Torsades de pointes
|Torsades de pointes|
|Classification and external resources|
|DiseasesDB = 29252|
Torsades de pointes (TdP or simply "torsades") (French: [tɔʁsad də pwɛ̃t], translated as "twisting of the spikes"), is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). It was described by Dessertenne in 1966.
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 hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness and syncope. Depending on their cause, most individual episodes of torsades de pointes revert to normal sinus rhythm within a few seconds, but may also persist and possibly degenerate into ventricular fibrillation, which will lead to sudden death in the absence of prompt 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 "short-coupled variant of torsade de pointes", which presents without long QT syndrome, was also described in 1994.
- 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)
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.
Most episodes revert spontaneously to sinus rhythm. Palpitations, dizziness, lightheadedness (short episodes) Syncope (longer episodes) Sudden death
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), levofloxacin, or haloperidol (Haldol), taken concomitantly with a specific cytochrome P450 inhibitor like fluoxetine (Prozac), cimetidine (Tagamet); 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 arrhythmia.
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.
Prescription drug interactions 
In September 2011 (and updated in March 2012), the FDA issued a warning concerning increased incidence of QT elongation with doses of the antidepressant Celexa (citalopram) above 40 mg per day, which is considered the maximum allowable dosage, increasing the risk of Torsades.
General risk factors 
Factors that are associated with an increased tendency toward torsades de pointes include:
- Heart failure
- Left ventricular hypertrophy
- Slow heart rate
- Subarachnoid hemorrhage
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.
- Dessertenne, F. (1966). "La tachycardie ventriculaire a deux foyers opposes variables". Archives des maladies du coeur et des vaisseaux (in French) 59 (2): 263–272. ISSN 0003-9683. PMID 4956181.
- John, J.; Amley, X.; Bombino, G.; Gitelis, C.; Topi, B.; Hollander, G.; Ghosh, J. (2010). "Torsade de Pointes due to Methadone Use in a Patient with HIV and Hepatitis C Coinfection". Cardiology Research and Practice 2010: 1–4. doi:10.4061/2010/524764. PMC 3021856. PMID 21253542.
- Leenhardt A, Glaser E, Burguera M, Nürnberg M, Maison-Blanche P, and Coumel P (January 1994). "Short-coupled variant of torsade de pointes. A new electrocardiographic entity in the spectrum of idiopathic ventricular tachyarrhythmias". Circulation 89 (1): 206–15. doi:10.1161/01.CIR.89.1.206. PMID 8281648.
- "FDA Drug Safety Communication: Revised recommendations for Celexa (citalopram hydrobromide) related to a potential risk of abnormal heart rhythms with high doses". FDA. March 28 2012. Retrieved May 13 2012.
- Deshmukh, A; Ulveling K, Alla V, Abuissa H, Airey K. (2012). "Prolonged QTc interval and torsades de pointes induced by citalopram.". Tex Heart Inst J. 39 (1): 68–70. PMC 3298934. PMID 22412232.
- Hoshino K, Ogawa K, Hishitani T, Isobe T, Eto Y (October 2004). "Optimal administration dosage of magnesium sulfate for torsades de pointes in children with long QT syndrome". J Am Coll Nutr 23 (5): 497S–500S. PMID 15466950.
- Hoshino K, Ogawa K, Hishitani T, Isobe T, Etoh Y (April 2006). "Successful uses of magnesium sulfate for torsades de pointes in children with long QT syndrome". Pediatr Int 48 (2): 112–7. doi:10.1111/j.1442-200X.2006.02177.x. PMID 16635167.