torsades de pointes/potaisiam

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Drug-induced block of cardiac HERG potassium channels and development of torsade de pointes arrhythmias: the case of antipsychotics.

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Logáil Isteach / Cláraigh

The prolongation of the cardiac repolarization process, a result of the blocking of the Human Ether-ago-go Related Gene potassium channel, is an undesired accessory property shared by many pharmacological classes of non-cardiovascular drugs. Often the delayed cardiac repolarization process can be

Potassium channel blockade amplifies cardiac instability numerical studies of torsades de pointes.

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Logáil Isteach / Cláraigh

Suppression of responses to premature stimulation has been the guiding principle in managing many cardiac arrhythmias. Recent clinical trails revealed that sodium channel blockade increased the incidence of re-entrant cardiac arrhythmias resulting in sudden cardiac death, although the physiologic

[Torsade de Pointes tachycardia during sotalol treatment of a patient with normal potassium levels].

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Logáil Isteach / Cláraigh

Proarrhythmia in the form of Torsade de Pointes tachycardia (TdP) is a well-known complication of sotalol treatment. It most often occurs in the setting of sotalol overdosing, renal impairment, bradycardia, hypokalaemia, hypomagnesiaemia or lengthening of the QT-interval due to other drugs. TdP is

Torsade de pointes with an antihistamine metabolite: potassium channel blockade with desmethylastemizole.

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Logáil Isteach / Cláraigh

OBJECTIVE Proarrhythmic effects have been observed with the selective histamine1 (H1) receptor antagonist drug astemizole, a widely prescribed antihistamine. The metabolites of astemizole and those of other antihistamine compounds have not been implicated as causative agents of cardiac arrhythmias.

Atypical antipsychotics: from potassium channels to torsade de pointes and sudden death.

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Logáil Isteach / Cláraigh

Syncope and sudden death are features of schizophrenia that can be attributed to ischaemic heart disease, the use of antipsychotics (because of proarrhythmia or other reasons such as pharyngeal dyskinesia) or the psychiatric disease itself. Cases have been described with most antipsychotics and have

Extracellular potassium modulation of drug block of IKr. Implications for torsade de pointes and reverse use-dependence.

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Logáil Isteach / Cláraigh

BACKGROUND Torsade de pointes often occurs with underlying hypokalemia and bradycardia. A common effect of many drugs producing torsade de pointes is block of the rapidly activating component of the cardiac delayed rectifier (IKr). In this study, we evaluated the effect of changing extracellular

Tedisamil and dofetilide-induced torsades de pointes, rate and potassium dependence.

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Logáil Isteach / Cláraigh

1. Tedisamil is a bradycardiac agent that prolongs the QT interval of the ECG and prevents cardiac arrhythmias. Given this profile, tedisamil might be expected to have proarrhythmic actions similar to Class III antiarrhythmic drugs. To address this question, the actions of dofetilide and tedisamil

Nicorandil, a potassium channel opener, abolished torsades de pointes in a patient with complete atrioventricular block.

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Logáil Isteach / Cláraigh

TdP is a serious complication of AV block. We report a case of complete AV block with QT prolongation who had bouts of TdP resistant to lidocaine and isoproterenol. Temporary pacing could not be performed, because insertion of a pacing lead triggered TdP that deteriorated into ventricular

The hERG potassium channel and hERG screening for drug-induced torsades de pointes.

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Logáil Isteach / Cláraigh

Drug-induced torsades de pointes (TdP) arrhythmia is a major safety concern in the process of drug design and development. The incidence of TdP tends to be low, so early pre-clinical screens rely on surrogate markers of TdP to highlight potential problems with new drugs. hERG (human

The degree of potassium channel blockade and the risk of torsade de pointes: the truth, nothing but the truth, but not the whole truth.

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Logáil Isteach / Cláraigh

hERG potassium channel inhibition by ivabradine may contribute to QT prolongation and risk of torsades de pointes.

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Logáil Isteach / Cláraigh

Fatal torsade de pointes with d,l-sotalol and low potassium.

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Logáil Isteach / Cláraigh

Cardiac arrest secondary to emotional stress and torsade de pointes in a patient with associated magnesium and potassium deficiency.

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Logáil Isteach / Cláraigh

Treatment of torsade de pointes with magnesium sulfate.

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Logáil Isteach / Cláraigh

Twelve consecutive patients who developed torsade de pointes (polymorphous ventricular tachycardia with marked QT prolongation, TdP) over a 4 year period were treated with intravenous injections of magnesium sulfate. In nine of the patients a single bolus of 2 g completely abolished the TdP within 1

Proton Pump Inhibitors and Serum Magnesium Levels in Patients With Torsades de Pointes.

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Logáil Isteach / Cláraigh

Background: Torsades de pointes (TdP) is a life-threatening ventricular tachycardia occurring in long QT-syndrome patients. It usually develops when multiple QT-prolonging factors are concomitantly present, more frequently drugs and electrolyte imbalances. Since proton-pump inhibitors

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