Peak SV (R² = 65%) and thigh muscle fat fraction (R² = 68%) were similarly strong independent predictors of VO₂peak in BCS and matched-CON combined. Post-anthracyclines, myocardial fibrosis is associated with impaired cardiac reserve, and thigh muscle fatty infiltration is associated with impaired oxygen extraction, which both contribute to VO₂peak.
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Kirkham et al. (2021) studied this question.
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