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Myocardial Cytoprotection by Trimetazidine Against Anthracycline-Induced Cardiotoxicity in Anticancer Chemotherapy

Department of Experimental Medicine and Pathology "La Sapienza" University of Rome, Rome, Italy.

Vito Rizzo, MD

Department of Clinical Medicine, Cardiac Rehabilitation Center,

Fernando di Maio, MD

Department of Clinical Medicine, Cardiac Rehabilitation Center, Rome, Italy.

Federica Petretto, MD

Department of Clinical Medicine, Cardiac Rehabilitation Center, Rome, Italy.

Gianluca Bianco, MD

Department of Experimental Medicine and Pathology "La Sapienza" University of Rome, Rome, Italy.

Giuseppe Placanica, MD

Department of Experimental Medicine and Pathology "La Sapienza" University of Rome, Rome, Italy.

Marta Marziali, MD

Department of Experimental Medicine and Pathology "La Sapienza" University of Rome, Rome, Italy.

Vincenzo Paravati, MD

Department of Experimental Medicine and Pathology "La Sapienza" University of Rome, Rome, Italy.

Nicolò Gueli, MD

Department of Clinical Medicine, Cardiac Rehabilitation Center, Rome, Italy.

Fortunato Meloni, MD

Department of Clinical Medicine, Cardiac Rehabilitation Center, Rome, Italy.

Stefano Villatico Campbell, MD

2nd Faculty of Medicine, Rome, Italy.

The ability of trimetazidine (2,3,4, trimethoxybenzylpiperazine dihydrochloride, TMZ) to protect the myocardium against anthracycline (ANT)-induced cardiotoxicity during chemotherapy has been evaluated in female patients with breast cancer. A clinical trial was conducted in 61 patients subdivided into three groups: group 1 (n = 15, G1) treated with standard ANT protocol and cardioprotection by dexrazoxane (DEX) plus TMZ (60 mg, daily dose); group 2 (n = 22, G2) treated with ANT and cardioprotection by TMZ only; and group 3 (n = 24, G3) scheduled to receive ANT therapy and DEX. All the patients submitted to an echocardiographic evaluation of diastolic function (E wave velocity, A wave velocity, isovolumetric relaxation time [IVRT], deceleration time [DT]) at enrollment (TO), at T1 time, at T2 time, and at T3 time. After a 12- month follow-up period, the patients showed a good conservation of diastolic function both in G1 and G2 groups. No statistically significant difference was observed in E wave and A wave velocity and E/A ratio after ANT treatment. TMZ produced a cardioprotective effect, compa rable to DEX protection, against subacute and chronic subclinical cardiotoxicity with no signif icant changes in diastolic function after 1 year of follow-up.

Angiology, Vol. 54, No. 2, 219-227 (2003)
DOI: 10.1177/000331970305400212


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