Fragmented endocardial signals and early afterdepolarizations during torsades de pointes tachycardia
Abstract
Background: Bradycardia-induced torsade de pointes (TdP) tachycardia in patients with spontaneous high-degree atrioventricular block (AVB) is common. The aim of this study was to analyze endocardial recordings during TdP in spontaneous high-degree AVB in humans to better understand the electrophysiological mechanisms underlying this phenomenon.
Methods: The study group consisted of 5 patients with typical episodes of TdP during spontaneous high-degree AVB. A standard (USCI) temporary bipolar endocardial catheter positioned at the apex of the right ventricle (RV) and bipolar chest leads from two precordial leads V1 and V4 were used to record the tracings during TdP.
Results: The presence of a wide spectrum of fragmentations was noted on endocardial electrograms (EGMs), which were invisible on the surface electrocardiogram (ECG) tracing. Endocardial signals indicated that TdP started in the proximity of the RV apex, since the local EGM began prior to the QRS complex on the surface ECG. Early afterdepolarizations (EADs) were observed in 2 out of 5 cases confirming a common opinion about the mechanism of TdP. However, this phenomenon was not observed in 3 other patients suggesting that the arrhythmia was the result of a different mechanism originating in proximity to the RV apex.
Conclusions: This work demonstrated early endocardial signals in the RV apex during TdP associated with high-degree AVB in humans, and exhibits a spectrum of fragmented signals in this area occurring on a single or multiple beats. These fragmentations indicate areas of poor conduction and various degrees of intramyocardial block, and therefore a new mechanism of TdP tachycardia in some patients with spontaneous high-degree AVB.
Keywords: early afterdepolarizationstorsades de pointeselectrocardiogramatrioventricular blockendocardial recordings
References
- Subbiah RN, Gollob MH, Gula LJ, et al. Torsades de pointes during complete atrioventricular block: Genetic factors and electrocardiogram correlates. Can J Cardiol. 2010; 26(4): 208–212.
- Varkevisser R, Vos MA, Beekman JD, et al. AV-block and conduction slowing prevail over TdP arrhythmias in the methoxamine-sensitized pro-arrhythmic rabbit model. J Cardiovasc Electrophysiol. 2015; 26(1): 82–89.
- Cho MS, Nam GB, Kim YG, et al. Electrocardiographic predictors of bradycardia-induced torsades de pointes in patients with acquired atrioventricular block. Heart Rhythm. 2015; 12(3): 498–505.
- Boulaksil M, Jungschleger JG, Antoons G, et al. Drug-induced torsade de pointes arrhythmias in the chronic AV block dog are perpetuated by focal activity. Circ Arrhythm Electrophysiol. 2011; 4(4): 566–576.
- Vandersickel N, Bossu A, De Neve J, et al. Short-lasting episodes of torsade de pointes in the chronic atrioventricular block dog model have a focal mechanism, while longer-lasting episodes are maintained by re-entry. JACC Clin Electrophysiol. 2017; 3(13): 1565–1576.
- Smith WM, Gallagher JJ. "Les torsades de pointes": an unusual ventricular arrhythmia. Ann Intern Med. 1980; 93(4): 578–584.
- Roden DM. Clinical practice. Long-QT syndrome. N Engl J Med. 2008; 358(2): 169–176.
- Liu JF, Jons C, Moss AJ, et al. International Long QT Syndrome Registry. Risk factors for recurrent syncope and subsequent fatal or near-fatal events in children and adolescents with long QT syndrome. J Am Coll Cardiol. 2011; 57(8): 941–950.
- Schwartz PJ, Woosley RL. Predicting the Unpredictable: Drug-Induced QT Prolongation and Torsades de Pointes. J Am Coll Cardiol. 2016; 67(13): 1639–1650.
- Brugada P, Wellens HJ. Early afterdepolarizations: role in conduction block, "prolonged repolarization-dependent reexcitation," and tachyarrhythmias in the human heart. Pacing Clin Electrophysiol. 1985; 8(6): 889–896.
- Dessertenne F. [Ventricular tachycardia with 2 variable opposing foci]. Arch Mal Coeur Vaiss. 1966; 59(2): 263–272.
- D'Alnoncourt CN, Zierhut W, Blüderitz B. "Torsade de pointes" tachycardia. Re-entry or focal activity? Br Heart J. 1982; 48(3): 213–216.
- Jensen G, Sigurd B, Sandoe E. Adams-Stokes seizures due to ventricular tachydysrhythmias in patients with heart block: prevalence and problems of management. Chest. 1975; 67(1): 43–48.
- Li G, Saguner AM, Akdis D, et al. Intramyocardial block in patients with atrioventricular block. J Investig Med. 2018; 66(5): 1–4.
- Antzelevitch C. Basic mechanisms of reentrant arrhythmias. Curr Opin Cardiol. 2001; 16(1): 1–7.
- Gilmour RF, Moïse NS. Triggered activity as a mechanism for inherited ventricular arrhythmias in German shepherd Dogs. J Am Coll Cardiol. 1996; 27(6): 1526–1533.
- Akar FG, Yan GX, Antzelevitch C, et al. Unique topographical distribution of M cells underlies reentrant mechanism of torsade de pointes in the long-QT syndrome. Circulation. 2002; 105(10): 1247–1253.
- Kim TY, Kunitomo Y, Pfeiffer Z, et al. Complex excitation dynamics underlie polymorphic ventricular tachycardia in a transgenic rabbit model of long QT syndrome type 1. Heart Rhythm. 2015; 12(1): 220–228.
- Han J, Millet D, Chizzonitti B, et al. Temporal dispersion of recovery of excitability in atrium and ventricle as a function of heart rate. Am Heart J. 1966; 71(4): 481–487.
- Han J, Moe GK. Nonuniform recovery of excitability in ventricular muscle. Circ Res. 1964; 14: 44–60.
- El-Sherif N, Caref EB, Yin H, et al. The electrophysiological mechanism of ventricular arrhythmias in the long QT syndrome. Tridimensional mapping of activation and recovery patterns. Circ Res. 1996; 79(3): 474–492.
- Birati EY, Belhassen B, Bardai A, et al. The site of origin of torsade de pointes. Heart. 2011; 97(20): 1650–1654.
- James TN. Anatomy of the crista supraventricularis: its importance for understanding right ventricular function, right ventricular infarction and related conditions. J Am Coll Cardiol. 1985; 6(5): 1083–1095.
- Fontaine G. A new look at torsades de pointes. Ann N Y Acad Sci. 1992; 644: 157–177.
