title: Heterogeneous effect of quinidine on the ventricular depolarization process assessed by the spatial velocity electrocardiogram of the QRS complex. Preliminary report of a new investigative method.
abstract: The negative conduction effect of quinidine on each of the successive phases of the ventricular depolarization was investigated using an original noninvasive method: the spatial velocity electrocardiogram of the QRS complex (SVECG-QRS). We performed a randomized placebo-controlled trial in 10 healthy subjects with a single oral dose of quinidine (330 mg) or placebo. Electrocardiographic acquisition and processing (220 recordings for the complete trial) were performed using the Lyon vectorcardiographic program. For each SVECG-QRS curve, the position of seven specific points from A (onset of QRS) to G (end of QRS) were determined precisely. The six successive time intervals between these points (AB-FG) and five velocity values (B-F) were then calculated. The QRS complex was longer under quinidine than placebo (102.4 +/- 1.6 vs. 100.3 +/- 1.5 ms). The difference was at the periphery of statistical significance (p = 0.05), and this lack of statistical difference may be mainly due to the low serum levels of quinidine obtained at the peak of the concentration (1.46 +/- 0.4 mg/1). All six QRS time intervals were longer under quinidine, but only the BC interval was significantly different (9.3 +/- 1.1 vs. 18.8 +/- 1.1 ms; p < 0.05) suggesting a more pronounced negative conduction effect at the onset of ventricular depolarization. No significant modifications were observed for the velocity values. We conclude that (1) the negative conduction effect of quinidine is heterogeneous, but a further study with a higher dose of quinidine (concentration-dependent effect) is required to confirm this hypothesis and (2) the spatial velocity electrocardiogram of the QRS complex allows a detailed analysis of the ventricular conduction phases. The results of the measurement were found to be reproducible. This noninvasive tool could be used in clinical practice to assess effects of antiarrhythmic drugs on successive ventricular depolarization phases.
authors.affiliation: INSERM Unit 121, Cardiovascular Hospital, Lyon, France.
authors.forename: S
authors.initials: S
authors.lastname: Fareh
authors.forename: P
authors.initials: P
authors.lastname: Arnaud
authors.forename: J
authors.initials: J
authors.lastname: Fayn
authors.forename: P
authors.initials: P
authors.lastname: Nony
authors.forename: P
authors.initials: P
authors.lastname: Girard
authors.forename: M
authors.initials: M
authors.lastname: Haugh
authors.forename: I
authors.initials: I
authors.lastname: Girard
authors.forename: S
authors.initials: S
authors.lastname: Ferry
authors.forename: J P
authors.initials: JP
authors.lastname: Boissel
authors.forename: P
authors.initials: P
authors.lastname: Rubel
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D004562:Electrocardiography / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects; D006801:Humans; D008297:Male; D011802:Quinidine / Q000494:pharmacology*; D012815:Signal Processing, Computer-Assisted; D014672:Vectorcardiography / Q000187:drug effects*
chemical_list: D000889:Anti-Arrhythmia Agents; D011802:Quinidine