A cardiac complication with relevant short-term toxicity is uncommon, but it is one of the severe complications after allogeneic hematopoietic stem cell transplantation (HSCT). 1 Recently, there has been increased performance of HSCT; hence late complications in long-term survivors are monitored closely. However, there are only a few reports about late-onset cardiac dysfunction. A few years ago, we experienced two patients with AML and a concomitant previously unrecognized form of very late-onset reversible cardiomyopathy in our long-term follow-up program after allogeneic HSCT.The first patient is a 46-year-old man, who underwent PBSC transplantation (PBSCT) from an HLA-matched sibling after a reduced-intensity conditioning regimen (fludarabine and busulfan). Cyclosporine A was used for GvHD prophylaxis. On day 120, he developed de novo chronic GvHD (cGvHD) with oral erosions and moderate elevation of liver enzymes, which were treated with FK506. Moreover, he experienced a cryptogenic organizing pneumonitis at 9 months post HSCT, which was treated successfully with steroid. After FK506 was discontinued and steroid was tapered, severe cGvHD developed gradually within 6 years with the following scores of severity: 2 performance status (PS) 1, oral 1, skin 2, eye 2, lung 3 (bronchiolitis obliterans), gut 1, and joints and fascia 1 with prednisolone 5 mg/day. Eight years post SCT, he experienced dyspnea and lightheadedness with sinus tachycardia (115 bpm) and hypertension (169/125 mm Hg). Hypoxemia was not observed.The second patient is a 40-year-old man, who underwent PBSCT from a 5/6 HLA-matched sibling after cyclophosphamide/TBI. FK506 and mycophenolate mofetil were used for GvHD prophylaxis. Three months post PBSCT, he developed acute GvHD (liver, stage 2), which was treated successfully with steroid. After FK506 and steroid were discontinued, he developed a quiescent-type moderate cGvHD within 2 years: PS 1, eye 2 and lung 1 without any immunosuppressant drugs. Five years after SCT, annual follow-up examination incidentally revealed deterioration of heart function, although mild exertional dyspnea had developed 1 month before. He presented with sinus tachycardia (120 bpm) with blood pressure of 136/90 mm Hg.Neither patient presented with signs and symptoms of infection and ischemic heart disease. Moreover, physical examinations and plain chest X-rays revealed the absence of congestive heart failure. Laboratory studies showed no significant elevation of creatine kinase and troponin I. However, echocardiogram demonstrated severe left ventricular global hypokinesia without bradycardia and pericardial effusion (left ventricular ejection fraction: 32% for patient 1 and 22% for patient 2). Cardiac functions, including left ventricular ejection fraction, were normal during the pretransplant and post-transplant annual follow-up period. Before transplantation, there were four rounds and one cycle of chemotherapy, and the cumulative doses of anthracycline were tolerable and equivalent to 315 and 107 mg/m 2 doxorubicin, ...