Key result
Postchemotherapy sarcopenia is strongly associated with anthracycline-induced cardiotoxicity.
Why the study?
Sarcopenia shares mechanistic pathways with anthracycline cardiotoxicity, including mitochondrial dysfunction, oxidative stress, and systemic inflammation, prompting investigation into the association between postchemotherapy sarcopenia and changes in cardiac function in patients with cancer.
Is postchemotherapy sarcopenia associated with anthracycline-induced cardiotoxicity in adult patients with cancer?
Observational (n=163)
No
Is postchemotherapy sarcopenia associated with anthracycline-induced cardiotoxicity in adult patients with cancer?
Postchemotherapy sarcopenia is independently associated with anthracycline-induced cardiac dysfunction, suggesting that CT-based muscle assessment and functional testing could enhance cardio-oncology risk stratification.
Answers are grounded in this paper and cite their sources.
Sarcopenia assessment may refine cardiotoxicity prediction; leaves open whether targeting muscle loss improves anthracycline outcomes.
Background: Anthracycline-based chemotherapy is associated with cancer therapy–related cardiac dysfunction, primarily manifested by a decline in left ventricular ejection fraction (LVEF). Sarcopenia, characterized by reduced skeletal muscle mass and strength, shares mechanistic pathways with anthracycline cardiotoxicity, including mitochondrial dysfunction, oxidative stress, and systemic inflammation. We aimed to investigate the association between postchemotherapy sarcopenia and changes in cardiac function in a heterogeneous cohort of patients with cancer. Methods: In this single-center prospective observational study, 163 adult patients scheduled to receive anthracycline-containing chemotherapy were enrolled. Transthoracic echocardiography was performed before treatment and 3 months after completion, with assessment of LVEF using the biplane Simpson method and global longitudinal strain. Sarcopenia was assessed postchemotherapy using computed tomography–derived skeletal muscle index at the L3 level combined with handgrip strength. Cardiotoxicity was defined as a reduction in LVEF of 10% or more to below normal and/or new diastolic dysfunction. Multivariable logistic regression was used to evaluate independent associations. Results: Sarcopenia was identified in 46% of patients following chemotherapy. Significant differences in echocardiographic outcomes were observed between sarcopenic and nonsarcopenic groups (P<.05). Sarcopenia was strongly associated with cardiotoxicity, with logistic regression demonstrating robust predictive performance (Nagelkerke R²=0.485; P<.001). Patients with low muscle mass and strength exhibited markedly higher odds of cardiac dysfunction. Conclusion: Postchemotherapy sarcopenia is independently associated with anthracycline-induced cardiac dysfunction. Integrating CT-based muscle assessment and functional testing into cardio-oncology risk stratification may enhance early identification of vulnerable patients and guide cardioprotective strategies.
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Alizadehasl et al. (2026) conducted an observational in Cancer scheduled for anthracycline-containing chemotherapy (n=163). Postchemotherapy sarcopenia vs. Nonsarcopenic patients was evaluated on Cardiotoxicity (reduction in LVEF of 10% or more to below normal and/or new diastolic dysfunction) (Nagelkerke R²=0.485, p=<.001). Postchemotherapy sarcopenia occurred in 46% of patients and was strongly associated with anthracycline-induced cardiotoxicity (Nagelkerke R²=0.485; P<.001).
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