Individuals suffering from torsades de pointes suffer recurrent palpitation events, syncope and dizziness. In addition to this, patients also experience shortness of breath, difficulty in breathing, pain in chest and nausea accompanied by cold sweats. In many instances sudden death can occur due to cardiac arrest.

Research has also shown that period of stress, fear, anxiety or physical exertion can trigger episodes of torsades. Patients may also exhibit signs of rapid pulse rate, and transient periods of unconsciousness. Other physical symptoms would depend on the type of congenital disorder present. Individuals who experience sustained episodes of torsades may suffer from diaphoresis and pallor.

Making an appropriate diagnosis of torsades de pointes is necessary to separate the condition from other variants of ventricular tachycardia. Failure to promptly diagnose the condition can lead to continuation of rhythm disturbances. Diagnosis of torsades de pointes includes the following tests:

• Electrocardiography (ECG): This is one of the most important and preliminary diagnostic procedure that should be carried out. The patient should be continuously monitored through ECG, when torsades has occurred as a secondary response to drug therapy or other chronic diseases [9].
• Laboratory studies: These include measuring calcium, potassium and magnesium levels. In addition, cardiac enzymes are also analyzed to determine myocardial ischemia as the underlying etiology.
• Imaging studies: Chest radiographs along with echocardiography are indicated in order to evaluate presence of structural abnormalities of heart.

• Short term and long term management is indicated in treatment of torsades de pointes. The short term management is similar for both the congenital and acquired forms of the condition; with an exception that β-1 adrenergic stimulation is given only in acquired form and should not be used for treatment of congenital form.
• Direct current (DC) cardioversion is kept as the last option and employed in cases when other treatment modes do not show the desired effect. Amongst the available drugs, magnesium is the treatment of choice and is extremely helpful in terminating the episodes of arrhythmia. It is administered at the rate of 1 – 2 g intravenously in 30 – 60 seconds initially [10]. The dosage is repeated every 5 – 15 minutes. Other drugs that can also be given include lidocaine, mexiletine and isoproterenol.

The condition resolves almost spontaneously; however can recur until the underlying etiology is completely treated. In untreated cases, or if there is a delay in initiation of treatment, there are chances of patients falling prey to sudden death. If the prolonged QT interval is acquired in nature, the prognosis is excellent, with correction of precipitating factor [8].

In many cases prolonged QT interval may be a congenital affair. Individuals with Jervell and Lange-Nielson syndrome and Romano Ward syndrome are likely to exhibit prolonged QT interval. These syndromes are associated with sudden death either due to primary onset of ventricular fibrillation or induced ventricular fibrillation due to torsades.

Electrolyte imbalances can predispose an individual to develop torsades de pointes. Certain drugs such as tricyclic antidepressants, cisapride, high-dose methadone, lithium carbonate, ziprasidone and chemotherapeutic agents can also increase the likelihood of prolonging QT interval [2] [3].

The exact incidence of torsades de pointes is unknown. It has been estimated that, women are 3 to 4 times more likely to have prolonged QT intervals. In addition, women also are at an increased risk of secondary development of torsades de pointes in response to drugs [4].

Torsades de pointes increases the risk of sudden death and it has been reported that about 300,000 sudden deaths occur in US every year. Of these, 5% of the cases occur due to torsades. Individuals in the age group of 35 to 50 years are more prone to suffer from prolonged QT interval [5].

The major and basic phenomenon behind the onset of lengthened QT interval in individuals is the current flow which is ionic in nature and that takes place during the repolarization phase. The morphology of QRS complex is different with each heart beat; however, the electrocardiogram appears like twisted ribbons, which is characteristic of torsades de pointes [6].

The appearance of twisted ribbons in electrocardiogram can be attributed to lengthened QT intervals which is the resultant reaction of delayed depolarization phase. This is considered to be the most vulnerable period, wherein majority of the myocardial tissue is ready to accept signals [7].

Individuals are advised to avoid those drugs that can lengthen the QT interval. Individuals with family history of torsades de pointes are at an increased risk of contracting the condition and therefore such families should be regularly screened. Certain predisposing factors such as hypomagnesemia, hypocalcemia and hypokalemia should be prevented.

Torsades de pointes is a type of ventricular tachycardia which may eventually resolve on its own; but can recur increasing the risk for other conditions. The ventricular heart rate in torsades de pointes is recorded to be 150 to 250 beats per minute. The condition is distinctly different from other forms of ventricular tachycardia due to its morphological characteristics, underlying etiology and types of therapy [1].

• Definition: Torsades de pointes is a form of ventricular tachycardia characterized by onset of prolonged QT intervals. Women are at a higher risk of contracting the condition than males. Drug-induced torsades de pointes is known to majorly strike the female population.
• Cause: Torsades de pointes can either be acquired or congenital in nature. Various factors such as drugs, underlying disease conditions and liver or renal failure can also lead to development of the characteristic prolonged QT interval.
• Symptoms: Affected individuals suffer from rapid pulse rate, arrhythmias, shortness of breath, diaphoresis, nausea along with dizziness, pallor, chest pain and cold sweats. In addition, other signs and symptoms of the underlying disease condition or congenital abnormality would also accompany.
• Diagnosis: Electrocardiography that shows prolonged QT interval is the characteristic finding in patients suffering from torsades de pointes. In addition, laboratory studies that are also conducted include evaluation of hypokalemia, hypocalcemia and hypomagnesemia. Imaging studies such as chest radiographs along with echocardiography is also indicated to determine presence of structural heart disease if any. Cardiac enzymes are also determined to evaluate myocardial ischemia.
• Treatment: Short term treatment of torsades de pointes is almost on similar lines for both congenital and acquired forms, except for β-1 adrenergic stimulation. Pharmacologic therapy includes intravenous administration of magnesium at rate of 1 – 2 g in 30 – 60 seconds. This remains the treatment of choice in majority of cases. Cardioversion is employed only when other methods do not work.

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