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• W2056102652 abstract "We report a case of tacrolimus-induced left ventricular apical hypertrophy in a 28-year-old Japanese man with post-allogeneic hematopoietic stem cell transplantation. He was diagnosed with acute myelomonocytic leukemia (FAB AML-M4) in July 2012. He failed to achieve complete remission after two courses of induction chemotherapies (one course of cytarabine plus idarubicin and one course of high-dose cytarabine plus mitoxantrone). Therefore, he underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) after conditioning with 12-Gy total body irradiation, high-dose cytarabine and high-dose cyclophosphamide in November 2012. He had no previous history of cardiovascular disease or hypertension. A 12-lead electrocardiography (ECG: Fig. 1A ) and echocardiography (Fig. 2A ) showed normal findings before allo-HSCT. For the prophylaxis against graft versus host disease (GVHD), tacrolimus was started as a continuous intravenous infusion at an initial dose of 0.03 mg/kg/day on the day before the transplantation (day −1) and continued for 60 days. Subsequently, oral tacrolimus was administered at a dose of 0.05 mg/kg/day for 24 days. The regimen related toxicity was minimal and his post-transplant course was uneventful. Since mixed hematopoietic chimerism was observed on day +80 post-transplant, tacrolimus was stopped on day +83 to establish complete donor chimerism. Four weeks after tacrolimus discontinuation, he developed severe acute GVHD manifested by a typical rash, diarrhea, and fever. Tacrolimus was readministered with a 0.03 mg/kg/day continuous intravenous infusion with prednisolone at a dose of 1.0 mg/kg/day on day +115. His tacrolimus blood concentrations were maintained between 10 and 15 ng/ml. Within four weeks after readministration of tacrolimus, he gradually gained body weight and peripheral edema appeared despite tapering of prednisolone. Serum brain natriuretic peptide (BNP) level was elevated to 670 pg/ml. His ECG was abnormal with negative T wave in both limb and chest leads including giant negative T waves in V3 and V4 (Fig. 1B). Echocardiography showed distinct left ventricular (LV) apical hypertrophy (Fig. 2B). Cardiac magnetic resonance imaging (MRI) also showed LV apical hypertrophy, and revealed focal late gadolinium enhancement (LGE) in the apical-lateral segment, indicating the presence of myocardial fibrosis (Fig. 3A ). His body weight decreased and edema improved with loop diuretics. Eight months after allo-HSCT, the patient achieved complete donor chimerism and tacrolimus was discontinued. Six months after discontinuation of tacrolimus, his ECG improved (Fig. 1C), plasma BNP level was normalized, and follow-up echocardiography (Fig. 2C) and cardiac MRI (Fig. 3B) showed marked improvement of LV apical hypertrophy without complete disappearance of LGE. Therefore, he was finally diagnosed with tacrolimus-induced LV apical hypertrophy. Fig. 2Echocardiography imaging in the apical four-chamber view. (A) before allogeneic hematopoietic stem cell transplantation, (B) during tacrolimus therapy, and (C) 6 months after discontinuation of tacrolimus therapy. View Large Image Figure Viewer Download Hi-res image Fig. 3A. Cardiac magnetic resonance imaging (MRI). (A) during tacrolimus therapy and (B) 6 months after discontinuation of tacrolimus therapy. White arrows indicate late gadolinium enhancement. View Large Image Figure Viewer Download Hi-res image" @default.
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• W2056102652 date "2014-11-01" @default.
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• W2056102652 title "Tacrolimus-induced left ventricular apical hypertrophy in a patient with post-allogeneic hematopoietic stem cell transplantation" @default.
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• W2056102652 doi "https://doi.org/10.1016/j.ijcard.2014.07.171" @default.
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