[Severe heart failure in consequence of late anthracycline-induced cardiotoxicity--case report]. / Tazké srdcové zlyhávanie ako prejav neskorej antracyklínovej kardiotoxicity--kazuistika.

BACKGROUND: Anthracyclines are known cardiotoxic agents. Anthracycline therapy increases the risk of long-term cardiac adverse effects in oncology patients. CASE REPORT: We report the case of a young male patient with severe congestive heart failure. The patient was treated for childhood acute myeloid leukemia by chemotherapy containing anthracyclines. Manifest dilated cardiomyopathy was developing ten years after the termination of chemotherapy with symptoms of left ventricular heart failure. Seventeen years following the end of cytostatic therapy the patient underwent heart transplantantation as ultimum refugium. CONCLUSIONS: Late cardiac complications may become a serious therapeutic problem. In such cases, the heart transplantation seems to be the only effective approach otherwise terminal forms of the heart failure.

Role of NT-proBNP in detection of myocardial damage in childhood leukemia survivors treated with and without anthracyclines.

BACKGROUND: Exposure to anthracyclines (ANT) during childhood represents a high risk for development of late cardiotoxicity. Cardiotoxicity is usually detected only when clinical symptoms or progressive cardiac dysfunction have already occurred. Early detection of cardiotoxicity may lead to better therapeutic outcome. N-terminal pro-brain natriuretic peptide (NTproBNP) has been hypothesized to reflect increased left ventricular wall stress before development of echocardiographic abnormalities. The aim of this study was to detect cardiac abnormalities using plasma NTproBNP and echocardiography in asymptomatic childhood leukemia survivors treated with or without cardiotoxic anthracycline therapy. METHODS: Serum levels of NTproBNP were determined in 69 asymptomatic survivors of childhood leukemia treated with or without anthracyclines and in 44 apparently healthy controls. The survivors were divided into two treatment groups: 36 patients after chemotherapy containing anthracyclines (ANT) and 33 patients after chemotherapy without anthracyclines (nonANT). Levels of NTproBNP were measured by using the Elecsys 2010 immunoassay analyzer (Roche Diagnostics). Echocardiography using M-mode, two-dimensional and Doppler measurements were performed on the same day as blood samples were obtained for NTproBNP analysis in survivors. RESULTS: Serum levels of NTproBNP were significantly higher in the ANT group than in controls (median 51.52 vs 17.37 pg/ml; p=0.0026). Survivors exposed to ANT had significantly increased levels of NTproBNP compared with patients treated without ANT (median 51.52 vs 12.24 pg/ml; p=0.0002). Female exposed and unexposed survivors had significantly higher NTproBNP levels than males. Four of the 36 survivors (11%) treated with ANT and two of the 33 patients (6%) not exposed to ANT had abnormal NTproBNP levels. Although no patient had echocardiographic abnormalities, significant differences were found in values of left ventricular ejection fraction (LVEF) and deceleration time (DT) between survivors treated with or without anthracyclines. CONCLUSIONS: Higher levels of NTproBNP detected in childhood leukemia survivors after low anthracycline cumulative doses might reflect an initial stage of ANT cardiotoxicity before the development of echocardiographic abnormalities. Although the current studies support NTproBNP as one of the best available biochemical markers of late anthracycline cardiotoxicity, a possible strategy toward further improvement and combination with other cardiac biomarkers and novel echocardiographic methods should be explored in additional studies.

Heart transplant in a childhood leukemia survivor: a case report.

OBJECTIVES: Children with acute leukemia often receive therapy that is potentially cardiotoxic. Development of irreversible cardiac impairment requiring heart transplant may appear many years after anticancer therapy. Other possible causes are discussed. MATERIAL AND METHODS: We describe a young leukemia survivor who developed severe heart failure needing a heart transplant. RESULTS: A 4-year-old boy was treated with standard doses of chemotherapy containing cardiotoxic daunorubicin and mitoxantrone, and later, with an allogeneic bone marrow transplant. Twelve years after the diagnosis of acute myeloid leukemia, and following a viral infection of an unknown cause, he developed symptoms of heart failure. Severe dilated cardiomyopathy; and severe, left ventricular dysfunction with ejection fraction of 12% were noted on echocardiography. The patient required a heart transplant 19 years after the diagnosis of leukemia. CONCLUSIONS: Cardiac failure may progressively occur in childhood leukemia survivors. Heart transplant is indicated in patients with refractory hemodynamic decompensation.