Torsades de pointes

[3] Prolongation of the QT interval can increase a person's risk of developing this abnormal heart rhythm, occurring in between 1% and 10% of patients who receive QT-prolonging antiarrhythmic drugs.

[8] Knowledge that TdP may occur in patients taking certain prescription drugs has been both a major liability and reason for removal of 14 medications from the marketplace.

[10][11] Examples of compounds linked to clinical observations of TdP include amiodarone, most fluoroquinolones, methadone, lithium, chloroquine, erythromycin, azithromycin, pimozide, and phenothiazines.

[13] In one example, the gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after it was linked to deaths caused by long QT syndrome-induced torsades de pointes.

In Torsades de pointes, however, the repolarization is prolonged; this can be due to electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia), bradycardia, certain drugs (disopyramide, sotalol, amiodarone, amitriptyline, chlorpromazine, erythromycin) and/or congenital syndromes.

As soon as the mid myocardial layer is no longer in a refractory period, excitation from nearby tissue will cause a retrograde current and a reentry circuit that will result in a positive chronotropic cycle, leading to tachycardia.

[19] A "short-coupled variant of torsade de pointes", which presents without long QT syndrome, was also described in 1994 as having the following characteristics:[20] The R-on-T phenomenon is the superimposition of a premature ventricular contraction on the T wave of a preceding heart beat.

[21] Not all premature chamber actions can trigger these dangerous arrhythmias; the risk is increased with ischemia of the heart muscle or with prolonged repolarization time (long QT syndrome).

[23] Treatment to prevent recurrent torsades includes infusion of magnesium sulphate,[24] correction of electrolyte imbalances such as low blood potassium levels (hypokalaemia), and withdrawal of any medications that prolong the QT interval.

[26] The phenomenon was originally described in a French medical journal by Dessertenne in 1966, when he observed this cardiac rhythm disorder in an 80-year-old female patient with complete intermittent atrioventricular block.

In coining the term, he referred his colleagues to the "Dictionnaire Le Robert", a bilingual French English dictionary, of which his wife had just given him a copy.

Lead II ECG showing a TdP patient being shocked by an implantable cardioverter-defibrillator back to their baseline cardiac rhythm