scholarly journals Takotsubo cardiomyopathy and the long-QT syndrome: an insult to repolarization reserve

EP Europace ◽  
2009 ◽  
Vol 11 (6) ◽  
pp. 697-700 ◽  
Author(s):  
E. R. Behr ◽  
S. Mahida
Keyword(s):  
Takotsubo Cardiomyopathy ◽  
Long Qt Syndrome ◽  
Long Qt ◽  
Repolarization Reserve ◽  
Qt Syndrome

scholarly journals Association of a congenital long QT syndrome type 1 with Takotsubo cardiomyopathy

2016 ◽  
Vol 4 (8) ◽  
pp. 789-792 ◽  
Author(s):  
Ibrahim El‐Battrawy ◽  
Michael Behnes ◽  
Martin Borggrefe ◽  
Ibrahim Akin
Keyword(s):  
Takotsubo Cardiomyopathy ◽  
Long Qt Syndrome ◽  
Syndrome Type ◽  
Long Qt ◽  
Qt Syndrome ◽  
Congenital Long Qt Syndrome

scholarly journals Transient Long QT Development in a Patient with Takotsubo Cardiomyopathy

2016 ◽  
Vol 2 (2) ◽  
pp. 81-84
Author(s):  
Dániel Czuriga ◽  
Andrea Szegedi ◽  
Ferenc Győry ◽  
Attila Szilágyi ◽  
Sándor Sipka ◽  
...  
Keyword(s):  
Takotsubo Cardiomyopathy ◽  
Long Qt Syndrome ◽  
Qt Interval ◽  
Ventricular Arrhythmias ◽  
Interval Prolongation ◽  
Long Qt ◽  
Electrolyte Disturbances ◽  
Acquired Long Qt Syndrome ◽  
Qt Interval Prolongation ◽  
Qt Syndrome

Abstract QT interval prolongation on the electrocardiogram is considered a precursory sign for imminent, potentially lethal ventricular arrhythmias. Beside the inherited condition of long QT syndrome, numerous drugs, certain electrolyte disturbances and early transmural ischemia have been identified to induce reversible prolongation of the QT interval, collectively called as acquired long QT syndrome. Herein we describe a case of a patient with transient QT prolongation and Takotsubo cardiomyopathy, a rather infrequent cause of long QT development. Serial changes of the repolarization pattern were documented to demonstrate progression and resolution of the abnormal QT interval.

scholarly journals Long QT Syndrome and Torsade de Pointes Associated with Takotsubo Cardiomyopathy

2011 ◽  
Vol 26 (7) ◽  
pp. 959 ◽  
Author(s):  
Ji Hun Ahn ◽  
Sang-Ho Park ◽  
Won Yong Shin ◽  
Se Whan Lee ◽  
Seung Jin Lee ◽  
...  
Keyword(s):  
Takotsubo Cardiomyopathy ◽  
Long Qt Syndrome ◽  
Torsade De Pointes ◽  
Long Qt ◽  
Qt Syndrome

scholarly journals Late I Na Blocker GS967 Supresses Polymorphic Ventricular Tachycardia in a Transgenic Rabbit Model of Long QT Type 2

2020 ◽  
Vol 13 (8) ◽  
Author(s):  
Jungmin Hwang ◽  
Tae Yun Kim ◽  
Dmitry Terentyev ◽  
Mingwang Zhong ◽  
Anatoli Y. Kabakov ◽  
...  
Keyword(s):  
Action Potential ◽  
Long Qt Syndrome ◽  
Rabbit Model ◽  
Syndrome Type ◽  
Long Qt ◽  
Repolarization Reserve ◽  
Action Potential Plateau ◽  
Qt Syndrome ◽  
Potential Plateau

Background: Long QT syndrome has been associated with sudden cardiac death likely caused by early afterdepolarizations (EADs) and polymorphic ventricular tachycardias (PVTs). Suppressing the late sodium current (I NaL ) may counterbalance the reduced repolarization reserve in long QT syndrome and prevent EADs and PVTs. Methods: We tested the effects of the selective I NaL blocker GS967 on PVT induction in a transgenic rabbit model of long QT syndrome type 2 using intact heart optical mapping, cellular electrophysiology and confocal Ca 2+ imaging, and computer modeling. Results: GS967 reduced ventricular fibrillation induction under a rapid pacing protocol (n=7/14 hearts in control versus 1/14 hearts at 100 nmol/L) without altering action potential duration or restitution and dispersion. GS967 suppressed PVT incidences by reducing Ca 2+ -mediated EADs and focal activity during isoproterenol perfusion (at 30 nmol/L, n=7/12 and 100 nmol/L n=8/12 hearts without EADs and PVTs). Confocal Ca 2+ imaging of long QT syndrome type 2 myocytes revealed that GS967 shortened Ca 2+ transient duration via accelerating Na + /Ca 2+ exchanger (I NCX )-mediated Ca 2+ efflux from cytosol, thereby reducing EADs. Computer modeling revealed that I NaL potentiates EADs in the long QT syndrome type 2 setting through (1) providing additional depolarizing currents during action potential plateau phase, (2) increasing intracellular Na + (Na i ) that decreases the depolarizing I NCX thereby suppressing the action potential plateau and delaying the activation of slowly activating delayed rectifier K + channels (I Ks ), suggesting important roles of I NaL in regulating Na i . Conclusions: Selective I NaL blockade by GS967 prevents EADs and abolishes PVT in long QT syndrome type 2 rabbits by counterbalancing the reduced repolarization reserve and normalizing Na i . Graphic Abstract: A graphic abstract is available for this article.

scholarly journals A novel transgenic rabbit model with reduced repolarization reserve: long QT syndrome caused by a dominant-negative mutation of theKCNE1gene

2016 ◽  
Vol 173 (12) ◽  
pp. 2046-2061 ◽  
Author(s):  
Péter Major ◽  
István Baczkó ◽  
László Hiripi ◽  
Katja E. Odening ◽  
Viktor Juhász ◽  
...  
Keyword(s):  
Long Qt Syndrome ◽  
Rabbit Model ◽  
Dominant Negative ◽  
Long Qt ◽  
Transgenic Rabbit ◽  
Dominant Negative Mutation ◽  
Repolarization Reserve ◽  
Qt Syndrome

Coronary occlusion and reperfusion promote early afterdepolarizations and ventricular tachycardia in a canine tissue model of type 3 long QT syndrome

2006 ◽  
Vol 290 (2) ◽  
pp. H607-H612 ◽  
Author(s):  
Norihiro Ueda ◽  
Douglas P. Zipes ◽  
Jiashin Wu
Keyword(s):  
Ventricular Tachycardia ◽  
Long Qt Syndrome ◽  
Coronary Occlusion ◽  
Arterial Occlusion ◽  
Interactive Effects ◽  
Long Qt ◽  
Early Afterdepolarizations ◽  
Repolarization Reserve ◽  
Qt Syndrome ◽  
Type 3

Although long QT syndrome (LQTS) and coronary occlusion-reperfusion (O/R) are arrhythmogenic, they affect ventricular action potential duration (APD) differently. In contrast to the prolonged APD in LQTS, ischemia abbreviates APD after a transient prolongation. Thus we hypothesized that the dynamic interactive effects of ischemia and LQTS on APD and its dispersion would affect ventricular arrhythmogenicity. We mapped transmural distribution of action potentials in 6 groups of 10 isolated wedges of canine ventricular walls: LQTS-O/R, LQTS only, and O/R only, with separate groups for pacing cycle lengths (PCL) of 1,000 and 2,000 ms. We created type 3 LQTS with anemone toxin (ATX) II followed >30 min later by arterial occlusion (40 min) and reperfusion (>100 min). Arterial occlusion initially (first 4 min) prolonged and then shortened APD. Early afterdepolarizations (EADs) occurred during the initial 4 min of occlusion in 4 of the 10 LQTS-O/R wedges at PCL of 2,000 ms but not in the other groups. Reperfusion restored APD in the O/R-only groups but caused APD to overshoot its original duration, indicating depressed repolarization reserve, in the LQTS-O/R group. Reperfusion increased the dispersion of APDs and initiated ventricular tachycardia-fibrillation in 7 of 10 and 6 of 10 LQTS-O/R wedges and in 2 of 10 and 1 of 10 O/R-only wedges at PCLs of 1,000 and 2,000 ms, respectively. The LQTS-only wedges exhibited neither EADs nor ventricular tachycardia. We conclude that coronary O/R increased the arrhythmogenicity of LQTS via cumulative prolongation of APD, increase in repolarization dispersion, and suppression of repolarization reserve.

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