Worsening of Ventricular Tachycardia by Amiodarone

Abstract

The details of worsening of ventricular tachycardia in 8 (4.1%) of 194 patients receiving treatment with amiodarone are reported. Two forms of amiodarone-induced tachycardia were recognized: first, the development of new tachycardias (three patients) and second, a change in the pattern of recurrence of clinical tachycardia (five patients). In retrospect, the time from the initiation of amiodarone to the initial documentation of worsening ranged from 1 to 23 days (mean +/- SD, 9.4 +/- 8.2 days) and the time from the initiation of therapy to the recognition of worsening ranged from 6 to 26 days (14.6 +/- 10.1 days). Seven patients survived the worsening of tachycardia and one died. The total dose of amiodarone received and the duration of administration did not correlate with time to manifestation or time to resolution of worsening. This report emphasizes that worsening of ventricular tachycardia as a result of amiodarone is often difficult to differentiate from inadequate drug loading or early recurrence of 2 patient's clinical tachycardia. Further, because of the pharmacokinetics of the drug, the manifestations of worsening may be prolonged. In the cases reported, it ranged from 2 to 26 days (7.9 +/- 8.3 days), which is longer than previously reported. Because of the potential for amiodarone to cause life-threatening worsening of ventricular tachycardia and in accordance with current results, a period of in-hospital monitoring of at least 10 days at the start of therapy with amiodarone is recommended.

Proarrhythmia: A Paradoxic Response to Antiarrhythmic Agents

“…Of interest, when patients were crossed over to flecainide, only 4 of 22 had proarrhythmic effects, a trend that also held true for those who were given quinidine, then procainamide or mexiletine, then t~c a i n i d e .~~ Type Ill Antiarrhythmics Amiodarone may also cause proarrhythmia (see Table 1). [55][56][57] patients who had received amiodarone, 8 (4.1 %) developed pr~arrhythmia.~~ Proarrhythmia was defined as the clinical occurrence of new VT or a significant change in the frequency of the underlying arrhythmia with subsequent resolution after amiodarone therapy was discontinued. All of the eight patients were males, age 50-71 years, seven had ischemic heart disease, and six had decreased ejection fractions (< 35%).…”

Torsade de Pointes Due to Dronedarone: Déjà Vu?

“…Drugs that are highly torsadogenic, such as quinidine or sotalol, do both in potent fashion—they block the rapid component of the potassium current ( I Kr ) in an inverse rate‐dependent manner and cause nonuniform ventricular recovery throughout the ventricle. Benzofurans are more complex; amiodarone, although a clear cause of torsade de pointes, does so less frequently than pure I Kr blockers. Amiodarone is a multichannel blocker (it blocks I Kr , the slow component of the potassium current [ I Ks ], and sodium and L‐type calcium channels) and causes less dispersion of refractoriness with a much lower frequency of EADs, despite potently delaying repolarization and lengthening QT interval.…”