Clinical aspects of ventricular arrhythmias associated with QT prolongation
Department of Cardiology and Angiology, Hospital of the University of Munster, and Institute for Arteriosclerosis Research at the University of Münster, Germany
* Correspondence: Dr Wilhelm Haverkamp, Medizinische Klinik and Poliklinik, Innere Medizin C (Kardiologie, Angiologie), Universitätsklinikum Munster, D-48129 Münster, Germany.
Abstract
QT interval prolongation is a risk factor in a number of cardiovascular as well as non-cardiovascular diseases. Apart from this, abnormal, i.e. excessive, QT prolongation is typical for patients with acquired as well as congenital long QT syndrome. In these syndromes, prolongation of repolarization is often associated with severe, potentially life-threatening, ventricular tachyarrhythmias of the type torsade de pointes (TdP). While the congenital long QT syndrome has recently been identified as an ion channelopathy, the mechanisms underlying acquired long QT syndrome, which is most often induced by drugs prolonging myocardial repolarization, are far from understood. Recent studies have yielded only a small number of individual cases in whom the clinical setting has suggested an acquired form of the syndrome and genetic analysis revealed a familial form.
In order to prevent an unwanted exposure to risk, physicians prescribing agents that may prolong repolarization need to be aware of their potential to cause excessive QT prolongation and TdP. A clearer delineation of the factors predisposing to abnormal prolongation of repolarization and TdP, and a more precise quantification of the torsadogenic potency of individual drugs appear mandatory in order to prevent, or at least minimize, the incidence of this potentially fatal adverse effect of certain drugs.
Key Words: Long QT syndrome • torsade de pointes • QT interval • proarrhythmia • ventricular tachycardia • sudden cardiac death • drug metabolism • adverse effect
References
- Roden DM, George-Al J, Bennett PB. Recent advances in understanding the molecular mechanisms of the long QT syndrome. J Cardiovasc Electrophysiol. 1995;6:1023–1031[Web of Science][Medline]
- Priori SG, Barhanin J, Hauer RN, et al. Genetic and molecular basis of cardiac arrhythmias; impact on clinical management. Eur Heart J. 1999;20:174–195
[Free Full Text] - Haverkamp W, Shenasa M, Borggrefe M, Breithardt G. Torsades de Pointes. Zipes DP, Jalife J. Cardiac Electrophysiology-From Cell to Bedside. 2nd ed. Philadelphia: WB Saunders; 1995. p. 886–899
- Haverkamp W, Breithardt G, Janse MJ, et al, with other speakers in the sessions and the chairs of the workshops. The potential for QT prolongation by non-antiarrhythmic drugs. Clinical and regulatory implications. Report on a policy conference of the European Society of Cardiology. Eur Heart. 12000;21:1216–1231
- Selzer A, Wray HW. Quinidine syncope. Paroxysmal ventricular fibrillation occurring during treatment of chronic atrial arrhythmias. Circulation. 1964;30:17–26
[Free Full Text] - Roden DM, Woosley RL, Primm RK. Incidence and clinical features of the quinidine-associated long QT syndrome: implications for patient care. Am Heart J. 1986;111:1088–1093[CrossRef][Web of Science][Medline]
- Kay GN, Plumb VJ, Arciniegas JG, Henthorn RW, Waldo AL. Torsade de pointes: the long-short initiating sequence and other clinical features: observations in 32 patients. J Am Coll Cardiol. 1983;2:806–817[Abstract]
- Bauman JL, Bauernfeind RA, Hoff JV, Strasberg B, Swiryn S, Rosen KM. Torsades de pointes due to quinidine: observations in 31 patients. Am Heart J. 1984;107:425–430[CrossRef][Web of Science][Medline]
- Haverkamp W, Martinez RA, Hief C, et al. Efficacy and safety of d,1-sotalol in patients with ventricular tachycardia and in survivors of cardiac arrest. J Am Coll Cardiol. 1997;30:487–495[Abstract]
- Lehmann MH, Hardy S, Archibald D, Quart B, McNeil DJ. Sex difference in risk of torsade de pointes with d,l-sotalol. Circulation. 1996;94:2535–2541
[Abstract/Free Full Text] - Hohnloser SH. Proarrhythmia with class III antiarrhythmic drugs: types, risks, and management. Am J Cardiol. 1997;80:82G–89G[CrossRef][Medline]
- Schulze-Bahr E, Guicheney P, Szafranski P et al. Mutations in cardiac ion channel genes associated with acquired long-QT-syndrome (in press).
- Sesti F, Abbott GW, Wei J, et al. A common polymorphism associated with antibiotic-induced cardiac arrhythmia. Proc Natl Acad Sci USA. 2nd ed. 2000. p. 10613–10618
- Dessertenne F. La tachycardie ventriculaire a deux foyers opposes veriables. Arch Mal Coeur. 1966;59:263–272
- Dessertenne F, Fabiato A, Coumel P. Un chapitre nouveau de l'ectrocardiographie: les variations progressive de l'amplitude de l'electrocardiogramme. Actual Cardiol Angeiol Int. 1966;15:241–258
- Hohnloser SH, Klingenheben T, Singh BN. Amiodaroneassociated proarrhythmic effects. A review with special reference to torsade de pointes tachycardia. Ann Intern Med. 1994;121:529–535
[Abstract/Free Full Text] - Nattel S, Singh BN. Evolution, mechanisms, and classification of antiarrhythmic drugs: focus on class III actions. Am J Cardiol. 1999;84:11R–19R[Web of Science][Medline]
- Zhang S, Zhou Z, Gong Q, Makielski JC, January CT. Mechanism of block and identification of the verapamil binding domain to HERG potassium channels. Circ Res. 1999;84:989–998
[Abstract/Free Full Text] - Chouabe C, Drici MD, Romey G, Barhanin J. Effects of calcium channel blockers on cloned cardiac K+channels Ikr and Iks. Therapie. 2000;55:195–202[Web of Science][Medline]
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