Abstract
Acetylcholine is widely used for a diagnostic provocation test of coronary spasm in patients with vasospastic angina. Acetylcholine usually induces coronary vasodilatation mediated by muscarinic receptor activation, but sometimes it evokes vasoconstriction of coronary arteries where the endothelium is damaged. Early repolarization syndrome is characterized by a J wave observed at the end of the QRS complex in a surface electrocardiogram. The J wave is attributed to the transmural voltage gradient at the early repolarization phase across the ventricular wall, which stems mainly from prominent transient outward current in the epicardium, but not in the endocardium. Transient high-dose application of acetylcholine into the epicardial coronary arteries provides a unique opportunity to augment net outward current, selectively, in the ventricular epicardium and unmask the J wave, irrespective of the cardiac ischemia based on coronary spasm. Acetylcholine augments cardiac membrane potassium conductance by enhancing acetylcholine-activated potassium current directly and by activating adenosine triphosphate-sensitive potassium current, in addition to the reduced sodium and calcium currents in the setting of severe ischemia due to vasospasm. However, the role of acetylcholine as an arrhythmogenic probe of the J wave induction in patients with suspected early repolarization syndrome warrants future prospective study.