Dear José,

An EAD can induce arrhythmias by two different mechanisms. It can cause triggered activity, this is, an EAD can trigger an action potential and become an ectopic focus. Also an EAD can cause a phase 2 reentry.

You can find very illustrative Figures of each possibility in:

Antzelevitch C. Brugada syndrome. Pacing Clin Electrophysiol. 2006 Oct;29(10):1130-59.

Antzelevitch C, Belardinelli L. The role of sodium channel current in modulating transmural dispersion of repolarization and arrhythmogenesis. J Cardiovasc Electrophysiol, Vol. 17, pp. S79-S85, Suppl. 1, May 2006

Sincerely,

  Oscar

With electrical depolarization of T-tubules Sarkvlma Calcium enters the cells through the T-tubules and myocytes contract calcium influx lead to the rapid release of large amounts of calcium into the  is Systolic network. Ca release calcium binding subunit of troponin molecule located on the actin filament attached sarcomere, which leads to changes in the environment is Tropomyosin troponin complex. This change facilitates interaction of actin, myosin, and finally the muscle contraction. The depolarization wave failed, calcium actively and quickly absorbed by Sarkvplasmyk reticulum and by proteins such as Calsequestrin stored until the next wave of depolarization begins. Calcium also through multiple calcium pumps in the cytosol Sarkvlma out. Sarkvplasmyk  reticulum calcium release into the cell through the determined intensity of the contraction of myocytes has more calcium, leading to better interaction of actin and myosin contraction will be more severe

There is a paper from Brian Hoffman from Columbia

Hoffman B.F., Feinmark S.J., Guo S.D.

Electrophysiologic Effects of Interactions Between Activated Canine Neutrophils and

Cardiac Myocytes.

J Cardiovasc Electrophysiology 1997 : 8, 679-687

Dear Josè i'll report an article (with citations) i found in this book:

Clinical Approaches to Tachyarrhythmias; Mechanisms of Arrhythmias Pag.18-20.

[...] By infusing dogs with cesium, pleomorphic ventricular tachycardias resembling torsades de points have been induced65. In such animals, oscillation resembling EADs have been seen in epicardial recording of monophasic action potentials66,67. Similar observations have been made in the dog's ventricle subjected to sudden outflow obstruction68, in cats during ischemia and reperfusion69, in humans undergoing valvuloplasty for pulmonary stenosis70, and in humans with prolonged repolarisation and the long QT syndrome71. [...] The arrhythmia most likely caused by EADs is torsade de pointes, a nonsustained ventricular tachycardia with a characteristic ECG pattern, where QRS complexes twist irregularly around the isoelectric line. It is frequently associated with a long QT interval and bradycardia and is often initiated by a premature beat following a long cycle73,74. The characteristics of this arrhythmia and the fact that it may occur in patients taking antiarrhytmic drugs that prolong the action potential duration strongly support the notion that is caused by triggered activity based on EADs74. Another argument in in favor of this mechanism is he fact that the most effective treatment in patients with an acquired long QT syndrome and torsade de points is pacing, which shortens the QT interval74. In addition, magnesium sulfate is effective, and this may be related to suppression of EADs75. Still, reentry based on dispersion of refractoriness76 and multiple foci, either automatic or triggered77, are possible as well.

In summary, Arrhythmias caused by EAD-induced triggered activity should appear as the heart rate slows and disappear as the heart rate increases. Predisposing factors are pauses, low extracellular potassium concentration, and situations where action potentials are prolonged (long QT syndrome and excess use of class III antiarrhythmic drugs). They should be suppressed by drugs that blocksodium and calcium currents, by magnesium, and by adrenergic blockade.

65. Brachmann J, Scherlag BJ, Rosenstraukh LV, Lazzara R. Bradycardia dependent trigger activity: relevance to drug-induced multiform ventricular tachycardia. Circulation 1983;68:846

66. Ben David J, Zipped DP. Differential response to right and left ansae sublaciae stimulation of early afterdepolarizations and ventricular tachycardia induced by cesium in dogs. Circulation 1988;78:1241

67. Levine JH, Spear JF, Guarnieri ML et al. Cesium cholride-induced long QTsyndrome: demonstration of afterdepolarizations and triggered activity in vivo. Circulation 1985;72:1092

68. Franz MR, Burghoff D, Yeu DT, Sagawa K. Mechanically induced action potential changes and arrhythmias in isolated and in situ canine hearts. Cardiovasc Res 1989;23:213

69. Priori SG, Mantica M, Napolitano C, Schwartz PJ. Early afterdepolarizations induced in vivo by reperfusion of ischaemic myocardium. A possible mechanism for reperfusion arrhythmias. Circulation 1990;81:1911

70. Levine Jh, Guarnieri T, Kadish AH, White RI, Calkins H, Kan JS. Changes in myocardial ripolarization in patients undergoing balloon valvuloplasty for congenital pulmonary stenosis: evidence for contraction-excitation feedback in humans. Circulation 1988;77:70

71.Bonatti V, Rolli A, Botti G. Monophasic action potential studies in human subjects with prolonged ventricular repolarization and long QT syndrome. Eur Heart J 1985;6 suppl D:131

73. Dessertenne F. La tachycardie ventriculaire a deux foyers opposés variables. Arch Mal Coeur 1966;59:263

74. Leenardt A, Coumel P, Slama R. Torsades de Pointes. J Cardiovasc Electrophysiol 1992;3:281

75. Bailie DS, Inoue H, Kaseda S, et al. Magnesium suppression of early afterdepolarisations and ventricular tachyarrhythmias induced by cesim in dogs. Circulation 1988;77:1395

76.Surawicz B, Knoebel SB. Long QT: good, bad or indifferent? J Am Coll Cardiol 1984;4:398

77. Naumann d'Alnoncourt C, Zierhut W, Lüderitz B. "Torsade de pointes" tachycardia: Re-entry or focal activity? Br Heart J 1982;48:213.

I hope to be usefull.

Best regards

Giacomo Rozzi