Effect of atropine on QT prolongation and torsade de pointes induced by intracoronary acetylcholine in the long QT syndrome

We recently reported a marked QT prolongation and torsade de pointes (TDP) induced by an intracoronary acetylcholine (ACh) administration in patients with long QT syndrome, but the mechanism was not determined. In the present study, the effect of atropine on the ACh-induced QT prolongation and TDP w as studied in long QT syndrome. Nine patients with congenital long QT syndr ome were studied. ACh at doses of 20, 50, and 100 mu g were injected in a s tepwise manner into the left main coronary artery, and the changes in the Q T interval were measured. In 4 of the 9 patients, ACh administration at a d ose of 100 mu g was repeated after an intravenous atropine administration a t a dose of 0.5 mg. The QT intervals were measured using 12-lead electrocar diograms, and the data were compared before and after atropine administrati on. The coronary angiograms were normal and coronary spasm was not induced by ACh in all patients. The intracoronary administration of ACh at a dose o f 100 mu g significantly prolonged the corrected QT interval (QT(c)), from 511 +/- 26 to 629 +/- 40 ms (p <0.05). In 5 of the 9 patients, TDP was indu ced and was spontaneously terminated within 10 seconds (n = 4) or required direct-current shock (n = 1). After atropine administration, intracoronary ACh at the same dose resulted in no QT prolongation, and the QT(c) interval remained unchanged (525 +/- 29 vs 520 +/- 21 ms before and after atropine) , and no TDP was induced. These findings indicate that the muscarinic recep tor is involved in ACh-induced QT prolongation and TDP, both of which were prevented by the atropine administration. (C)1999 by Excerpta Medica, Inc.