Torsade de pointes complicating drug treatment of low‐malignant forms of arrhythmia: Four case reports

Abstract

Summary:In patients with malignant ventricular arrhythmias, antiarrhythniic therapy is known to c x y a substantial risk of proarrhythmia. This risk is usually considered to be low when supraventricular arrhythmias or benign ventricular arrhythmias are considered. We were able to collect data on four patients without a history of life-threatening arrhythmias. in whom witiarrhythmic therapy was used and resulted in documented ventriculx fibrillation or torsade de pointes. In Cases No. 1 and 2.amal fibrillation was treated with either quinidine or quinidine and sotalol in combination. In both patients Holter monitoring, 4-I2 h :]tier conversion to sinus rhythm, documented the spmtaneous Occurrence of toixade de pointes degenerating into ventriculm fibrillation and requiring DC shock for termination. In Case No. 3, atrial fibrillation was treated with sotalol and amiodarone for 2 months when incessant episodes of torsade de pointes were documented. In Case No. 4, frequent but unsustained ventricular arrhythmias were treated with amiodarone in a patient sutfering dilative cardiomyopathy. After 6 days of treatment at a hem rate of 54 beats/inin, a mdrked QT increase was associated with the occurrence of repetitive episodes of polymorphic ventricular tachycardia degenerating into ventricular fibrillalion. None of the patients presented significant electrolyte abnormalities in the laboratory. A pathologic increase of' the QTc-lime was documented in Cases No. 1,3, and 4. In all pati en r s an ti m h yt hmic therapy was withdrawn after the proarrhythmic event and the patient became free of malignant tachyan-hythnuas. Antiarrhythmic therapy also carries a considerable risk of proarrhythmia when "benign" cardiac mhythtnias are treated. The risk seems to be lower than in patients with malignant arrhythmias, however it includes the occurrence of lethal tachyarrhythmias. Special attention should be paid to the selection ofantiarrhythmic agents when used in combination.

Time-Dependent Changes in QT Dynamics after Initiation and Termination of Paroxysmal Atrial Fibrillation

“…This study showed that attenuated bradycardia‐dependent prolongation of QT interval during AF was gradually corrected after restoration of SR from AF. This could be consistent with the finding that TdP developed a few hours after restoration of SR rather than immediately after restoration of SR . VR (SDQT/SDRR) as a measure of QT dynamics became greater at SR 4‐5h than at AF 4‐5h , and this could also be related to increases in risk of fatal arrhythmia after restoration of SR.…”

“…When such drugs are used to treat atrial fibrillation (AF), TdP could develop after restoration of sinus rhythm (SR); however, this rarely happens when the underlying rhythm remains in AF . TdP could occur a few hours after rather than immediately after restoration of SR, when AADs that prolong QT interval are given …”

“…2 TdP could occur a few hours after rather than immediately after restoration of SR, when AADs that prolong QT interval are given. 3 A rate correction of QT interval using standard Bazett 4 and Fridericia 5 formulae can induce significant errors in assessment of drug effects on QT interval. 6 There are no established methods Financial support: This work was partly supported by JSPS KAKENHI C 24591040. for evaluating QT interval during irregular RR intervals as seen in AF.…”

“Torsade de Pointes” in Patients with Structural Heart Disease and Atrial Fibrillation Treated with Amiodarone, β‐Blockers, and Digitalis

“…Despite the small number of cases, a causation between the medication and the induction of Tdp thus seems likely, though the exact proarrhythmic mechanism remains unclear. Yet, several investigators found an increased proarrhythmia risk associated to therapy with antiarrhythmic agents in combination with heart rate suppressing drugs, 12 , 21 supporting our thesis. Patients with chronic heart failure are nowadays more likely to be treated with such combination therapies of two or more cardiovascular and/or antiarrhythmic drugs.…”

Programming a fixed long atrioventricular delay is not effective in preventing ventricular pacing in patients with sick sinus syndrome

“…In the case of an inappropriately short QT interval after AF conversion, the potential protective effect of a longer QT interval at lower heart rates is transiently abolished. It seems possible that reentrant and polymorphic tachyarrhythmias could be facilitated in this situation, an effect which may become of crucial importance when the additional influence of sotalol is considered [9].…”