LAUSR

Coronary artery vasospasm is an important cause of chest pain syndromes that can lead to angina or even myocardial infarction. Prinzmetal et al. first described a syndrome of nonexertional chest pain with ST segment elevation on electrocardiography. Although coronary artery vasospasm can be suspected clinically, proof cannot usually be obtained by non-invasive means unless via cardiac catheterization. Patients with vasospastic angina are repeatedly exposed to this invasive procedure as most cardiologists suspect a coronary lesion which requires intervention. Calcium antagonists are extremely effective in treating as well as preventing coronary spasm, and may provide long-lasting relief for the patient, avoid repeated coronary angioplasty. Lambda-like ST segment pattern was first described by Riera et al. [1] and further characterised by Gussak and Bjerregaard in their editorial [2], which resembled the Greek letter lambda, called then by Gussak ‘action potential-like’ shape. This specific ST segment elevation was accompanied by an upsloping ST segment depression in other leads, which was once called atypical Brugada syndrome [1]. We present a patient with acute inferior myocardial infarction (AMI) due to vasospasm and lambda-like atypical ST segment elevation during subsequent vasospastic angina. A 57-year-old man presented with a typical chest pain lasting for 8 h was admitted to the emergency department. Based on the persistent symptom of chest pain, the electrocardiographic change of ST segment, and increased Troponin, a diagnosis of acute inferior myocardial infarction was established. He had none of the classical risk factors for coronary artery disease, and did not use alcohol, tobacco, or cocaine. After receiving loading doses of aspirin and clopidogrel, the patient underwent an urgent coronary angiography which revealed total occlusion in the right coronary artery (RCA) and 70% stenosis in the proximal left anterior descending artery (LAD). However, after intracoronary nitroglycerine administered, the right coronary artery turned almost normal (Fig. 1a–f). Pathological Q wave and ST segment changes were not observed after the intervention compared to the admission (Fig. 1g, h). He had a history of recurrent chest pain which was milder in the past 1 month. During the year after this angiography, although sustained release tablets of diltiazem and isosorbide mononitrate were regularly taken, Prinzmetal’s variant angina pectoris happened once. In the latest event of his chest pain, an ECG first revealed almost normal (Fig. 2a). 30 min later, his repeated ECG showed remarkable downsloping ST segment elevation in leads II, III and aVF with mirror image in precordial leads, which is known as lambda-like pattern [2] (Fig. 2b). Then, a third ECG showed mild horizontal ST segment elevation in the inferior leads (Fig. 2C), and the ST elevation in leads II, III and aVF turned to baseline soon with symptom disappearance (Fig. 2d). None of antiarrhythmic drugs which could explain the widening of the QRS were used for our patient. Given that he had a history of emergency coronary angiogram 1 year before due to similar chest pain and negative Troponin, we decided to follow the patient. The lambda-like J wave caused by coronary artery spasm was rarely reported in literature. Our patient first suffered from AMI due to vasospasm and 1 year later he encountered an event of vasospastic angina resulted from the same reason. During his vasospastic angina, a diffuse ST segment elevation on electrocardiogram resembling the Greek letter lambda was observed in leads II, III and aVF, which was accompanied by an upsloping ST segment depression in precordial leads. Originally, the “lambda wave” was named for a case with idiopathic cardiac asystole whose ECG showed a nonischemic “action potential-like” Manli Yu and Qin Zhang have contributed equally.