| Torsades de pointes | |
|---|---|
| Other names | Torsade(s) |
 | |
| 12-lead ECG oftorsades de pointes (TdP) in a 56-year-old white female withlow blood potassium (2.4 mmol/L) andlow blood magnesium (1.6 mg/dL) | |
| Specialty | Cardiology |
| Complications | Cardiac arrest |
| Causes | Hereditary, certain drugs, electrolyte disorders which causeincreased QT interval |
| Risk factors | Medications, hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, heart failure, left ventricular hypertrophy, hypothermia, subarachnoid hemorrhage, hypothyroidism |
| Deaths | ~5% of 300,000 sudden cardiac deaths in the US[1] |
Torsades de pointes,torsade de pointes ortorsades des pointes (TdP; also calledtorsades) (/tɔːrˌsɑːddəˈpwæ̃t/,[2]French:[tɔʁsaddəpwɛ̃t̪], translated as "twisting of peaks") is a specific type ofabnormal heart rhythm that can lead tosudden cardiac death. It is a polymorphicventricular tachycardia that exhibits distinct characteristics on theelectrocardiogram (ECG). It was described by French physicianFrançois Dessertenne in 1966.[3] Prolongation of theQT 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.[4]
Most episodes will revert spontaneously to a normalsinus rhythm.[5] Symptoms and consequences includepalpitations,dizziness,lightheadedness (during shorter episodes),fainting (during longer episodes), andsudden cardiac death.[citation needed]
Torsades occurs as both an inherited (linked to at least 17 genes)[6] and as an acquired form caused most often by drugs and/or electrolyte disorders that cause excessive lengthening of the QT interval.[7]
Common causes for torsades de pointes include drug-induced QT prolongation and, less oftendiarrhea,low serum magnesium, andlow serum potassium or congenital long QT syndrome. It can be seen in malnourished individuals and chronicalcoholics, due to a deficiency in potassium and/or magnesium. Certain drugs and combinations of drugs resulting indrug interactions are common contributors to torsades de pointes risk.QT-prolonging medications such asclarithromycin,levofloxacin, orhaloperidol, when taken concurrently withcytochrome P450 inhibitors, such asfluoxetine,cimetidine, or particular foods includinggrapefruit, 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 byloperamide has been reported (although the dose was well beyond the therapeutic range of the medication).[8]
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.[9] 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.[10][11] Examples of compounds linked to clinical observations of TdP includeamiodarone, mostfluoroquinolones,methadone,lithium,chloroquine,erythromycin,azithromycin,pimozide, andphenothiazines.[11] Theanti-emetic agentondansetron may also increase the risk of developing TdP.[12] It has also been shown as a side effect of certain anti-arrhythmic medications, such assotalol,procainamide,quinidine,ibutilide, anddofetilide.[13] In one example, the gastrokinetic drugcisapride (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 thehERG channel and, in some cases, augmentation of the latesodium channel.[14]
The following is a partial list of factors associated with an increased tendency towards developing torsades de pointes:[15]
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.[16]
The prolongation of repolarisation may result in subsequent activation of an inward depolarisation current, known as anearly after-depolarisation, which may promote triggered activity.[17] Re-entry, due to a dispersion of refractory periods, is also possible;[18] this is because M Cells (found in the mid-myocardial layer) show a more prolonged repolarization phase in response to potassium blockage than other cells. In turn, this produces a zone of functional refractoriness (inability to depolarize) in the mid-myocardial layer.[17] When a new action potential is generated, the mid-myocardial layer will remain in a refractory period, but the surrounding tissue will depolarize. As soon as the mid-myocardial layer is no longer in a refractory period, excitation from nearby tissue will cause a retrograde current and a reentry circuit that will result in a positive chronotropic cycle, leading to tachycardia.[citation needed]
The ECG tracing in torsades demonstrates apolymorphic ventricular tachycardia with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline (peaks, which are at first pointing up, appear to be pointing down for subsequent "beats" when looking at ECG traces of the "heartbeat"). It is hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness andfainting. Depending on their cause, most individual episodes of torsades de pointes revert to normal sinus rhythm within a few seconds; however, episodes may also persist and possibly degenerate intoventricular fibrillation, leading to sudden death in the absence of prompt medical intervention. Torsades de pointes is associated withlong QT syndrome, a condition whereby prolonged QT intervals are visible on an ECG. Long QT intervals predispose the patient to anR-on-T phenomenon, wherein the R-wave, representing ventricular depolarization, occurs during the relative refractory period at the end of repolarization (represented by the latter half of the T-wave). An R-on-T can initiate torsades. Sometimes, pathologicT-U waves may be seen in the ECG before the initiation of torsades.[19]
A "short-coupled variant of torsade de pointes", which presents without long QT syndrome, was also described in 1994 as having the following characteristics:[20]
The R-on-T phenomenon is the superimposition of a premature ventricular contraction on the T wave of a preceding heartbeat. Studies suggest that the R-on-T phenomenon is likely to start a sustainedventricular tachycardia andventricular fibrillation.[21] It's considered a cardiac arrhythmia in which the ventricles of the heart become again excited during the repolarization of the previous heart action. Because part of the heart muscle cannot be excited at this early point in time, a premature chamber action can trigger life-threatening cardiac arrhythmias (e.g., ventricular fibrillation or Torsades de pointes).
On the ECG, this phenomenon is shown when aventricular extrasystole (R) (T-wave) is superimposed during the repolarization phase of the previous action of the heart.[21] Not all premature chamber actions can trigger these dangerous arrhythmias; the risk is increased withischemia of the heart muscle or with prolonged repolarization time (long QT syndrome).[22] The arrhythmia can also be triggered when an external stimulus such ascardioversion falls in the vulnerable phase of thecardiac cycle.
In the Lown grading system of ventricular arrhythmias, the R-on-T phenomenon is the fifth, most threatening class.
The treatment of torsades de pointes aims to restore a normal rhythm and to prevent the arrhythmia from recurring. While torsades may spontaneously revert to a normalsinus rhythm, sustained torsades requires emergency treatment to preventcardiac arrest.[23] The most effective treatment to terminate torsades is anelectrical cardioversion – a procedure in which an electrical current is applied across the heart to temporarily stop and then resynchronise the heart's cells.[23] Treatment to prevent recurrent torsades includes infusion ofmagnesium sulphate,[24] correction of electrolyte imbalances such as low blood potassium levels (hypokalaemia), and withdrawal of anymedications that prolong the QT interval. Treatments used to prevent torsades in specific circumstances includebeta blockers ormexiletine in long QT syndrome.[25] Occasionally apacemaker may be used to accelerate the heart's own sinus rhythm, and those at risk of further torsades may be offered animplantable defibrillator to automatically detect and defibrillate further episodes of the arrhythmia.[25]
Magnesium is used in the treatment of torsades de pointes because it functions as a physiologiccalcium channel blocker. By blocking the calcium channels in phase 2 of the myocardial action potential, magnesium suppresses theearly afterdepolarizations that occur in this phase with calcium influx into the cell.[26]
The phenomenon was originally described in a Frenchmedical journal byDessertenne in 1966, when he observed this cardiac rhythm disorder in an 80-year-old female patient with complete intermittentatrioventricular block. In coining the term, he referred his colleagues to the "Dictionnaire Le Robert", a bilingual French English dictionary, of which his wife had just given him a copy. Here, "torsade" is defined as:[citation needed]
The singular and plural forms (torsade de pointes,torsades de pointes) have often been used. The question of whether each one is grammatically "correct" and the others "incorrect" has repeatedly arisen. This is seen among major medical dictionaries, where one enters only the plural form, another enters the plural form as theheadword but lists the singular as a variant, and yet another enters the singular form as the headword and gives a usage comment saying that the plural is not preferred. One group of physicians has suggested that it would make the most sense to use the singular form to refer to the arrhythmia entity (where an arrhythmia may involve one or multiple episodes), and that one might best reserve the plural form for describing repeated twisting during a single episode.[27] Other authors have suggested all three words should be plural.[28] Regarding thenatural language variation, they concluded, in good nature, "Wasn't it the French who coined the termvive la difference?"[27]
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