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Torsades de pointes is a distinctive polymorphic ventricular tachycardia in which the QRS amplitude varies and the QRS complexes appear to twist around the baseline. Torsades de pointes is associated with a prolonged QT interval, which may be built or acquired.^{[1, 2]}

Torsades de pointes is usually non sustained and terminates spontaneously just frequently recurs unless the underlying cause is corrected. Torsades de pointes may degenerate into sustained ventricular tachycardia or ventricular fibrillation. Torsades is a life-threatening arrhythmia and may present as sudden cardiac expiry in patients with structurally normal hearts.

Epidemiology^[3]

The corrected QT interval is longer in the white population than in the black population, and longer in females than males. Therefore, torsades de pointes is more than mutual in white races and in females.^[four]
Torsades occurs at whatsoever age. If it occurs at an early age, the cause is usually due to congenital long QT syndrome. In later years, the cause is usually due to acquired long QT syndrome.

Risk factors

Congenital long QT syndromes - eg, Jervell and Lange-Nielsen syndrome, Romano-Ward syndrome.
Acquired long QT syndromes:
- Acute myocardial infarction.
- Drugs - eg, antiarrhythmic agents of classes Ia and Three, erythromycin, ketoconazole, tricyclic antidepressants, methadone, antipsychotics.^{[5, 6]}
- Electrolyte disturbances; hypokalaemia, hypomagnesaemia, hypocalcaemia.
- Acute kidney injury, liver failure.
- Metabolic; hypothyroidism, anorexia nervosa, malnutrition.
- Bradycardia; sinoatrial disease, atrioventricular (AV) block.
- Toxins; heavy metals, insecticides.

Presentation

Episodes of torsades in patients with congenital long QT syndromes may exist triggered by stress, fearfulness or physical exertion.
Patients with torsades usually present with recurrent episodes of palpitations, dizziness, and syncope.^[7] Sudden cardiac death can occur with the beginning episode.
Nausea, pallor, common cold sweats, shortness of breath and chest hurting may occur.
A history of congenital deafness or a family history of sudden death may indicate a long QT syndrome.
Physical findings depend on the rate and duration of tachycardia and the degree of cerebral hypoperfusion. Findings include rapid pulse, depression or normal claret pressure level, and transient or prolonged loss of consciousness.
Other physical signs depend on the cause - eg, features of a congenital disorder.

Differential diagnosis

Ventricular tachycardia.
Supraventricular tachycardia with aberrant conduction.
Other causes of syncope or sudden cardiac death.

Investigations

ECG:^[viii]
- Paroxysms of five-xx beats, with a heart rate faster than 200 beats per minute. Sustained episodes are occasionally seen.
- Progressive change in polarity of QRS about the isoelectric line occurs with complete 180° twist of QRS complexes in 10-12 beats.
- Usually, a prolonged QT interval and pathological U waves are nowadays. The most consistent indicator of QT prolongation is a QT of 0.60 seconds or longer or a QTc (corrected for heart charge per unit) of 0.45 seconds or longer. QTc = QT interval divided by the square root of the interval (in seconds) between the onset of each QRS complex (Bazett's formula).
- A short-long-short sequence between the R-R interval occurs before the trigger response.
Electrolytes; hypokalaemia, hypomagnesaemia and hypocalcaemia.
Cardiac enzymes; cess for myocardial ischaemia.
CXR and echocardiography, to rule out structural heart illness.

Management

Short-term treatment

Resuscitation
Defibrillation:
- Although torsades is frequently self-terminating, it may develop into ventricular fibrillation, which requires defibrillation.^[9]
- In an otherwise stable patient, direct current (DC) cardioversion is unremarkably a last resort because torsades is paroxysmal in nature and oft recurs after cardioversion.
Discontinuation of whatsoever offending agent (cease all QT-prolonging drugs) and correction of any underlying cause such as hypokalaemia, hypomagnesaemia and bradycardia.
Intravenous magnesium is the drug of option for torsades de pointes. Magnesium is effective fifty-fifty in patients with normal magnesium levels.
Acceleration of the eye rate tin be achieved by using beta ane-adrenergic agonists such as isoprenaline or overdrive electrical pacing.
Isoprenaline is used as an acting treatment until overdrive pacing can be started:
- Isoprenaline accelerates AV conduction and decreases the QT interval.
- It can be used in bradycardia-dependent torsades that is usually associated with acquired long QT syndrome.
- Isoprenaline is given as a continuous intravenous infusion to keep the heart charge per unit faster than 90 beats per minute.
- Beta-adrenergic agonists are contra-indicated in the congenital form of long QT syndrome.
Temporary transvenous pacing:
- Pacing tin be effective in terminating torsades by increasing the heart rate so reducing the QT interval.
- Atrial pacing is the preferred mode because it preserves the atrial contribution to ventricular filling. In patients with AV block, ventricular pacing can exist used to suppress torsades.

Long-term treatment

Patients without syncope, ventricular tachyarrhythmia or a family history of sudden cardiac expiry can be observed without starting any treatment.
Congenital long QT syndrome:
- Beta-adrenergic antagonists are used every bit a showtime-line long-term therapy in congenital long QT syndrome. Propranolol is has been the most extensively used.
- Beta-blockers are contra-indicated in acquired cases considering bradycardia produced by these agents can precipitate torsades. They should also be avoided in those congenital cases in which bradycardia is a prominent feature.
- Permanent pacing benefits patients who remain symptomatic despite receiving the maximally tolerated dose of beta-blockers and tin be used in add-on to beta-blockers.
- High left thoracic sympathectomy is constructive in patients who remain refractory to beta-occludent and pacing.
- Implantable cardioverter-defibrillators (ICDs) are useful in rare instances when torsades still continues despite all of these treatments. Beta-blockers should be used forth with ICDs considering daze can further precipitate torsades by adrenergic stimulation.
Acquired long QT syndrome:
- Long-term handling in acquired cases is usually not required because the QT interval returns to normal one time the predisposing cistron has been corrected.
- Pacemaker implantation is effective in cases that are associated with heart block or bradycardia.
- ICDs are indicated in cases that cannot be managed by avoidance of any specific precipitating factor.

Complications

Prognosis

Patients may revert spontaneously or convert to a non-polymorphic ventricular tachycardia or ventricular fibrillation.^[9]
Torsades is a life-threatening arrhythmia and may nowadays equally sudden cardiac decease in patients with structurally normal hearts.
In acquired long QT syndrome, the prognosis is excellent once any precipitating factor has been removed.

Prevention^[9]

Avoid offending drugs that prolong the QT interval.
Preclude predisposing conditions such as hypokalaemia, hypomagnesaemia, and hypocalcaemia, especially in patients shown to have long QT interval.
Screen families of patients with torsades for whom the cause for prolonged QT is suggested to be built.

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Behr ER, Roden D ; Drug-induced arrhythmia: pharmacogenomic prescribing? Eur Heart J. 2013 Jan34(ii):89-95. doi: 10.1093/eurheartj/ehs351. Epub 2012 Oct 22.
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ECG Library
Drew BJ, Ackerman MJ, Funk Thousand, et al ; Prevention of torsade de pointes in hospital settings: a scientific statement from the American Eye Association and the American College of Cardiology Foundation. J Am Coll Cardiol. 2010 Mar 255(9):934-47. doi: 10.1016/j.jacc.2010.01.001.