Vasospastic angina (VSA) is a variant form of
angina pectoris, which occurs at night or at rest, with transient electrocardiogram modifications and preserved exercise capacity. Its association with
stable angina,
sudden cardiac death,
acute coronary syndrome,
arrhythmia, and
syncope has previously been established. Its presentation can occur with or without existing
coronary artery disease and may present with focal or diffuse alteration and dysfunction of the coronary vasculature. VSA diagnosis involves patient response to
nitrates, transient ischemic electrocardiogram (ECG) changes, and
coronary artery spasms. The mechanisms proposed to constitute the substrate for susceptibility to VSA include vascular smooth muscle cell hyperreactivity, endothelial dysfunction,
magnesium deficiency, low-grade
inflammation, altered autonomic nervous system response,
hypothyroidism, and oxidative stress. Herein, we present the rare case of a patient with ST-segment elevation in the inferior leads, increased
troponin, and an episode of
ventricular fibrillation initially thought to be due to lateral wall
ST-elevation myocardial infarction (
STEMI), although it was revealed to be vasospastic angina. We will also review the literature. Vasospastic angina remains underdiagnosed and a timely diagnosis is crucial to prevent major
cardiac events. In patients with diffuse ST-segment elevation on ECG (independently of angiographic findings), VSA should be considered as one of the differential diagnoses and treated if found to be the cause of pathological changes.