ABSTRACT. We report an 8-year-old girl who presented with clinical features of an acute myocardial infarction. The angiographic appearance of the coronary arteries was normal. A thrombophilic state caused by a homozygote genotype for the prothrombin G20210A mutation was detected, and a patent foramen ovale (PFO) with right-to-left shunting after Valsalva maneuver was demonstrated by transesophageal contrast echocardiography. No other embolic source was identified. We suggest that paradoxical embolization through a PFO resulted in a myocardial infarction in this young patient with hereditary thrombophilia. We closed the patient's PFO with a 25-mm PFO occluder. She was anticoagulated with warfarin for 6 months. S tudies of cryptogenic stroke in young patients have shown that the incidence of patent foramen ovale (PFO) is higher than in patients with established causes of stroke. [1][2][3][4][5] The suggested mechanism for a cerebrovascular event in patients with a PFO is based on a transient increase in right heart pressure, which would cause a transient right-to-left shunt through the PFO, with the possibility that a venous embolus could cross the PFO and embolize the cerebral circulation (paradoxical embolism). Paradoxical emboli could also reach other vascular beds, such as the coronary arteries, and cause acute myocardial infarction (MI). 6 Recent studies have shown that genetic or acquired prothrombotic disorders may represent risk factors for thromboembolic disease also in children. [7][8][9] We report a case of acute MI in an 8-year-old girl in whom, because of the presence of a PFO and inherited prothrombotic abnormality, after excluding all other possible causes, we presume that the MI had been caused by a paradoxical embolism.
CASE REPORTSThis 8-year-old girl, who previously had been well except for asthma and allergic rhinitis and conjunctivitis caused by pollen allergy, experienced acute chest pain, localized at the sternal area, while she was playing basketball at school. She stopped playing and the pain disappeared within 20 minutes. Her mother arrived when the pain had already ceased and noted that she was pale. In the evening, she developed a mild fever. On the following day, she awoke early in the morning because of a severe precordial pain. She stated that the pain felt like a weight pushing on her chest. The girl appeared extremely ill, pale, and sweaty; therefore, she was taken to the local hospital. On admission, the pain had persisted for ϳ45 minutes, but the intensity had decreased. The pain disappeared completely in 1 hour. Physical examination did not reveal any abnormality, heart rate was 96 beats/min, blood pressure was 105/60 mm Hg, respiratory rate was 20 breaths/min, and transcutaneous oxygen saturation was 97%. The electrocardiogram (ECG) showed a sinus rhythm with 2.5-mm ST elevation in lead I, aVL, V 4 , V 5 , and V 6 and ST depression in V 1 , V 2 , and aVR (Fig 1). The markers of myocardial damage were significantly increased: myoglobin was 224 ng/mL (normal values: 0 -70 ng/mL),...