Key result
ACT chemotherapy significantly prolonged the QTc interval from 439.7 ms at baseline to 472.5 ms after the AC phase and 467.9 ms after taxane treatment in patients with non-metastatic breast cancer.
Why the study?
Does the ACT chemotherapy regimen (doxorubicin, cyclophosphamide, paclitaxel) prolong the QTc interval in patients with non-metastatic breast cancer?
Observational (n=23)
No
Does the ACT chemotherapy regimen (doxorubicin, cyclophosphamide, paclitaxel) prolong the QTc interval in patients with non-metastatic breast cancer?
In patients with non-metastatic breast cancer, the ACT chemotherapy regimen is associated with acute and subacute cardiotoxicity, evidenced by significant QTc prolongation and elevated serum troponin levels.
Supports QTc monitoring during ACT chemotherapy in breast cancer; leaves open arrhythmic risk and needs prospective validation.
AIM: Acute and subacute cardiotoxicity are characterized by prolongation of the corrected QT interval (QTc) and other measures derived from the QTc interval, such as QTc dispersion (QTdc) and transmural dispersion of repolarization (DTpTe). Although anthracyclines prolong the QTc interval, it is unclear whether breast cancer patients who undergo the ACT chemotherapy regimen of anthracycline (doxorubicin: A), cyclophosphamide (C) and taxane (T) may present with QTc, QTdc and DTpTe prolongation. METHODS: Twenty-three consecutive patients with breast cancer were followed prospectively during ACT chemotherapy and were analyzed according to their QT measurements. QTc, QTdc and DTpTe measurements were determined by a 12-lead electrocardiogram (EKG) prior to chemotherapy (baseline), immediately after the first phase of anthracycline and cyclophosphamide (AC) treatment, and immediately after T treatment. Serum troponin and B-type natriuretic peptide (BNP) levels were also measured. RESULTS: Compared to baseline values, the QTc interval was significantly prolonged after the AC phase (439.7 ± 33.2 ms vs. 472.5 ± 36.3 ms, p = 0.001) and after T treatment (439.7 ± 33.2 ms vs. 467.9 ± 42.6 ms, p < 0.001). Troponin levels were elevated after the AC phase (23.0 pg/mL [min-max: 6.0-85.0] vs. 6.0 pg/mL [min-max: 6.0-22.0], p < 0.001) and after T treatment (25.0 pg/mL [min-max: 6.0-80.0] vs. 6.0 pg/mL [min-max: 6.0-22.0], p < 0.001) compared to baseline values. CONCLUSION: In this prospective study of patients with non-metastatic breast cancer who underwent ACT chemotherapy, significant QTc prolongation and an elevation in serum troponin levels were observed.
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Veronese et al. (2018) conducted an observational in Non-metastatic breast cancer (n=23). ACT chemotherapy (doxorubicin, cyclophosphamide, paclitaxel) vs. Baseline was evaluated on QTc interval after the AC phase of chemotherapy (ms) (p=0.001). ACT chemotherapy significantly prolonged the QTc interval from 439.7 ms at baseline to 472.5 ms after the AC phase and 467.9 ms after taxane treatment in patients with non-metastatic breast cancer.
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