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the occurrence of myocardial infarction in newborns has been associated with cardiac malformations and abnormalities of the coronary arteries or thromboembolism .
the syndrome of hypoxemia - related myocardial dysfunction in newborns occurs in about 30% of asphyxiated infants and is usually more relevant in preterm infants , due to   immature myocardial contractility and respiratory distress syndrome .
myocardial ischemia in full term   infants with normal heart is an extremely rare and serious event .
we report a case of a full   term newborn affected by neonatal asphyxia and severe anemia , with normal heart and coronary arteries anatomy , who developed a massive myocardial infarction .
after delivery , the baby needed   immediate cardiopulmonary resuscitation with intubation , external cardiac massage , ventilatory assistance ( a / c with pip 20 , peep + 5 , ti 350  msec , fr 50/minute , map 9.9 , fio2 0.80 ) , and an immediate blood transfusion for severe anemia ( hb 2.5  g / dl ) .
severe metabolic acidosis was present ( ph 6.81 ) , with arterial hypotension ( 41/19  mmhg ) . correction of acidosis and treatment with dopamine , dobutamine , hydrocortisone , and furosemide was started .  
on ecg there were small q waves in d2 - 3 and marked signs of subendocardial ischemia - lesion  with diffused st - t segment elevation ( figure 1c ) .
echocardiography ( figure 1b ) showed   normal anatomy with the coronary arteries originated from the aorta ; dilated and hypocontratile left ventricle ( lv ) , with hypertrophic walls , mitral regurgitation , dilated right ventricle with tricuspid regurgitation and estimated pulmonary pressure of 35  mmhg , left - to - right shunt at atrial and ductal level , and moderate pericardial effusion .  
serum enzymes , at 10 hours of life , were : ck = 14.895  u / l , ck - mb = 2.472 
rh isoimmunization   was excluded and no specific infective agents were found by laboratory tests .   despite of the treatment ,
the clinical conditions of the baby worsened , with appearance of anuria , hepatic insufficiency , massive haemorrhage of the right cerebral hemisphere , and disseminated intravascular coagulation .
post - mortem examination ( figure 2 ) showed massive subendocardial infarction of the lv , diffused parenchymal hemorrhages in lungs , kidneys , adrenal glands , and brain ; with histological appearance of myocardial hypertrophy , increase of eosinophilia   and polymorphonucleated cells .
myocardial ischemia is a rare event in childhood and can occur in the immediate postnatal period , usually due to perinatal asphyxia and respiratory problems .
this complication is more frequent in premature infants with severe respiratory distress    that present abnormal left ventricular function and abnormal values of ck and ck - mb .
previously , a rare case of myocardial necrosis - infarction was reported in a premature infant with asphyxia , and the infant recovered , using the conventional treatment .   in full term infants , the etiology of myocardial dysfunction - ischemia is   mostly related to asphyxia .
another case was reported of a full term infant who presented at 12 days of age with myocardial infarction complicated by late mitral regurgitation and   heart failure that improved after mitral valve annuloplasty at 6 months of age .
our case suffered apparently from   a   longstanding anemia of unknown etiology , also due to a lack of routine controls in pregnancy ; this fact induced a compensatory mechanism of myocardial hypertrophy that was observed at echocardiography and at post - mortem examination . the entity of anemia has worsened toward the end of pregnancy ( as evident from the very low value of haemoglobin ) and led to a severe fetal and postnatal distress   due to the severe hypoxia .
myocardial - subendocardial necrosis was very diffused and the general state was very severe since the moment of birth , and all the therapeutic measures remained inefficacious . neither a hypothetical use of ecmo , reported to be employed in   another full term infant who   presented however later   on ,   at 9 days of age ,   could have saved our infant with   a more precocious and severe symptomatology .
our case regards a very unusual event   of a massive myocardial infarction in a full term neonate that occurred on the basis of a longstanding fetal anemia of unknown etiology leading   to the perinatal distress with severe hypoxia and multiorgan failure not improvable by the treatment .
a full - term female newborn with neonatal asphyxia and severe anemia ( hb 2.5  g / dl ) with normal heart developed a massive myocardial infarction . 
 no examinations were performed during pregnancy for parental nomadism . 
 the baby had immediate external cardiac massage , ventilatory assistance , and blood transfusion . 
 cardiomegaly was evident at chest x - ray and marked signs of ischemia - lesion at ecg . 
 echocardiography showed dilated , hypertrophic , and hypocontractile left ventricle ( lv ) , mitral and tricuspid regurgitation , and moderate pericardial effusion . 
 rh isoimmunization and infective agents were excluded at laboratory tests . despite the treatment with inotropes , hydrocortisone , and furosemide , the baby worsened and died at 45 hours of life . 
 postmortem examination showed diffuse subendocardial infarction of lv and diffuse parenchymal hemorrhages and myocardial hypertrophy , increase of eosinophilia , and polymorphonucleated cells at histology . 
 our patient suffered apparently from longstanding fetal anemia of unknown etiology that led to perinatal distress , severe hypoxia , and massive myocardial infarction , unresponsive to the therapy .