Torsades de Pointes

Torsades de Pointes (TdP), which mean “twisting of the point” in French, is a type of polymorphic ventricular tachycardia (fast heart rate originating in the ventricles) characterized on electrocardiogram (ECG) by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line that can potentially lead to sudden cardiac death if not diagnosed and treated ¹, ², ³, ⁴, ⁵, ⁶, ⁷. Torsades de Pointes is often associated with QTc interval prolongation (the time it takes for the ventricles to depolarize and repolarize), which is the heart rate adjusted lengthening of the QT interval. The rate of Torsades de Pointes ranges from 160 to 240 beats per minute, which is slower than ventricular fibrillation ⁶. Torsades de Pointes rhythm may terminate spontaneously or may degenerate into ventricular fibrillation (VFib) and therefore can be fatal if not diagnosed and managed ⁸, ⁶. Torsades de Pointes is usually self-terminating and may cause palpitations (the sensation of your heart beating rapidly, irregularly, or with a forceful beat), dizziness, or fainting (syncope). Fainting (syncope) is typically precipitous and without warning.

Torsades de Pointes (TdP) can be caused by either congenital due to inherited Long QT syndrome or acquired due to electrolyte disturbances such as low blood potassium (hypokalemia), low blood calcium (hypocalcemia) and low blood magnesium (hypomagnesemia), and can be triggered by certain medications ⁹, ³, ¹⁰, ¹¹, ¹². More often, certain medications such as antiarrhythmics, antipsychotics, antibiotics, and antidepressants are the most frequent cause Torsades de Pointes ¹³.

The prevalence of Torsades de Pointes is unknown. Torsades de Pointes is a life-threatening arrhythmia and may present as sudden cardiac death in patients with structurally normal hearts ¹⁴. In the United States, 300,000 sudden cardiac deaths occur per year. Torsades de Pointes probably accounts for fewer than 5% ¹⁵.

Torsades de Pointes is 2-3 times more common in women than in men ¹⁵. Women have longer QT intervals as well as have more QT prolongation secondary to drug therapy ¹⁶.

Long QT syndrome usually falls into 2 groups ¹⁷, ¹⁸, ¹⁹:

1. Congenital long QT syndrome. You’re born with this type of long QT syndrome. It’s estimated to affect about 1 in 2,000 people ²⁰, ²¹. It’s caused by changes in DNA that are passed down through families. That means it is inherited. Congenital long QT syndrome has been shown to be caused by mutations in one of at least 15 different ion-channel genes ²²: the KCNQ1 gene causing LQTS1; KCNH2 causing LQT2; SCN5A causing LQT3; ANK2 causing LQTS4; KCNE1 causing LQTS5; KCNE2 causing LQT6; KCNJ2 causing LQTS7; CACNA1c causing LQTS8; CAV3 causing LQTS9; SCN4B causing LQTS10; AKAB9 causing LQTS11; SNTA1 causing LQTS12; KCNJ5 causing LQTS13; CALM1 causing LQTS14; and CALM2 causing LQTS15. Mutations in KCNQ1, KCNH2, and SCN5A correlate to Long QT types 1-3 and account for the majority (60-75%) of genetically identifiable cases.
   • There are 2 types of congenital long QT syndrome:
     • Romano-Ward syndrome. This more common type happens in people who get only a single gene change from one parent. Receiving a changed gene from one parent is known as an autosomal dominant inheritance pattern.
     • Jervell and Lange-Nielsen syndrome. This rare form of long QT syndrome usually happens very early in life and is severe. Children with this type of long QT syndrome also are deaf. In Jervell and Lange-Nielsen syndrome, children get the gene change from both parents. This is called an autosomal recessive inheritance pattern.
2. Acquired long QT syndrome. Acquired long QT syndrome is caused by another health condition or medicine. It usually can be reversed when the specific cause is found and treated.
   • If a medicine causes acquired long QT syndrome, the disorder may be called drug-induced long QT syndrome. More than 100 medicines can cause prolonged QT intervals in otherwise healthy people. Medicines that can cause long QT syndrome include ²³:
     • Some antibiotics, such as erythromycin (Eryc, Erythrocin, others), azithromycin (Zithromax) and others.
     • Some antifungal medicines used to treat yeast infections.
     • Water pills, also called diuretics, that cause the body to remove too much potassium or other minerals.
     • Heart rhythm medicines called anti-arrhythmics, which can make the QT interval longer.
     • Some medicines used to treat mental health conditions such as anxiety and depression.
     • Some medicines used to treat upset stomach.
   • Always tell your healthcare professional about all the medicines you take, including those you buy without a prescription.
   • Health conditions that can cause acquired long QT syndrome include ²³:
     • Body temperature below 95 degrees Fahrenheit (35 degrees Celsius), a condition called hypothermia.
     • Low calcium, also called hypocalcemia.
     • Low magnesium, also called hypomagnesemia.
     • Low potassium, also called hypokalemia.
     • A tumor of the adrenal gland that usually is not cancer, called pheochromocytoma.
     • Stroke or brain bleed.
     • Underactive thyroid, also called hypothyroidism.

Congenital Long QT syndrome is autosomal in genetic transmission but shows a greater frequency of expression and a greater lengthening of the QT interval in women than in men. You should avoid competitive sports if you have congenital long QT syndrome ²⁴. If you inherited Long QT syndrome from a parent, you should talk to a heart rhythm specialist before your start exercising. In congenital long QT syndrome, the mortality rate for untreated patients is 50% in 10 years, which can be reduced to 3-4% with therapeutic intervention. A systematic review of babies born with long QT syndrome from 83 studies comprising 265 newborns with postnatal confirmation of long QT syndrome found that a longer fetal QTc was more predictive of death than any other antenatal factor, and the mortality risk was significantly raised when the fetal QTc was longer than 600 ms ²⁵. Other factors that were highly predictive of death included the combination of ventricular tachycardia/Torsade de Pointes or functional 2:1 heart block and lack of a family history of long QT syndrome ²⁵. However, fetal heart rate and heart z-score did not predict death ²⁵.

Torsades de Pointes occurs in patients of a wide age range, from newborns to the very elderly ¹⁵. The highest frequency is in patients aged 35-50 years. Torsades de Pointes that occurs at an early age usually is due to congenital long QT syndrome. In older persons, it usually is due to acquired long QT syndrome ¹⁵. In a systematic review, investigators found that slightly over half (50.8%) of elderly patients age ≥80 years with drug-induced Torsades de Pointes experienced it as the result of “reckless administration” of a QT-interval prolonging agent ²⁶. The most common occurrences of reckless administration of a QT-interval prolonging drugs were in conjunction with another such agent (51.6%) or despite a known QT-interval prolongation (25.8%) ²⁶. Several European centers estimate that the annual reporting rate of drug-induced Torsades de Pointes is between 0.8 and 1.2 per million person-years ³. The incidence of drug-induced Torsades de Pointes also varies based on the drug in question and the population being studied ²⁷, ²⁸, ²⁹.

Torsades de Pointes is an electrocardiographic (ECG) diagnosis, and obtaining an ECG is essential. Frequent ECG monitoring is indicated for patients who are at risk due to chronic conditions or drug therapy. When the patient is in sinus rhythm, examine the QT interval. Usually, a prolonged QT interval and pathological U waves are present, reflecting abnormal ventricular repolarization ³⁰. The most consistent indicator of QT prolongation is a QT of 0.60 second or longer or a QTc (corrected for heart rate) of 0.45 second or longer ³⁰.

Tests to diagnose Torsades de Pointes include:

• Electrocardiogram (EKG).
• Blood tests to check electrolyte levels.
• Echocardiogram.
• A heart monitor you wear at home.

Treatment of Torsades de Pointes can be divided into short-term or immediate management and long-term management ²⁴. The goal of short-term management or immediate management is to assess for, achieve, and maintain hemodynamic stability. Short-term management or immediate management of Torsades de Pointes is the same in both acquired and congenital long QT syndrome, except that beta1-adrenergic stimulation may be tried in the acquired form but is contraindicated in the congenital form ²⁴. If you inherited Long QT syndrome from your parents, your treatment will include more long-term solutions than someone who got Long QT syndrome from a medication.

In an otherwise stable patient, direct current (DC) cardioversion is kept as a last resort, because Torsades de Pointes is paroxysmal in nature and is characterized by its frequent recurrences following cardioversion ²⁴. Although Torsades de Pointes frequently is self-terminating, it may degenerate into ventricular fibrillation, which requires direct current (DC) defibrillation ²⁴.

Any offending agent should be withdrawn. Predisposing conditions such as hypokalemia, hypomagnesemia, and bradycardia should be identified and corrected ²⁴.

Figure 1. Torsades de Pointes

Footnotes: In 1966, the French cardiologist Dessertenne ¹ described the electrocardiographic (ECG) pattern of ventricular tachycardia (VT), which he named “torsades de pointes” or “twisting of the points” and noted its association with a markedly prolonged QT interval.

[Source ¹³ ]

Figure 2. Onset of Torsades de Pointes

Footnotes: Onset of Torsades de Pointes during the recording of a standard 12-lead ECG in a young male with a history of drug addiction treated with chronic methadone therapy who presented to a hospital emergency department after ingesting an overdose of prescription and over-the-counter drugs from his parent’s drug cabinet. Classic ECG features evident in this rhythm strip include a prolonged QT interval with distorted T-U complex, initiation of the arrhythmia after a short-long-short cycle sequence by a Premature Ventricular Contraction (PVC) that falls near the peak of the distorted T-U complex, “warm-up” phenomenon with initial R-R cycles longer than subsequent cycles, and abrupt switching of QRS morphology from predominately positive to predominately negative complexes (asterisk).

[Source ⁶ ]

Figure 3. Torsade de Pointes ECG

Footnotes: A normal sinus beat is followed by a ventricular extrasystole (shortly after the sinus beat), the compensatory pause results in a longer interval to the next beat. This longer beat therefore has a longer QT interval. The next beat follows shortly thereafter, within the QT interval. Not all ventricular cells have been repolarized by that time and a ventricular arrhythmia results. This short-long-short sequence is typical for Torsades de Pointes.

[Source ³¹ ]

Figure 4. Torsades de Pointes ECG

Footnotes: Torsades de Pointes ECG with prolonged QT interval and the “twisting” or oscillating pattern of the QRS complexes, with the amplitude changing around the baseline.  12-lead ECG of Torsades de Pointes in a 56-year-old white female with low blood potassium (2.4 mmol/L) and low blood magnesium (1.6 mg/dL).

[Source ³² ]

Figure 5. Prolonged QT interval ECG

What is the difference between Torsades de Pointes and ventricular fibrillation?

Torsades de Pointes (TdP) is actually ventricular tachycardia that happens in the setting of Long QT interval. During Torsades de Pointes, your electrocardiogram (ECG) have a specific pattern of ventricular tachycardia (VT) that looks like “twisting” or “oscillating” points or peaks on an electrocardiogram (ECG). Torsades de Pointes can lead to ventricular fibrillation, a dangerous heart rhythm where the heart’s lower chambers quiver erratically instead of pumping blood effectively, that can lead to sudden cardiac arrest and death if not treated immediately.

How common is Torsades de Pointes?

Researchers aren’t sure how many people get Torsades de Pointes because of side effects from medicines, but getting Long QT syndrome from medicines is common. This can put you at risk for Torsades de Pointes. Anywhere from one in 2,000 people to one in 20,000 people may have been born with a genetic problem that can lead to Torsades de Pointes.

Torsades de Pointes causes

Some people are born with Long QT syndrome, which can lead to Torsades de Pointes ³³, ³⁴. 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) ¹⁰. Both of Jervell and Lange-Nielsen syndrome and the Romano Ward syndrome are associated with sudden death due to either primary ventricular fibrillation or Torsades de Pointes that degenerates into ventricular fibrillation.

Brugada syndrome is characterized by a coved ST segment in the right precordial leads ¹⁰. Brugada syndrome may cause sudden death due to polymorphic ventricular tachycardia resembling Torsades de Pointes.

Takotsubo cardiomyopathy, also known as “broken heart syndrome” or stress-induced cardiomyopathy, is a temporary heart condition triggered by intense emotional or physical stress. Takotsubo cardiomyopathy causes a part of the heart to weaken and change shape, similar to an octopus trap (tako-tsubo in Japanese), leading to symptoms like chest pain and shortness of breath and Torsades de Pointes ³⁵, ³⁶.

The acquired conditions that predispose someone to Torsades de Pointes include electrolyte disturbances that 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 low blood potassium (hypokalemia) and low blood magnesium (hypomagnesemia) ¹⁰. These electrolyte abnormalities cause a delay in phase III (ie, reprolongation) and form the substrate for emergence of the irregular heartbeat ¹⁰. Close observation is required in predisposed patients, such as those with cirrhosis of the liver or hypothyroidism (underactive thyroid).

Medications that are used to treat and prevent irregular heart rhythms or arrhythmias called antiarrhythmic drugs have been reported to cause Torsades de Pointes include class 1A agents (eg, quinidine, procainamide, disopyramide), class 1C agents (eg, flecainide [encainide was withdrawn in 1991]), and class 3 agents (eg, sotalol, amiodarone) ¹⁰.

Other drugs that prolong the QT interval and have been implicated in cases of Torsades de Pointes include phenothiazines (first-generation typical antipsychotic medications used for the treatment of psychosis, schizophrenia, bipolar disorders, control nausea and vomiting), tricyclic antidepressants, lithium carbonate, ziprasidone, cisapride, highly active antiretroviral drugs, high-dose methadone, anthracycline chemotherapeutic agents (eg, doxorubicin, daunomycin), some fluoroquinolones, and any other medication using the CYP3A metabolic pathway ¹², ³⁷, ¹⁰. Ranolazine, an antiangina agent, also prolongs the QTc, but Torsades is a rare complication of this therapy ³⁸, ³⁹, ⁴⁰.. Often, multiple agents act synergistically. Because QT prolongation is highly variable among and even in a single individual, the specific “causative” agent is often speculative ¹⁰. Accordingly, lists of agents suspected of increasing the QT interval may include some drugs that do not have this particular effect ¹⁰.

Medicines that can cause Torsades de Pointes include ¹³, ⁴¹, ²⁷, ²⁸, ²⁹:

• Antifungals.
• Antibiotics.
• Antipsychotics.
• Antiemetics (for nausea and vomiting).
• Antiarrhythmics.
• Cancer medicines.

A single-center, retrospective (2008-2019), observational study of the effects of 272 medications on 310,335 electrocardiograms (ECGs) from 159,397 individuals found that drugs associated with the greatest QT interval prolongation were dofetilide, mexiletine, amiodarone, rifaximin, and sotalol ⁴¹. However, the investigators also noted that several top drugs not previously known to prolong QT included rifaximin, lactulose, cinacalcet, and lenlidomide ⁴¹.

A 2023 case report described emergency department administration of a small dose (4 mg) of intravenous ondansetron resulting in QT prolongation, Torsades de pointes, and cardiac arrest in a middle-aged woman with alcohol disuse disorder who was not on any medications or supplements ⁴². Another 2023 case report described a rare presentation of levetiracetam-induced Torsades de pointes and cardiac arrest in a middle-age man with a history of a seizure disorder but noncompliance with valproic acid ⁴³. The patient received a total of 1000 mg intravenous levetiracetam as well as 4 mg of intramuscular lorazepam for two sets of episodes of tonic-clonic seizures in the emergency department ⁴³.

Risk factors for developing Torsades de Pointes

Risk factors for developing Torsades de Pointes include ⁶:

• Having Long QT syndrome that you inherited from your parents.
• Having a parent, brother, sister or child with long QT syndrome.
• Having heart disease.
• A history of cardiac arrest.
• Being a woman.
• Being older than 65.
• Using medicines known to cause prolonged QT intervals.
• Taking diuretics.
• Having profound bradycardia (very slow heart rate).
• Having low levels of calcium (hypocalcemia), magnesium (hypomagnesemia) or potassium (hypokalemia).
• Eating disorders such as anorexia nervosa, which also cause changes in the levels of body minerals.
• Having excessive diarrhea and vomiting, which can cause changes in body minerals such as potassium.

Torsades de Pointes Prevention

You can reduce your risk of Torsades de Pointes:

• Avoid medications that can cause Long QT interval and can put you at risk for Torsades de Pointes.
• Stop taking medicines that can cause Long QT syndrome. Your doctor can find an alternative.
• Increase your levels of calcium, magnesium and potassium if your doctor recommends it.

If Long QT syndrome runs in your family, your doctor can test your family members to see if they have it. With proper treatment, you can manage and prevent the dangerous heartbeats that can lead to Long QT syndrome complications.

Regular health checkups and good communication with your doctor also may help prevent causes of some types of acquired long QT syndrome. It’s especially important not to take medicines that can affect the heart rhythm and cause a prolonged QT interval.

Torsades de Pointes signs and symptoms

Half of the people with Torsades de Pointes don’t have any symptoms.

People with Torsades de Pointes who get symptoms can experience:

• Dizziness.
• Palpitations (feeling your heart pounding).
• Lightheadedness.
• Syncope (fainting).
• Cardiac arrest.
• Sudden cardiac death – an unexpected death due to cardiac causes that occurs in a short time period (generally within 1 hour of symptom onset) in a person with known or unknown cardiac disease.

Torsades de Pointes Complications

Complications of Torsades de Pointes include:

• Ventricular fibrillation. This type of irregular heartbeat causes the lower heart chambers to beat so fast that the heart trembles and stops pumping blood. Unless a device called a defibrillator is quickly used to correct the heart’s rhythm, brain damage and death can happen.
• Syncope (fainting).
• Sudden cardiac death. This is the swift and not expected ending of all heart activity. Torsades de Pointes has been linked to sudden cardiac death in young people who otherwise appear healthy. Long QT syndrome might be responsible for some unexplained events in children and young adults, such as unexplained fainting, drownings or seizures.

Torsades de Pointes diagnosis

Doctor can diagnose Torsades de Pointes on an electrocardiogram (EKG or ECG) ³⁰, ⁴⁴. Patients with Torsades de Pointes usually present with recurrent episodes of palpitations, dizziness, and syncope (fainting) that correspond to arrhythmia episodes; however, sudden cardiac death can occur with the first episode ⁴⁵. Nausea, cold sweats, shortness of breath, and chest pain also may occur but are nonspecific and can be produced by any form of tachyarrhythmia ⁴⁵.

In a young patient with Torsades de Pointes, a diagnosis of congenital long QT syndrome should be considered, especially if a family history of sudden cardiac death or sudden infant death syndrome is present ⁴⁵. In these patients, episodes of Torsades de Pointes are triggered by adrenergic stimulation such as stress, fear, or physical exertion, but other predisposing factors also should be considered ⁴⁶.

A family history of congenital deafness may also be suggestive, although a prolonged QT is found in only 0.25-0.3% of deaf-mute children ⁴⁵. Patients with Jervell and Lange-Nielsen syndrome commonly have congenital sensorineural deafness representing an autosomal dominant pattern of inheritance for cardiac abnormalities, whereas deafness usually is autosomal recessive ⁴⁵.

Another form of familial or congenital long QT syndrome is Romano-Ward syndrome, in which hearing is normal and an autosomal dominant pattern of inheritance is observed ⁴⁵.

Patients with acquired long QT syndrome usually develop Torsades de Pointes during periods of bradycardia. The most common causes of acquired long QT syndrome are medications and electrolyte disorders (eg, hypokalemia, hypomagnesemia, hypocalcemia). Drug-associated Torsades de Pointes is relatively rare, but is becoming increasingly common; its incidence is as high as 2-3% with certain drugs ⁴¹, ⁶. Hence, asking your patient about all current medications is important.

Tests to diagnose Torsades de Pointes include:

• Electrocardiogram (EKG or ECG). An ECG is the most common test used to diagnose Torsades de Pointes and long QT syndrome (LQTS). It records the electrical signals in the heart and shows how fast or how slow the heart is beating. Sticky patches called electrodes attach to the chest and sometimes the arms and legs. Wires connect the electrodes to a computer, which prints or displays the test results. The heart’s signals are shown as waves on the test results.
  
• Blood tests to check electrolyte levels.
• Echocardiogram.
• A heart monitor you wear at home.
  • Holter monitor. This small, portable ECG device records the heart’s activity. It’s worn for a day or two while you do your regular activities.
  • Event recorder. This device is like a Holter monitor, but it records only at certain times for a few minutes at a time. It’s typically worn for about 30 days. You usually push a button when you feel symptoms. Some devices automatically record when an irregular heart rhythm is detected.
• Genetic testing. A genetic test is available to confirm long QT syndrome (LQTS). The test checks for gene changes that can cause long QT syndrome (LQTS). If you have long QT syndrome, your heart doctor may suggest that other family members also get genetic testing to check for the disorder. Genetic tests for long QT syndrome can’t find all inherited cases of long QT syndrome. It’s recommended that families speak to a genetic counselor before and after testing.

Physical examination

The physical findings in Torsades de Pointes depend on the rate and duration of tachycardia and the degree of cerebral hypoperfusion ⁴⁵. Findings include rapid pulse, low or normal blood pressure, or transient or prolonged loss of consciousness ⁴⁵. This could be preceded by bradycardia or premature ventricular contractions (PVC) ⁴⁵. An increase in premaure ventricular contractions in individuals with prolonged QTc may be useful in predicting imminent Torsades de Pointes ⁴⁷.

Pallor and diaphoresis may be noted, especially with a sustained episode.

Other physical signs depend on the cause of Torsades de Pointes.

Electrocardiographic (ECG)

Torsades de Pointes is an electrocardiographic (ECG) diagnosis, and obtaining an ECG is essential.

Frequent ECG monitoring is indicated for patients who are at risk due to chronic conditions or drug therapy. When the patient is in sinus rhythm, examine the QT interval. Usually, a prolonged QT interval and pathological U waves are present, reflecting abnormal ventricular repolarization ³⁰. The most consistent indicator of QT prolongation is a QT of 0.60 second or longer or a QTc (corrected for heart rate) of 0.45 second or longer ³⁰.

Other electrocardiographic features helpful in diagnosing Torsades de Pointes include its typical mode of onset and its morphology, as follows ³⁰:

• Patients have paroxysms of 5-20 beats at a rate faster than 200 bpm; sustained episodes occasionally can be seen
• Progressive change in polarity of QRS about the isoelectric line occurs
• Complete 180° twist of QRS complexes in 10-12 beats is present
• A short-long-short sequence between the R-R intervals occurs before the trigger response.
• Torsades de Pointes may revert spontaneously or convert to a nonpolymorphic ventricular tachycardia or ventricular fibrillation
• Occasionally, T-wave alternans may be seen before Torsades de Pointes.

Torsades de Pointes occurring in the setting of acquired long QT syndrome is preceded by pauses in almost all cases ³⁰. In congenital long QT syndrome (adrenergic-dependent), pause dependence is found in most of the adult cases, whereas onset of Torsades de Pointes in children is not pause-dependent ³⁰.

Failure to identify Torsades de Pointes may occur for various reasons. During very short runs of Torsades de Pointes, the typical oscillatory QRS complexes around the isoelectric line may not be apparent. Early events usually are short lived. In the case of a single-lead recording, the typical morphology of Torsades de Pointes may not be obvious.

The diagnosis of Torsades de Pointes should be considered in any patient with pause-dependent ventricular tachycardia, and ventricular bigeminy in a patient with long QT interval may be a sign of an impending Torsades de Pointes ³⁰.

Findings from electrophysiological studies usually are negative in Torsades de Pointes ³⁰.

Other Tests

Other tests, including lab and imaging studies, should be ordered based on the underlying causal factors ⁴⁸:

• Laboratory studies
  • Electrolytes: Check for hypoglycemia, hypokalemia, hypomagnesemia, and hypocalcemia.
  • Cardiac enzymes: Rule out myocardial ischemia, especially in patients without QT prolongation.
• Imaging studies
  • Chest radiographs and echocardiography should be performed to rule out structural heart disease, if any clinical suggestion is present.

Torsades de Pointes Differential Diagnosis

The differential diagnosis of Torsades de Pointes includes ⁴⁹:

• Ventricular Tachycardia
• Atrial Tachycardia
• Syncope
• Dialysis Complications of Chronic Renal Failure
• Antidysrhythmic Toxicity
• Cough, Cold, and Allergy Preparation Toxicity. Because these medications are available over the counter (OTC) and are found in most households, they are frequently implicated in toxic ingestions, particularly in children. Antihistamines and cough and cold preparations, respectively, rank seventh and twenty-third on the list of substance categories most frequently involved in human exposures in the United States ⁵⁰.
• Ventricular Fibrillation
• Sudden Cardiac Death – an unexpected death due to cardiac causes that occurs in a short time period (generally within 1 hour of symptom onset) in a person with known or unknown cardiac disease

Other considerations are the differentiation of acquired long QT syndrome from congenital long QT syndrome. In addition, Torsades de Pointes should be differentiated from polymorphic ventricular tachycardia or rarely, monomorphic ventricular tachycardia.

Supraventricular tachycardia (SVT) with aberrant conduction may be confused with Torsades de Pointes, especially when the degree of aberration is variable. One clue to supraventricular tachycardia (SVT) is that atrial fibrillation may be intermixed with narrower and typical QRS complexes.

Torsades de Pointes treatment

Treatment of Torsades de Pointes can be divided into short-term or immediate management and long-term management ²⁴. The goal of short-term management or immediate management is to assess for, achieve, and maintain hemodynamic stability. Short-term management or immediate management of Torsades de Pointes is the same in both acquired and congenital long QT syndrome, except that beta1-adrenergic stimulation may be tried in the acquired form but is contraindicated in the congenital form ²⁴.

In an otherwise stable patient, direct current (DC) cardioversion is kept as a last resort, because Torsades de Pointes is paroxysmal in nature and is characterized by its frequent recurrences following cardioversion ²⁴. Although Torsades de Pointes frequently is self-terminating, it may degenerate into ventricular fibrillation, which requires direct current (DC) defibrillation ²⁴.

Any offending agent should be withdrawn. Predisposing conditions such as hypokalemia, hypomagnesemia, and bradycardia should be identified and corrected ²⁴.

Medical therapy

Magnesium is the drug of choice for suppressing early afterdepolarizations and terminating Torsades de Pointes arrhythmia ⁵¹, ²⁴, ⁵², ⁵³. Magnesium achieves this by decreasing the influx of calcium, thus lowering the amplitude of early afterdepolarizations ⁵⁴. Magnesium can be given at 1 to 2 g IV initially in 30-60 seconds, which then can be repeated in 5-15 minutes ²⁴. Alternatively, a continuous magnesium infusion can be started at a rate of 3-10 mg/minute ²⁴. Magnesium is effective even in patients with normal magnesium levels. Because of the danger of hypermagnesemia (depression of neuromuscular function), the patient requires close monitoring ²⁴.

Some authorities recommend supplemental potassium to increase the potassium concentration to high normal, which increases the efflux of potassium from myocardial cells, thus causing rapid repolarization ²⁴.

Lidocaine usually has no effect in Torsades de Pointes. Occasionally, lidocaine can have an initial beneficial effect, but Torsades de Pointes recurs in all cases ²⁴, ⁵¹.

Mexiletine also may be helpful in suppressing Torsades de Pointes ²⁴. In one study, mexiletine was used in patients with HIV who had acquired long QT interval and Torsades de Pointes ⁵⁵. Mexiletine effectively suppressed the torsade on a long-term basis ⁵⁵. Nakashima et al ⁵⁶ reported Mexiletine successfully preventing refractory Torsades de Pointes and ventricular fibrillation in a 28-year-old patient with congenital type 2 long QT syndrome.

Patients with congenital long QT syndromes are thought to have an abnormality of sympathetic balance or tone and are treated with beta-blockers ²⁴. If the patient experiences breakthrough Torsades de Pointes, a short-acting beta-blocker, such as esmolol, can be tried ⁵⁷.

Isoproterenol can be used in bradycardia-dependent Torsades de Pointes that usually is associated with acquired long QT syndrome (pause-dependent) ²⁴. Isoproterenol should be administered as a continuous IV infusion to keep the heart rate above 90 bpm ²⁴.

Isoproterenol accelerates AV conduction and decreases the QT interval by increasing the heart rate and reducing temporal dispersion of repolarization ²⁴. Beta-adrenergic agonists such as isoproterenol are contraindicated in the congenital form of long QT syndrome (adrenergic-dependent) ²⁴. Because of precautions, contraindications, and adverse effects associated with its use, Isoproterenol is used as an interim agent until overdrive pacing can be started ²⁴.

Temporary transvenous pacing

Based on the fact that the QT interval shortens with a faster heart rate, pacing can be effective in terminating Torsades de Pointes ²⁴. Pacing is effective in both forms of the long QT syndrome because it facilitates the repolarizing potassium currents and prevents long pauses, suppressing early afterdepolarizations and decreasing the QT interval.

Atrial pacing is the preferred mode because it preserves the atrial contribution to ventricular filling and also results in a narrower QRS complex and hence a shorter QT ²⁴. In patients with AV block, ventricular pacing can be used to suppress Torsades de Pointes ²⁴. This is dependent on intact atrial-to-ventricular conduction at the pacing rate found necessary.

Pacing should be instituted at a rate of 90-110 bpm until the QT interval is normalized. Overdrive pacing may be necessary at a rate of up to 140 bpm to control the rhythm ²⁴.

Patient with Torsades de Pointes who is in extremis should be treated with electrical cardioversion or defibrillation ²⁴. Anecdotal reports cite successful conversion with phenytoin (Dilantin) and lidocaine. A few cases of successful conversion using phenytoin and overdrive pacing have been reported ²⁴.

If patient is unresponsive to cardioconversion with phenytoin and overdrive pacing, attempt electrical cardioversion ²⁴.

Long-term treatment

Beta-adrenergic antagonists (beta blockers) at maximally tolerated doses are used as a first-line long-term therapy in congenital long QT syndrome ²⁴. Propranolol is used most extensively, but other agents such as esmolol or nadolol also can be used ²⁴. Beta-blockers should be avoided in those congenital cases in which bradycardia is a prominent feature ²⁴. Beta-blockers are contraindicated in acquired long QT syndrome because bradycardia produced by these agents can precipitate Torsades de Pointes ²⁴. One approach to assess the adequacy of beta-blockade is by exercise testing. One investigator recommends aiming for at least a 20% reduction in maximum heart rate compared to that of the baseline (pre-beta blocker therapy). Another approach is to check the blood levels of beta blockers (eg, propranolol) when possible ⁵⁸.

Patients without syncope, ventricular tachyarrhythmia, or a family history of sudden cardiac death can be observed without starting any treatment ²⁴.

Permanent pacing benefits patients who remain symptomatic despite receiving the maximally tolerated dose of beta-blockers and can be used adjunctively with beta-blockers ²⁴. Permanent pacing decreases the QT interval by enhancing the repolarizing potassium currents and suppressing early afterdepolarizations ²⁴.

High left thoracic sympathectomy or left cardiac sympathetic denervation (LCSD) surgery, another antiadrenergic therapy, is effective in patients who remain refractory to beta-blockade and pacing ²⁴. This surgery may be done if you have long QT syndrome and continuing heart rhythm changes but beta blockers don’t work for you. It doesn’t cure long QT syndrome. Instead, the surgery helps lower the risk of sudden cardiac death. In this treatment, surgeons remove specific nerves along the left side of the spine. These nerves are part of the body’s sympathetic nervous system, which helps control the heart rhythm. Accidental ablation of ocular efferent sympathetic nerves may result in Horner syndrome ²⁴.

Implantable cardioverter-defibrillators (ICDs) are useful in instances when Torsades de pointes recurs despite treatment with beta-blockers, pacing, and possibly left thoracic sympathectomy ²⁴. Beta-blockers should be used along with implantable cardioverter-defibrillators (ICDs) because shock can further precipitate Torsades de pointes by adrenergic stimulation. In the United States, an implantable cardioverter-defibrillator (ICD) for refractory cases may often precede sympathectomy ²⁴. The implantable cardioverter-defibrillator (ICD) device is placed under your skin near the collarbone. Placing an implantable cardioverter-defibrillator (ICD) requires surgery. It continuously checks the heart rhythm. If the device finds an irregular heartbeat, it sends out low- or high-energy shocks to reset the heart’s rhythm.

Most people with long QT syndrome don’t need an implantable cardioverter-defibrillator (ICD). But the device may be suggested for some athletes to help them return to competitive sports. The decision to place an implantable cardioverter-defibrillator (ICD), especially in children, needs to be carefully considered. Sometimes the device may send out shocks that aren’t needed. Talk with your heart specialist about the benefits and risks of an implantable cardioverter-defibrillator (ICD).

Long-term treatment in acquired long QT syndrome usually is not required because the QT interval returns to normal once the inciting factor or predisposing condition has been corrected ²⁴. Pacemaker implantation is effective in cases that are associated with heart block or bradycardia ²⁴. Implantable cardioverter-defibrillators (ICDs) are indicated in cases that cannot be managed by avoidance of the offending agent.

The boundary between acquired and congenital may not always be clear. Additive factors are often present, and individuals may show increased susceptibility to QT effects.

Exercise and physical activity warning

Competitive sports are prohibited in patients with congenital long QT syndrome ²⁴.

Complications of Torsades de Pointes may include:

• Monomorphic ventricular tachycardia
• Ventricular fibrillation
• Sudden cardiac death.

Living with Torsades de Pointes

There are several things you should do to take care of yourself with Torsades de Pointes.

• If you inherited Long QT syndrome from a parent, you should talk to a heart rhythm specialist before your start exercising.
• Keep taking your medicines to keep Torsades de Pointes from happening again.
• Learn how to take your pulse and what’s normal.
• Eat a diet rich in magnesium and potassium.
• Drink plenty of fluids.
• If your heart doctor gave you a heart monitor to use, be sure to wear it.
• You should go to the emergency room (ER) if you have a very fast pulse rate or if you feel palpitations, dizziness or lightheadedness or you get fainting episodes.

Torsades de Pointes prognosis

Without treatment, Torsades de Pointes can keep coming back or may lead to ventricular fibrillation, which can be deadly. With treatment, your chances of survival are good, especially if you stop taking the medicine that caused Long QT interval.

In congenital long QT syndrome, the mortality rate for untreated patients is 50% in 5 years, which can be reduced to 3-4% with therapeutic intervention ⁵⁹, ⁶⁰. A systematic review of babies born with long QT syndrome from 83 studies comprising 265 newborns with postnatal confirmation of long QT syndrome found that a longer fetal QTc was more predictive of death than any other antenatal factor, and the mortality risk was significantly raised when the fetal QTc was longer than 600 ms ²⁵. Other factors that were highly predictive of death included the combination of ventricular tachycardia/Torsade de Pointes or functional 2:1 heart block and lack of a family history of long QT syndrome ²⁵. However, fetal heart rate and heart z-score did not predict death ²⁵.

In acquired long QT syndrome, the prognosis is excellent once the inciting factor has been identified and discontinued ³.

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