Vasospastic angina (VSA), initially described by Prinzmetal as a form of angina occurring at rest, in the second part of the night and associated with transient changes in repolarization such as ST segment elevation on the electrocardiogram. The phenomenon of coronary spasm can occur in patients with or without coronary atherosclerosis. It can be focal or diffuse in one or more epicardial arteries. Its incidence is unknown and highly dependent on the population studied, with higher rates in Asian populations. Several pathophysiological mechanisms have been put forward to explain its occurrence, in particular endothelial dysfunction and hyperreactivity of smooth muscle cells related to damage to Rhokinase. Increased sympathetic nerve activity at night has shown to be involved in the mechanism underlying multivessel coronary spasm and predisposing genetic factors. Diagnosis can be easily establish using Coronary Artery Vasospastic Disorders Summit diagnostic criteria for vasospastic angina; adapted from Beltrame et al. VSA is one of the main aetiologies of MINOCA as stipulated in the last guidelines of ESC on ACS. Management of vasospastic angina is well codified based on lifestyle changes, established pharmacological therapies, control of risk factors, avoidance of triggering factors and possibly the use of percutaneous coronary intervention in cases of associated obstructive coronary artery disease, or an automatic implantable defibrillator.