P316Cardioprotective role of lisinopril and rosuvastatin in the prevention of anthracycline induced cardiotoxicity


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Abstract

Purpose: In the present study we aimed to evaluate by echo-Doppler echocardiography the cardioprotective effect of an angiotensin-converting enzyme inhibitor and a statin added to the standard chemotherapy regimen in the prevention of anthracycline induced cardiotoxicity.Methods: In this prospective study we evaluated by Doppler echocardiography 26 patients with various malignant tumors treated with epirubicin in doses up to 500 mg/2, who were receiving a cardioprotective treatment with Lisinopril 10 mg and Rosuvastatin 10 mg (study group- SG) and a gender and age matched group of 31 oncologic patients who were not receiving the cardioprotective treatment (control group- CG). None of the patients had any history of cardiovascular disease. The left ventricular ( LV) systolic function was assessed by measuring the LV ejection fraction ( LVEF) by Simpson method and the LV diastolic function was assessed by measuring transmitral flow: the maximal velocity of the E wave (rapid filling) and A wave (atrial filling), the ratio of E max/ Amax, the pressure half time (PHT) of the E wave, the E wave deceleration time (EDT) and the isovolumic relaxation time (IVRT). The echo-Doppler study was performed at the beginning and at the end of chemotherapy.Results: We documented a further deterioration of LV diastolic function in patients without cardioprotection with Lisinopril 10 mg and Rosuvastatin 10 mg compared with those in the SG by finding a significant decrease of Emax, an increased Amax and subunitary E/A ratio (p<0.02), the prolongation of IVRT ( p<0.2), of PHT (p<0.02) and of the EDT (p<0.01) in the CG. LV systolic function was less influenced by this treatment ( p< 0.21).Conclusions: In our echo-Doppler study we have documented the cardioprotective role of Lisinopril and Rosuvastatin in the prevention of cardiac disfunction. The patients who were not receiving the above mentioned cardioprotective treatement had a much rapid deterioration of the LV diastolic function. It appears that the LV systolic function was less influenced by this cardioprotective treatment.

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