LAUSR

150 J of biphasic shock. After confirming the diagnosis of vasospastic angina (VSA), we resumed the medication, and the patient had an uneventful course without recurrence of chest symptoms after discharge. VSA is mainly observed in middle-aged or older males who are at risk for atherosclerotic cardiovascular disease. VSA in premenopausal females is considered very rare due to high estrogen levels, which regulate endothelial function and prevent coronary spasm [1]. However, this 16-year-old female was diagnosed with VSA in the absence of risk factors or family history, and the attack was not related to the menstrual cycle [2]. There are few reports of VSA in females under 20 years of age, but the prevalence might be underestimated. Unexpected sudden death in young adults has been a subject of discussion for over two decades, and about 40% of cases remain unexplained [3]. Most previous reports of VSA in young females were diagnosed following serious cardiac events [4]. It is possible that VSA may account for a significant proportion of unexpected sudden deaths. Our case suggests that VSA can occur in young females in the absence of specific contributors. Further research is required to determine the true prevalence and contribution to unexpected sudden death in young patients. A 16-year-old female presented to our hospital with frequent chest tightness radiating to the left shoulder, which had persisted for several years. Her symptoms usually occurred on the way to school in the morning regardless of menstrual cycle, and disappeared after a period of rest. She had no coronary risk factors; congenital heart disease, Kawasaki disease, or menstrual disorder; or family history of sudden death, coronary artery disease, or hyperlipidemia. She and her family members had never smoked. The electrocardiogram, treadmill exercise testing, chest X-ray, laboratory data, and echocardiography were within normal limits. However, because of persistent symptoms, we decided to treat her as for angina pectoris. Her symptoms completely disappeared after starting diltiazem (200 mg/ day) and isosorbide mononitrate (40 mg/day). However, accurate diagnosis was thought necessary, and we planned additional evaluation following discontinuation of medication. Holter ECG revealed ST depression with symptoms. Coronary angiography showed no fixed stenosis. We then performed a spasm provocation test. Administration of 10 μg acetylcholine into the right coronary artery induced chest pain and significant ST changes, and the angiogram showed diffuse 90% stenosis (Fig. 1). Ventricular fibrillation occurred following ventricular premature conduction at R on T, but sinus rhythm was immediately restored with