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Precordial QT interval dispersion as a marker of torsade de pointes. Disparate effects of class Ia antiarrhythmic drugs and amiodarone.
Open accessAbstract
BACKGROUND: Patients with a history of class Ia drug-induced torsade de pointes have been treated with chronic amiodarone without recurrence of torsade de pointes despite comparable prolongation of the QT interval. We hypothesized that in such patients, class Ia drugs cause nonhomogeneous prolongation of cardiac repolarization times, whereas amiodarone causes homogeneous prolongation of cardiac repolarization times. METHODS AND RESULTS: Thirty-eight consecutive patients who received both class Ia drug therapy and chronic amiodarone therapy were evaluated. Standard 12-lead ECGs at baseline and during each therapy were used to calculate precordial QT interval dispersion (maximum QT in leads V1 through V6 minus minimum QT leads V1 through V6) as a measure of regional variabilities in ventricular repolarization times. Nine of these patients had torsade de pointes during class Ia drug therapy. In these nine patients, class Ia drug therapy and amiodarone significantly prolonged the maximum QT interval to comparable extents. However, class Ia drug therapy but not amiodarone therapy significantly increased precordial QT interval dispersion (101 +/- 37 versus 49 +/- 26 msec; baseline, 44 +/- 12 msec; p = 0.002). In the 29 patients without class Ia drug-induced torsade de pointes, neither class Ia drug therapy nor amiodarone therapy significantly increased QT interval dispersion (50 +/- 6 versus 69 +/- 7 msec; baseline, 54 +/- 5 msec). None of the patients with class Ia drug-induced torsade de pointes had recurrent torsade de pointes during chronic amiodarone therapy. CONCLUSIONS: An increase in regional QT interval dispersion during class Ia antiarrhythmic drug therapy is associated with torsade de pointes. Chronic amiodarone therapy in patients with a history of class Ia drug-induced torsade de pointes produces comparable maximum QT interval prolongation but does not increase QT interval dispersion. This characteristic may explain its apparent safe use in patients with a history of class Ia drug-induced torsade de pointes.
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Citations
Cited by
Taking the “Idio” out of “Idiosyncratic”: Predicting Torsades de Pointes
RODEN, D. M. (1998) · Pacing and Clinical Electrophysiology · doi:10.1111/j.1540-8159.1998.tb00148.x · Cited by 667
Measurement, interpretation and clinical potential of QT dispersion
Malik, M., & Batchvarov, V. N. (2000) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(00)00962-1 · Cited by 631
QTc-interval abnormalities and psychotropic drug therapy in psychiatric patients
Reilly, J., Ayis, S., Ferrier, I., Jones, S., & Thomas, S. (2000) · The Lancet · doi:10.1016/s0140-6736(00)02035-3 · Cited by 602
Mechanisms of abnormal cardiac repolarization during insulin-induced hypoglycemia
Robinson, R. T. C. E., Harris, N. D., Ireland, R. H., Lee, S., Newman, C., & Heller, S. R. (2003) · Diabetes · doi:10.2337/diabetes.52.6.1469 · Cited by 264
Metadata
- Authors
- Hii, J. T., Wyse, D. G., Gillis, A. M., Duff, H. J., Solylo, M. A., & Mitchell, L. B.
- Venue
- Circulation
- Published
- 1992-11
- Volume
- 86
- Issue
- 5
- Pages
- 1376-1382
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2074093573
- Cited by
- 385
- References
- 0
- FWCI
- 12.88
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Hii, J. T., Wyse, D. G., Gillis, A. M., Duff, H. J., Solylo, M. A., & Mitchell, L. B. (1992). Precordial QT interval dispersion as a marker of torsade de pointes. Disparate effects of class Ia antiarrhythmic drugs and amiodarone. Circulation. https://doi.org/10.1161/01.cir.86.5.1376
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