Acquired long QT syndrome: Risperidone-facilitated triggered activity and Torsades de Pointes during complete AV block. I

Acquired long QT syndrome: Unequal regression of Amiodarone-induced repolarization lengthening

“…Recent advances in myocardial-cell biology and organ physiology are making it possible to establish relations between specific membrane ionic currents, APD and the ECG waveforms [18]; having this approach in mind, the ECGs presented here support the contention that the U wave is not a separate entity but a component of an interrupted T wave [19,20].…”

Acquired long QT syndrome: Long-term electrocardiographic (Holter) recording of Torsades de Pointes ending in asystole: II

“…The QTa interval of escapes (measured when more than two were not interrupted) was 0.76 s; the automatic QT/RR ratio reading was beyond 526 ms; the density of beats arising in the ventricle was 58%, and many of them evoke a single response, as described in Fig. 1 [2]. Six bursts of Torsades de Pointes (TdP), lasting from 3 beats to 21 beats (the longest one, ending in asystole and death) were documented.…”

“…However these drawbacks, we think worth reporting the Holter obtained in the old lady patient on Risperidone treatment who developed Torsades de Pointes (TdP) just at the onset of a complete AV block whose tracings were commented by large in [2]. The surface ECG presentation of (likely) phase 2 early afterdepolarizations (EAD), the TdP formation and extinction, and a final TdP episode which ended in asystole, are the main focus of this report.…”

“…1) trigger or do not TdP bursts depending on critical TDR, a major engine in wave formation, as exposed in [2]. The cycle length (rotating period) of the TdP (around 360 ms = 160 bpm) and the TDR determined (200 ms) [2] are so close that the diastolic interval left (160 ms) precludes the formation/extinction of spirals (sites in the ventricle, unpredictable behaviour, duration, at least as from a surface ECG can be predicted). In all panels in Fig.…”

Isoproterenol enhancement of IKs current in Amiodarone-induced Long QT Syndrome

“…The I Kr protein is encoded by a HERG gene, while I Ks is the result of assembly of hKCNQ1 (the alpha subunit of I Ks ) and minK (the beta subunit), encoded by hKCNQ1 and hKCNE1 genes, respectively. Overt mutations and/or DNA polymorphisms in these genes, especially when associated to non-genetic causes, such as bradycardia, hypokalemia, female gender… [3,4] may decrease the function of their products leading to a prolong QT interval (congenital or acquired long QT syndrome, LQTS). Amiodarone, a widely used class III antiarrhythmic drug, block the I Kr and I Ks components of the delayed rectifier potassium channel, the slow inward Ca 2+ current mediated through the L-calcium channels and has a noncompetitive antisympathetic effect; usually, and as a result, it may prolong, even uniformly and in a modest proportion, the QT interval; however, when a subclinical deficiency in genes encoding potassium channel is present, an unexpected, acquired QT interval lengthening may result (aLQTS) [5].…”