Key result
Imatinib linked to higher baseline hs-cTnI and CK in CML without augmenting exercise-induced biomarker release.
Why the study?
It is unclear if exercise acutely increases cardiac or skeletal muscle damage in patients with CML receiving TKI therapy and whether this differs between TKIs.
Does exercise acutely increase cardiac or skeletal muscle damage biomarkers in patients with chronic myeloid leukemia receiving TKI therapy, and does this differ between TKIs?
Does exercise acutely increase cardiac or skeletal muscle damage biomarkers in patients with chronic myeloid leukemia receiving TKI therapy, and does this differ between TKIs?
This text outlines the rationale for investigating whether exercise induces the release of cardiac or skeletal muscle injury biomarkers in CML patients on TKI therapy.
Patients with chronic myeloid leukemia (CML) often require lifelong treatment with tyrosine kinase inhibitors (TKIs). Although TKI treatment results in an excellent prognosis, adverse events are frequently reported and may differ between first- and second-generation TKIs. Imatinib has been associated with a higher risk of skeletal muscle complaints compared to nilotinib, while cardiovascular events are more frequently reported with nilotinib [ 1 ]. Physical activity is a non-pharmaceutical strategy to enhance both muscle function and reduce cardiovascular disease risk [ 2 ], and hence could be of added significance in patients receiving TKI treatment. However, physical activity may provoke or exacerbate muscle complaints, which is supported by our observation that patients who experience adverse events on TKIs are less physically active [ 3 ]. It is unclear if exercise acutely increases cardiac or skeletal muscle damage in TKI users and whether this differs between TKIs.
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Janssen et al. (2023) conducted a letter in Chronic myeloid leukemia (n=42). Imatinib and nilotinib (TKI therapy) vs. Non-CML controls was evaluated on Baseline high-sensitivity cardiac Troponin I (hs-cTnI) levels (p=0.002). Imatinib-treated CML patients had significantly higher baseline hs-cTnI (5.0 vs 2.1 ng/L) and CK levels compared to controls, but exercise-induced biomarker release was not augmented by either TKI.
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