Introduction
Background
Torsade de pointes (TDP), often referred to as torsade, is an uncommon variant of ventricular tachycardia (VT). The underlying etiology and management of torsade are, in general, quite different from those of garden-variety VT. The management of torsade with group IA antidysrhythmic drugs can have disastrous consequences. Differentiating between these entities, therefore, is critically important.
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Pathophysiology
Torsade is defined as a polymorphous VT in which the morphology of the QRS complexes varies from beat to beat. The ventricular rate can range from 150 beats per minute (bpm) to 250 bpm. The original report described regular variation of the morphology of the QRS vector from positive to net negative and back again. This was symbolically termed torsade de pointes, or "twisting of the point" about the isoelectric axis, because it reminded the original authors of the torsade de pointes movement in ballet. Most cases exhibit polymorphism, but the axis changes may not have regularity.
The definition also requires that the QT interval be increased markedly (usually to 600 msec or greater). Cases of polymorphous VT, which are not associated with a prolonged QT interval, are treated as generic VT. Torsade usually occurs in bursts that are not sustained; thus, the rhythm strip usually shows the patient's baseline QT prolongation.
The underlying basis for rhythm disturbance is delay in phase III of the action potential. The delay is mediated by the hERG potassium channel. This prolonged period of repolarization and the inhomogeneity of repolarization times among myocardial fibers allow the dysrhythmia to emerge. The initiating electrophysiologic mechanism may be triggered activity or reentry.
Six genetic variants currently are recognized. Genotypes LQT1 and LQT2 have slow potassium channels, while LQT3 shows defects in the sodium channels. Treatment modalities soon may be based on the genotype of the individual.
Frequency
United States
Prevalence of torsade is still unknown.
Mortality/Morbidity
In the United States, 300,000 sudden cardiac deaths occur per year. TDP probably accounts for fewer than 5%.
Race
Brugada syndrome is more frequent in Southeast Asians.1
Sex
Women are 2-3 times more likely to develop TDP than men.
- Women have more QT prolongation secondary to drug therapy.
- Congenital long QT syndrome is autosomal dominant but shows greater frequency of expression and a greater lengthening of the QT interval in women than in men.
Age
The highest frequency is in patients aged 35-50 years.
Clinical
History
- Ask the patient about previous cardiac events or syncope and any medications that the patient is presently using.
- History of congenital deafness or family history of sudden death may indicate a long QT syndrome.
Physical
No physical findings are typical of torsade de pointes (TDP).
Causes
- Prolongation of the QT interval may be congenital, as seen in the Jervell and Lange-Nielsen syndrome (ie, congenitally long QT associated with congenital deafness) and the Romano Ward syndrome (ie, isolated prolongation of QT interval). Both of these syndromes are associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation.
- Prolonged QT is found in only 0.25-0.3% of deaf-mute children.
- Brugada syndrome is characterized by a coved ST segment in the right precordial leads. The syndrome may cause sudden death due to polymorphic VT resembling TdP.
- The acquired conditions that predispose one to torsade either decrease the outward potassium current or interfere with the inward sodium and calcium currents, or fluxes.
- The electrolyte disturbances that have been reported to precipitate torsade include hypokalemia and hypomagnesemia. Close observation is required in predisposed patients, such as those with cirrhosis or hypothyroidism.
- Hypokalemia and hypomagnesemia, in turn, cause a delay in phase III (ie, reprolongation) and form the substrate for emergence of the dysrhythmia.
- Antiarrhythmic drugs reported to be etiologic include class IA agents (eg, quinidine, procainamide, disopyramide), class IC agents (eg, encainide, flecainide), and class III agents (eg, sotalol, amiodarone).
- Drug interactions with the antihistamines astemizole (recalled from US market) and terfenadine (recalled from US market) can precipitate torsade; these drugs should never be used with class IA, IC, or III agents.
- Astemizole and terfenadine, in high dosages or when used in combination with the azole antifungal drugs or the macrolide antibiotics, have been reported to precipitate torsade and sudden death.
- Grapefruit juice has been shown to slow the hepatic metabolism of these antihistamines as well as other drugs and to prolong the QT interval in patients taking astemizole or terfenadine (recently taken off the market by the US Food and Drug Administration [FDA]).
- Clinical implications of this interaction are unclear.
- Other drugs that prolong the QT interval and have been implicated in cases of torsade include phenothiazines, tricyclic antidepressants, lithium carbonate, cisapride, highly active antiretrovirals (HAARTs), high-methadone, anthracycline chemotherapeutic agents (eg, doxorubicin, daunomycin), some fluoroquinolones, and any other medication using the CYP3A metabolic pathway. Ranolazine, an antiangina agent, also prolongs the QTc, but torsade is a rare complication of this therapy.
- Risk factors
- Female gender
- History of syncope or resuscitated arrest
- Congenital deafness
- Family history of sudden death
More on Torsade de Pointes |
 Overview: Torsade de Pointes |
| Differential Diagnoses & Workup: Torsade de Pointes |
| Treatment & Medication: Torsade de Pointes |
| Follow-up: Torsade de Pointes |
| Multimedia: Torsade de Pointes |
| References |
| Next Page » |
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Further Reading
Keywords
torsade de pointes, TDP, torsade, ventricular tachycardia, VT, polymorphous VT, twisting of the point, cardiac syncope, vasovagal syncope, QT syndrome, QT interval, sudden death, unstable heart beat rhythm, TDP rhythm, dysrhythmia, Brugada syndrome
