Key result
Telmisartan preserved systolic function, assessed by strain rate, and prevented epirubicin-induced increases in inflammation and oxidative stress up to 18 months of follow-up compared to placebo.
Why the study?
Does telmisartan prevent epirubicin-induced systolic dysfunction and inflammation in cancer patients?
RCT (n=49)
Single-blind
Block randomization
No
Does telmisartan prevent epirubicin-induced systolic dysfunction and inflammation in cancer patients?
Telmisartan provides long-term protection against epirubicin-induced cardiotoxicity, preserving systolic function and reducing inflammation and oxidative stress.
Answers are grounded in this paper and cite their sources.
Telmisartan warrants consideration with epirubicin to prevent cardiotoxicity; extends randomized evidence for ARBs to 18-month systolic preservation in cancer patients.
PURPOSE: The primary objective of the present study was to show the long lasting cardioprotective activity, at different time-points, up to 18 month-follow-up, of telmisartan in preserving the systolic function (assessed as Strain Rate-SR) in cancer patients treated with EPI both in the adjuvant and metastatic setting; the secondary objective was to confirm the correlation of the cardioprotective activity of telmisartan with a reduction of inflammation and oxidative stress induced by EPI. METHODS: Phase II single blind placebo-controlled randomized trial. Sample size 50 patients per arm: based on a pre-planned interim analysis for early stopping rules, the study was discontinued for ethical reasons at 49 patients. Cardiovascular disease-free patients with cancer at different sites eligible for EPI-based treatment randomized to: telmisartan n = 25 or placebo n = 24. Echocardiography Tissue Doppler imaging (TDI) strain and strain rate was performed, serum levels of proinflammatory cytokines (IL-6, TNF-α) and oxidative stress (reactive oxygen species, ROS) were assessed at baseline, every 100 mg/m(2) EPI dose and at 6-, 12- and 18-month follow-up (FU). RESULTS: Significant SR peak reduction in both arms was observed at t2 (cumulative dose EPI 200 mg/m(2)) vs t0. Conversely, at t3, t4, 6-, 12- and 18-month FU SR increased towards normal range in the telmisartan arm, while in the placebo arm SR remained significantly lower. Differences between SR changes in the placebo and telmisartan arm were significant from t3 up to 18 month-FU. IL-6 and ROS increased significantly in the placebo arm at t2 but did not change in the telmisartan arm. A significant (p < 0.05) correlation between changes of SR vs IL-6 and ROS was observed. CONCLUSIONS: Our results suggest that the protective effect of telmisartan is long lasting, probably by ensuring a permanent (at least up to 18-month FU) defense against chronic or late-onset types of anthracycline-induced cardiotoxicity.
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Dessì et al. (2013) conducted an RCT in Cancer patients eligible for epirubicin-based chemotherapy (n=49). Telmisartan vs. Placebo was evaluated on Change in systolic function assessed as Strain Rate (SR) up to 18-month follow-up (p=<0.05). Telmisartan preserved systolic function, assessed by strain rate, and prevented epirubicin-induced increases in inflammation and oxidative stress up to 18 months of follow-up compared to placebo.
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