Introduction; Transient hypertrophic cardiomyopathy (HCM) has been known in preterm infants associated with medication of steroids such as dexamethasone and methylprednisolone in the prenatal and the neonatal period and maternal diabetes. We describe one case of transient HCM with severe anemia, and nonimmune hydrops fetalis in the preterm infant. Case; A 29 year-old multipara was transferred because of the fetal pericardial effusion at 26 weeks of gestation. The male neonate was born at 30 weeks and 1 day of gestation by emergent Cesarean section due to severe fetal distress. He was pale, poorly perfused, and edematous. The respiratory effort was nearly absent, and the immediate endotracheal intubation, surfactant treatment, and positive ventilation were done in the delivery room. His birth weight was 1170g. The initial laboratory findings revealed pancytopenia. His blood type was AB Rh positive as same his mother. The markers of TORCH infection revealed negative. Clinically it suggested fetomaternal hemorrhage strongly, unfortunately we did not examine Kleihauer-Betke test and flow cytometry on maternal blood. The echocardiography on day 1 showed the 4mm-sized pericardial effusion and decreased left ventricular contractility (fractional shortening (FS) 24%, ejection fraction (EF) 52%). The continuous intravenous dobutamine (10mcg/kg/hr) mediation was started. The echocardiogram was followed up on day 5, the left ventricular contractility was improved, the dobutamine administration was stopped. On day 11, the grade III harsh systolic murmur at the cardiac base, tachypnea and tachycardia developed. The hypertrophy of myocardial walls were markedly aggravated, predominantly LVPW and dynamic left ventricular out-let obstruction was present. The beta-blocker was started, it was tapered and off after confirming that the hypertrophy of myocardium affecting IVS and LVPW were resolved on day 30. We reconfirmed no intracardiac abnormality before his discharge on day 61. Conclusion; Acute distress caused by fetal hydrops, severe anemia, and perinatal asphyxia induced myocardial ischemia, which led to impair cardiac function. In addition, it was considered that transient HCM was developed to compensate for decreased myocardial contractility, and aggravated by hypovolemia and dobutamine administration.