Valsartan Attenuates Cardiotoxicity in Breast Cancer Patients A fter Chemotherapy

Objective: To determine whether valsartan would be useful in attenuating Adriamycin/Cyclophosphamide/ Herceptin (ACH)-induced cardiotoxicity and to assess the role of biomarkers as indicators of cardiotoxicity in patients with breast cancer undergoing cancer therapy.Background: Valsartan is indicated to reduce the risk of cardiovascular death and hospitalization in patients with chronic heart disease. The administration of cancer drugs, in particular (ACH) is associated with increased risk of cardiotoxicity. The use of herceptin improves survival of women with early-stage positive human epidermal growth factor receptor 2 (HER2) breast cancer but also adds substantially to cost, toxicity, and inconvenience. Little is known about the potential role of valsartan in the prevention of ACH-mediated cardiotoxicity and the predictive role of biomarkers.Method: A total of 60 untreated HER-2 positive breast cancer patients (ages 24 –70 yr, mean 56 yr) were enrolled in this study and were divided to two groups. Group 1 and 2 had 30 patients each, and group 1 received ACH plus valsartan, group 2 received ACH alone. HER2- positive patients were recruited at the Cancer Therapy Center in Najaf, Iraq. Ejection fraction % (EF%), cardiac Troponin I (cTnI) and high sensitivity C-reactive protein (hsCRP) were measured at baseline and at six months after ACH administration.Results: Chemotherapy induced significant transient increase in EF%, cTnI, and hsCRP compared to baseline values (P < 0.001). Within one week after valsartan treatment, all these increases returned back to nearly normal levels. Notably, valsartan administration caused a significant decrease in cTnI and hsCRP values compared to baseline (P < 0.001) and it improved EF% value.Conclusion: This study demonstrated that prophylactic administration of valsartan resulted in the partial attenuation of cardiotoxicity caused by chemotherapy which was characterized by the improvement of EF% and in lowering serum level of cTnI and hsCRP.