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Torsades de pointes
Torsades de pointes, torsade de pointes or torsades des pointes (TdP; also called torsades) (/tɔːrˌsɑːd də ˈpwæ̃t/, French: [tɔʁsad də pwɛ̃t̪], translated as "twisting of peaks") is a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). It was described by French physician François Dessertenne in 1966. Prolongation of the QT interval can increase a person's risk of developing this abnormal heart rhythm, occurring in between 1% and 10% of patients who receive QT-prolonging antiarrhythmic drugs.
Most episodes will revert spontaneously to a normal sinus rhythm. Symptoms and consequences include palpitations, dizziness, lightheadedness (during shorter episodes), fainting (during longer episodes), and sudden cardiac death.[citation needed]
Torsades occurs as both an inherited (linked to at least 17 genes) and as an acquired form caused most often by drugs and/or electrolyte disorders that cause excessive lengthening of the QT interval.
Common causes for torsades de pointes include drug-induced QT prolongation and, less often diarrhea, low serum magnesium, and low serum potassium or congenital long QT syndrome. It can be seen in malnourished individuals and chronic alcoholics, due to a deficiency in potassium and/or magnesium. Certain drugs and combinations of drugs resulting in drug interactions are common contributors to torsades de pointes risk. QT-prolonging medications such as clarithromycin, levofloxacin, or haloperidol, when taken concurrently with cytochrome P450 inhibitors, such as fluoxetine, cimetidine, or particular foods including grapefruit, can result in higher-than-normal levels of medications that prolong the QT interval in the bloodstream and therefore increase a person's risk of developing torsades de pointes. A TdP cardiac event precipitated by loperamide has been reported (although the dose was well beyond the therapeutic range of the medication).
Knowledge that TdP may occur in patients taking certain prescription drugs has been both a major liability and a reason for the removal of 14 medications from the marketplace. Forty-nine drugs known to cause TdP and another 170 that are known to prolong QT remain on the market because the drugs provide medical benefit and the risk of TdP can be managed and mitigated by instructions in the drug label. Examples of compounds linked to clinical observations of TdP include amiodarone, most fluoroquinolones, methadone, lithium, chloroquine, erythromycin, azithromycin, pimozide, and phenothiazines. The anti-emetic agent ondansetron may also increase the risk of developing TdP. It has also been shown as a side effect of certain anti-arrhythmic medications, such as sotalol, procainamide, quinidine, ibutilide, and dofetilide. In one example, the gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after it was linked to deaths caused by long QT syndrome-induced torsades de pointes. This effect can be directly linked to QT prolongation mediated predominantly by inhibition of the hERG channel and, in some cases, augmentation of the late sodium channel.
The following is a partial list of factors associated with an increased tendency towards developing torsades de pointes:
The action potential of cardiac muscles can be broken down into five phases:[citation needed]
Repolarization of the cardiomyocytes occurs in phases 1–3 and is caused predominantly by the outward movement of potassium ions. In Torsades de pointes, however, the repolarization is prolonged; this can be due to electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia), bradycardia, certain drugs (disopyramide, sotalol, amiodarone, amitriptyline, chlorpromazine, erythromycin) and/or congenital syndromes.
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Torsades de pointes
Torsades de pointes, torsade de pointes or torsades des pointes (TdP; also called torsades) (/tɔːrˌsɑːd də ˈpwæ̃t/, French: [tɔʁsad də pwɛ̃t̪], translated as "twisting of peaks") is a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). It was described by French physician François Dessertenne in 1966. Prolongation of the QT interval can increase a person's risk of developing this abnormal heart rhythm, occurring in between 1% and 10% of patients who receive QT-prolonging antiarrhythmic drugs.
Most episodes will revert spontaneously to a normal sinus rhythm. Symptoms and consequences include palpitations, dizziness, lightheadedness (during shorter episodes), fainting (during longer episodes), and sudden cardiac death.[citation needed]
Torsades occurs as both an inherited (linked to at least 17 genes) and as an acquired form caused most often by drugs and/or electrolyte disorders that cause excessive lengthening of the QT interval.
Common causes for torsades de pointes include drug-induced QT prolongation and, less often diarrhea, low serum magnesium, and low serum potassium or congenital long QT syndrome. It can be seen in malnourished individuals and chronic alcoholics, due to a deficiency in potassium and/or magnesium. Certain drugs and combinations of drugs resulting in drug interactions are common contributors to torsades de pointes risk. QT-prolonging medications such as clarithromycin, levofloxacin, or haloperidol, when taken concurrently with cytochrome P450 inhibitors, such as fluoxetine, cimetidine, or particular foods including grapefruit, can result in higher-than-normal levels of medications that prolong the QT interval in the bloodstream and therefore increase a person's risk of developing torsades de pointes. A TdP cardiac event precipitated by loperamide has been reported (although the dose was well beyond the therapeutic range of the medication).
Knowledge that TdP may occur in patients taking certain prescription drugs has been both a major liability and a reason for the removal of 14 medications from the marketplace. Forty-nine drugs known to cause TdP and another 170 that are known to prolong QT remain on the market because the drugs provide medical benefit and the risk of TdP can be managed and mitigated by instructions in the drug label. Examples of compounds linked to clinical observations of TdP include amiodarone, most fluoroquinolones, methadone, lithium, chloroquine, erythromycin, azithromycin, pimozide, and phenothiazines. The anti-emetic agent ondansetron may also increase the risk of developing TdP. It has also been shown as a side effect of certain anti-arrhythmic medications, such as sotalol, procainamide, quinidine, ibutilide, and dofetilide. In one example, the gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after it was linked to deaths caused by long QT syndrome-induced torsades de pointes. This effect can be directly linked to QT prolongation mediated predominantly by inhibition of the hERG channel and, in some cases, augmentation of the late sodium channel.
The following is a partial list of factors associated with an increased tendency towards developing torsades de pointes:
The action potential of cardiac muscles can be broken down into five phases:[citation needed]
Repolarization of the cardiomyocytes occurs in phases 1–3 and is caused predominantly by the outward movement of potassium ions. In Torsades de pointes, however, the repolarization is prolonged; this can be due to electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia), bradycardia, certain drugs (disopyramide, sotalol, amiodarone, amitriptyline, chlorpromazine, erythromycin) and/or congenital syndromes.