Torsades de pointes

Torsades de pointes
Classification and external resources
DiseasesDB	29252
eMedicine	med/2286 emerg/596
MeSH	D016171

Torsades de pointes, or simply torsades, is a French term that literally means "twisting of the points." It was first described by Dessertenne in 1966 and refers to a specific, rare variety of ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG).

Presentation

The ECG tracing in torsades demonstrates a polymorphic ventricular tachycardia with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline. It is also associated with a fall in arterial blood pressure, which can produce syncope. Torsades de pointes can degenerate into ventricular fibrillation, which will lead to sudden death in the absence of medical intervention. Torsades de pointes is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on the ECG. Long QT intervals predispose the patient to an R-on-T phenomenon, where the R wave representing ventricular depolarization occurs during the relative refractory period at the end of repolarization (represented by the latter half of the T-wave). An R-on-T can initiate torsades. Sometimes pathologic T-U waves may be seen in the ECG before the initiation of torsades.

A variant of Torsades de pointes which presents without Long QT syndrome exists, referred to as the "Short-coupled variant of torsade de pointes" in literature and first described in 1994.

Characteristics

• Rotation of the heart's electrical axis by at least 180°
• Prolonged QT interval (LQTS) - not present in the short-coupled variant of torsade de pointes
• Preceded by long and short RR-intervals
• Triggered by an early premature ventricular contraction (R-on-T PVC)

Causes

Long QT syndrome can either be inherited as congenital mutations of ion channels carrying the cardiac impulse/action potential or acquired as a result of drugs that block these cardiac ion currents.

Common causes for torsades de pointes include diarrhea, hypomagnesemia and hypokalemia. It is commonly seen in malnourished individuals and chronic alcoholics. Certain combinations of drugs resulting in drug interactions may contribute: decreasing the metabolism of a medication causing QT elongation such as clarithromycin (Biaxin) or haloperidol (Haldol), taken concomitantly with a specific cytochrome P450 inhibitor like fluoxetine (Prozac) or cimetidine (Tagamet), some dietary supplements like St John's wort, foods like grapefruit will result in higher than normal doses of the medication responsible for the QT elongation. Since these specific drugs worsen the elongation of the QT wave in a dose-dependent manner, inhibition of drug metabolism raises the risks of developing a malignant torsades de pointes arrythmia. Various other medications are known to cause QT elongation. Examples include amiodarone, methadone, lithium, chloroquine, erythromycin, and phenothiazines. It can also be the side effect of some antiarrhythmic medications such as sotalol, procainamide and quinidine. The gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after such interactions lead to deaths caused by long QT syndrome-induced torsades de pointes.

An FDA warning was issued in September 2011 concerning high doses of the antidepressant Celexa (citalopram). Specifically, ECG analyses revealed an increased frequency of prolongation of the QT interval in patients receiving doses above 40 mg. per day (thereby increasing the risk of Torsades). Physicians were advised that 40 mg. per day is considered the maximum allowable dosage.

An FDA warning was issued in September 2011 concerning use of ondansetron (Zofran) in patients with low magnesium or potassium levels, or certain heart conditions, as they may lead to torsades de pointes. http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm272041.htm

Factors that are associated with an increased tendency toward torsades de pointes include:

Lead II ECG showing torsades being shocked by an implantable cardioverter-defibrillator back to the patients baseline cardiac rhythm.

• Familial long QT syndrome
• Class IA antiarrhythmics
• Class III antiarrhythmics
• Hypomagnesemia
• Hypokalemia
• Hypocalcemia
• Hypoxia
• Acidosis
• Heart failure
• Left ventricular hypertrophy
• Slow heart rate
• Female gender
• Hypothermia
• Subarachnoid hemorrhage

Treatment

Treatment is directed at withdrawal of the offending agent, infusion of magnesium sulfate, antiarrhythmic drugs, and electrical therapy as needed.

Because of the polymorphic nature of torsades de pointes, synchronized cardioversion may not be possible, and the patient may require an unsynchronized shock (or defibrillation).

History and terminology

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.