Synephrine-containing dietary supplement precipitating apical ballooning syndrome in a young female
A 21-year-old female presented to the emergency room with disturbed consciousness and a seizure. She had no relevant medical history. She had been taking dietary supplements purchased via the internet for the proceeding week in order to lose weight. The supplements contained caffeine and synephrine. The physical examination revealed a blood pressure of 115/84 mmHg and pulse of 110 beats per minute. On auscultation, the lungs were clear and heart sounds normal, with no murmur or gallop. The 12-lead electrocardiograph revealed sinus tachycardia, T wave inversion in leads II, III, aVF, and V3-6, and a prolonged QTc interval of 537 ms (). Laboratory analysis revealed creatine kinase (CK) 374 U/L (normal range, 21 to 215), CK-MB 9.9 ng/mL (normal range, < 4.3), troponin I 0.59 ng/mL (normal range, < 0.07), brain natriuretic peptide 734 pg/mL (normal range, < 100), and C-reactive protein 3.6 mg/L (normal range, 0.1 to 6.0). The serum catecholamine levels measured 3 days after admission showed dopamine 6.03 ng/mL (normal range, 0.5 to 6.2), epinephrine 0.03 ng/mL (normal range, < 0.3), and norepinephrine 0.48 ng/mL (normal range, < 0.8). Transthoracic echocardiography (TTE) performed at the day of admission showed apical ballooning of the left ventricle due to akinesis from the apical to midventricular segments, and hyperkinesis of the basal segments, with a markedly reduced left ventricular ejection fraction of 28% (). The impairment extended across the coronary artery distribution. Cardiac magnetic resonance (CMR) was performed 2 days after admission. The cine CMR findings were consistent with TTE () and the late enhancement CMR revealed no late gadolinium enhancement (). In addition, reconstructed CMR images of the coronary arteries revealed no significant stenosis (). Under a working diagnosis of ABS, she was treated conservatively with a β-blocker, angiotensin converting enzyme inhibitor, and loop diuretics. Gradually, her symptoms improved. Another TTE performed 9 days after admission revealed a normal ejection fraction of 63%, with complete recovery of the apical and midventricular wall motion. While hospitalized, neurological evaluations including electroencephalography and brain magnetic resonance imaging were performed to determine whether epilepsy was the cause of her seizure. However, there was no definite evidence of epilepsy or other organic brain abnormalities. Therefore, she was not given any antiepileptic medication. She remained stable clinically and hemodynamically for 10 days of hospitalization and was discharged home without cardiological or neurological sequelae. In the year since, there has been no recurrence of ABS or seizures.