A 13-year-old boy was brought to our hospital after recovering from ventricular fibrillation that occurred after an episode of chest pain during training with his soccer team. Subsequent 64-slice multidetector computed tomography revealed the left coronary artery arising from the right sinus of Valsalva, which coursed between the ascending aorta and root of the main pulmonary artery. Surgical correction including unroofing of the left coronary ostium and pulmonary artery translocation was performed successfully. One year later, he remained asymptomatic and was back on his soccer team.
Case ReportA 13-year-old male junior high school student without any past history or familial history of cardiac disease or sudden death had been suffering from occasional chest pain during training with his soccer team. In August 2012, he felt chest pain during training, which required him to take a rest at the school infirmary, where he suddenly fell down and lost consciousness. The patient was resuscitated immediately by the school nurse with cardiac compression and an automated external defibrillator, which detected ventricular fibrillation (Fig. 1). He regained consciousness while being taken to our hospital.Laboratory data showed no significant elevation of either the creatine kinase or troponin I levels. An electrocardiogram (ECG) showed a regular sinus rhythm without J waves, delta waves or Brugada type ST patterns, which were also not detected when using modified precordial leads. The corrected QT interval was 0.442. ECGs of the patient's family members were also examined, which did not show any abnormal findings. Late potential and T-wave alternans were both negative. Transthoracic echocardiography revealed a normal ventricular morphology without segmental wall-motion abnormalities, or valvular disease. Blood-pool scintigraphy using technetium-99m showed normal right and left ventricular systolic functions. No late gadolinium enhancement was noted on cardiac magnetic resonance imaging, and gallium-67 scintigraphy indicated no abnormal accumulation. An epinephrine provocation test showed no significant QT prolongation. A genetic analysis of the most common gene loci (KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2) was negative for long QT syndrome.Subsequent 64-slice multidetector computed tomography revealed an anomalous origin of the left coronary artery arising from the right coronary sinus of Valsalva (Fig. 2A). The left main coronary artery passed between the ascending artery and the root of the main pulmonary artery, which was