Abstract
Prinzmetal (vasospastic) angina is an uncommon cause of transient ST-segment elevation and potentially life-threatening arrhythmias, typically occurring at rest. Identification of precipitating factors, including metabolic and electrolyte disturbances, is critical for targeted management. We report the case of a 46-year-old female smoker with a family history of coronary artery disease and prior non-obstructive coronary angiography who presented with recurrent nocturnal chest pain radiating to the left arm and associated with diaphoresis. Initial electrocardiography demonstrated transient 1-mm ST-segment elevation in lead II, which resolved with anti-ischemic therapy. Two hours after discontinuation of intravenous nitroglycerin due to hypotension, the patient developed recurrent chest pain with 3-mm ST-segment elevation in the inferior leads and sinus bradycardia. Urgent coronary angiography revealed severe right coronary artery spasm, promptly relieved by intracoronary nitroglycerin. Subsequent laboratory evaluation identified significant hypophosphatemia (1.6 mg/dL) and vitamin D deficiency. Phosphate replacement was initiated, after which no further vasospastic episodes occurred. Hypophosphatemia may promote coronary vasospasm through impaired myocardial energy metabolism and endothelial dysfunction. This case highlights the importance of clarifying the temporal relationship between electrolyte abnormalities and vasospastic events and recognizing hypophosphatemia as a possible reversible contributor to refractory vasospastic angina. Severe right coronary artery spasm can closely mimic acute coronary syndrome and result in hemodynamic instability; prompt angiographic diagnosis, intracoronary vasodilator therapy, and correction of underlying metabolic disturbances are essential for effective management.