Key result
Intracoronary acetylcholine transiently prolonged QT intervals in all 3 patients with congenital long QT syndrome and induced torsades de pointes in 2 patients, without inducing coronary vasospasm.
Why the study?
Does intracoronary acetylcholine induce coronary vasospasm or alter repolarization in patients with long QT syndrome?
Case Report (n=3)
No
Does intracoronary acetylcholine induce coronary vasospasm or alter repolarization in patients with long QT syndrome?
Intracoronary acetylcholine prolongs QT intervals and enhances dispersion of repolarization in LQTS patients, consistent with experimental arrhythmogenic mechanisms.
May provoke torsades in LQTS without vasospasm; hypothesis-generating and should not yet change practice.
We injected acetylcholine (Ach) into the coronary artery to ascertain whether coronary vasospasm contributed to the syncopal events or chest oppression suffered by 3 patients with long QT syndrome (LQTS). During the test, a quadripolar electrode catheter was placed in the right ventricle and the activation-recovery interval was reanalyzed from the stored data. Intracoronary Ach transiently prolonged the QT intervals in all 3 patients without inducing coronary vasospasm. The Ach-induced QT prolongation was associated with enhanced spatial and temporal dispersion of intra-ventricular repolarization. The electrophysiological abnormalities were consistent with the putative arrhythmogenic mechanisms identified in experimental studies of LQTS.
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Chinushi et al. (2011) conducted a case report in Congenital Long QT Syndrome (LQTS) (n=3). Intracoronary acetylcholine vs. Baseline (before injection) was evaluated on QT/QTc interval prolongation and induction of Torsades de Pointes (Tdp). Intracoronary acetylcholine transiently prolonged QT intervals in all 3 patients with congenital long QT syndrome and induced torsades de pointes in 2 patients, without inducing coronary vasospasm.
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