Troponin-T and myoglobin plus echocardiographic evaluation for monitoring early cardiotoxicity of weekly epirubicin–paclitaxel in metastatic breast cancer patients

Increased serum level of troponin-T and myoglobin has been recently reported to be related to cumulative anthracycline exposure. Left ventricular ejection fraction seems accurate in monitoring systolic function according to the latest version of Toxicity Criteria by chemotherapeutics 3.0. From January 2002, 20 patients with untreated advanced breast cancer received epirubicin (25 mg/m/week) and paclitaxel (80 mg/m/week) for 24 weeks. Troponin-T, myoglobin and biochemical serum enzymes circulating levels were measured immediately before and 4 h after epirubicin administration every week. Patients underwent electrocardiography and echocardiography at weeks 0, 8, 16 and 24. The number of courses administered was 352 (median 18, range 4-24). Epirubicin median dose administered was 600 mg/m and paclitaxel median dose administered was 1760 mg/m. Troponin-T never overcame the upper normal limit; one patient experienced troponin-T elevation without any clinical or instrumental sign of cardiac failure. Myoglobin never significantly increased with the exception of a patient who underwent several abdominal fluid drainages. Creatine kinase MB and C-reactive protein never moved outside the upper normal limit. No symptomatic cardiac event was recorded. In 55 performed echocardiograms at weeks 0, 8, 16 and 24, neither left ventricular ejection fraction nor early peak flow/atrial flow velocity registered any significant decrease. No troponin-T or myoglobin serum elevations and Left ventricular ejection fraction/early peak flow/atrial flow velocity changes were registered in our series of nonsymptomatic women during epirubicin/paclitaxel weekly chemotherapy in the absence of clinical cardiac toxicity. Longer follow-up is needed, however, to understand whether the troponin-T or myoglobin circulating level measurement is able to detect subclinical, early-stage doxorubicin-induced cardiotoxicity.