Stop cardiotoxicity: the role of statin therapy in anthracycline treated patients

Introduction Anthracyclines (AC) have been the mainstay therapy for breast cancer (BC) for many decades. However, the cardiotoxic potential of this class of drugs still represents a major concern. Statins have pleiotropic effects independent of their cholesterol-lowering properties, arousing interest in their potential as cardioprotective agents for patients with BC receiving AC. Although there have been multiple studies showing their beneficial effect on AC toxicity, there were others where the beneficial effects of statins are less prominent, highlighting the need for further research to identify the subgroups of patients who may benefit the most from up-front statin therapy. Purpose To assess whether statins prevent development of cancer therapy-related cardiac dysfunction (CTRCD) in anthracycline-treated BC patients. Methods BC patients treated with AC and followed in Cardio-oncology consultation in a local portuguese hospital were retrospectively divided depending on whether they were taking a statin at baseline or not. The primary endpoint was development of CTRCD (classified according to the HFA-ICOS risk proforma). All-cause and cardiovascular (CV) mortality were secondary endpoints. Results We included 57 pts (100% women; mean age 60 ± 10 years; 40% ≥65 years). 11 (19%) had metastatic disease. According to the HFA-ICOS tool, 20 pts (35%) were classified as low risk, 23 (40%) as moderate risk, 10 (18%) as high risk, and 4 (7%) as very high risk. 14 (24%) were treated with a statin at baseline. Median follow-up was 31 months (interquartile range 19-67). 12 pts (21%) developed CTRCD: 11 (92%) moderate to severe, 7 (58%) symptomatic. 6 pts (10%) died, 2 by CV cause. A statistically significant association between statin use at baseline and development of CTRCD was found (p 0.027). The odds of not developing CTRCD after anthracycline treatment was 1.4 times greater for participants treated with a statin at baseline compared with those without a statin (OR=1.4, 95% CI [1.1;1.6]). We also observed that, from the patients with symptomatic CTRCD, none had a statin at baseline. However, we found no difference in the rates of all-cause and CV mortality between study groups (p 0.6 and 1, respectively). Conclusion In our population of patients with BC treated with AC, the use of statins was associated with a significant reduction in CTRCD. Further prospective studies with larger populations and longer follow-up are needed to clarify which subgroups of patients may benefit most from this strategy and to study if statin therapy prevents symptomatic CTRCD.