|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
|
|
|
|||||||||
|
|||||||||||
|
J Am Coll Cardiol, 1998; 31:1400-1405 © 1998 by the American College of Cardiology Foundation |
Helsinki University Central Hospital, Finland.
OBJECTIVES: Measurement of QT interval dispersion during pharmacologic adrenergic stimulation was used to assess the effect of alpha- and beta-adrenergic stimulation on arrhythmic vulnerability in familial long QT syndrome (LQTS). BACKGROUND: Nonhomogeneity in the ventricular action potential duration causes electrical instability leading to life-threatening ventricular arrhythmias and is markedly increased in LQTS. QT interval dispersion measured from the electrocardiogram (ECG) can be used as an index of nonhomogeneous ventricular repolarization. METHODS: Sixteen symptomatic patients with LQTS and nine healthy control subjects were examined at baseline and during epinephrine (mainly beta-adrenergic agonist, 0.05 microg/kg body weight per min) and phenylephrine infusions (alpha-adrenergic agonist, mean 1.4 microg/kg per min). QT interval dispersion was determined from a 12-lead ECG as interlead range and coefficient of variation measured to the end (QTend) and apex (QTapex) of the T wave. RESULTS: At baseline QTend dispersion was greater in patients with LQTS compared with control subjects (mean [+/-SD] 68+/-34 vs. 36+/-7 ms, p=0.001). QTend dispersion was markedly increased in patients with LQTS by use of epinephrine (from 68+/-34 to 90+/-36 ms, p=0.002), but remained unchanged in control subjects. Phenylephrine did not affect QT dispersion in either group (all p=NS). Atrial pacing to achieve comparable heart rates during baseline and epinephrine and phenylephrine infusions did not influence the magnitude of QT dispersion in either group. QTapex dispersion analysis gave congruent results. CONCLUSIONS: Epinephrine but not phenylephrine increased QT dispersion, suggesting that beta-adrenergic stimulation provokes arrhythmias in patients with LQTS by aggravating nonhomogeneity of ventricular repolarization, whereas alpha-adrenergic stimulation is less important for arrhythmic vulnerability. The results also suggest that rapid pacing may not reduce vulnerability to arrhythmias in congenital LQTS.
This article has been cited by other articles:
|
|
 |
|
  J. D. Hunter, P. Sharma, and S. Rathi Long QT syndrome CEACCP, April 1, 2008; 8(2): 67 - 70. [Full Text] [PDF]
|
|
|
|
 |
|
 E. Drake, R. Preston, and J. Douglas Brief review: Anesthetic implications of long QT syndrome in pregnancy: [Article de synthese court : Implications anesthesiques du syndrome du QT long pendant la grossesse] Can J Anesth, July 1, 2007; 54(7): 561 - 572. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. F. McBride and C. M. White Critical Differences Among Beta-Adrenoreceptor Antagonists in Myocardial Failure: Debating the MERIT of COMET J. Clin. Pharmacol., January 1, 2005; 45(1): 6 - 24. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. S. Baker, N. S. Talner, A. S. Milazzo Jr, S. P. Sanders, A. M. Valente, R. J. Kanter, I. M. Paul, and J. S. Li Measures of Cardiac Repolarization and Body Position in Infants Clinical Pediatrics, January 1, 2003; 42(1): 67 - 70. [Abstract] [PDF]
|
|
|
|
 |
|
 W. Shimizu, Y. Tanabe, T. Aiba, M. Inagaki, T. Kurita, K. Suyama, N. Nagaya, A. Taguchi, N. Aihara, K. Sunagawa, et al. Differential effects of beta-blockade on dispersion of repolarization in the absence and presence of sympathetic stimulation between the lqt1 and lqt2 forms of congenital long qt syndrome J. Am. Coll. Cardiol., June 19, 2002; 39(12): 1984 - 1991. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Tanabe, M. Inagaki, T. Kurita, N. Nagaya, A. Taguchi, K. Suyama, N. Aihara, S. Kamakura, K. Sunagawa, K. Nakamura, et al. Sympathetic stimulation produces a greater increase in both transmural and spatial dispersion of repolarization in LQT1 than LQT2 forms of congenital long QT syndrome J. Am. Coll. Cardiol., March 1, 2001; 37(3): 911 - 919. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W Haverkamp, G Breithardt, A.J Camm, M.J Janse, M.R Rosen, C Antzelevitch, D Escande, M Franz, M Malik, A Moss, et al. The potential for QT prolongation and proarrhythmia by non-antiarrhythmic drugs: clinical and regulatory implications. Report on a Policy Conference of the European Society of Cardiology Eur. Heart J., August 1, 2000; 21(15): 1216 - 1231. [PDF]
|
|
|
|
 |
|
 W. Haverkamp, G. Breithardt, A.J. Camm, M. J Janse, M. R Rosen, C. Antzelevitch, D. Escande, M. Franz, M. Malik, A. Moss, et al. The potential for QT prolongation and pro-arrhythmia by non-anti-arrhythmic drugs: Clinical and regulatory implications: Report on a Policy Conference of the European Society of Cardiology Cardiovasc Res, August 1, 2000; 47(2): 219 - 233. [Full Text] [PDF]
|
|
|
|
 |
|
 D. Thomas, W. Zhang, C. A. Karle, S. Kathofer, W. Schols, W. Kubler, and J. Kiehn Deletion of Protein Kinase A Phosphorylation Sites in the HERG Potassium Channel Inhibits Activation Shift by Protein Kinase A J. Biol. Chem., September 24, 1999; 274(39): 27457 - 27462. [Abstract] [Full Text] [PDF]
|
|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
