Torsades de pointes

As torsade de pointes ( TdP ), torsade de pointes tachycardia, Spitzenumkehrtachykardie, Schraubentachykardie or short torsade tachycardia (partly also as a plural " torsades " ) is in cardiology a special type of ventricular tachycardia called that by a wave or helical ( also called a spindle- shaped) image of the ventricular complexes is characterized in the electrocardiogram (ECG) and heart rates above 150 bpm has. Since they can go into ventricular fibrillation, is a potentially life-threatening cardiac arrhythmia.

History

The torsade tachycardia could for the first time in 1932 by Schwartz et al. have been described. The first ECG recording a caused by a drug torsade tachycardia was published in 1964 by the US-based cardiologist Arthur Selzer and H. Wesley Wray.

1966 coined the French cardiologist François Dessertenne the term used today torsades de pointes. The French term describes the helical winding of the ECG curve around the isoelectric line.

Formation

Enabling factors

  • Prolonged QT interval by: Drugs (especially class III antiarrhythmics such as amiodarone or sotalol)
  • Congenital long QT syndrome
  • Bradycardia ( physiologically long QT interval at slow heart beat)
  • Electrolyte disturbances ( hypomagnesemia or hypokalemia, so too little magnesium or potassium in the blood)
  • Heart failure
  • Cardiac hypertrophy (thickening of the heart wall )

Pathomechanism of the QT interval prolonging drugs

Hauptangriffsort these drugs is usually the hERG potassium channel, but due to its size and structure (large pore) very susceptible to various substances even for large molecules. By blocking the channel, the repolarization of the heart muscle cell is delayed and there is a prolongation of the plateau phase and thus in a prolongation of the action potential. In addition, there is an intracellular accumulation of calcium ions ( by a delayed inactivation or reactivation of cardiac calcium channels), which promotes early afterdepolarizations ( "early after depolarization " = EADs ). This can emerge as pathological U waves in the ECG.

The delay in repolarization can also excessive, spatial spread (dispersion) favor of repolarization in addition to the emergence of the above-mentioned EADs. Both mechanisms thus contribute to the emergence of a torsade tachycardia.

Not all drugs that prolong the QT interval, also cause torsade tachycardia. A facility in Arizona to maintain a detailed English-language database (see links).

Trigger

Cause of the tachycardia in pre-existing contributing factors is usually a falling into the vulnerable phase extrasystole (which is more likely with prolonged vulnerable phase of course).

Clinic

  • Dizziness
  • Syncope
  • Nausea

Therapy

Torsade tachycardia often end after a short time by itself, but may recur. In a sustained tachycardia torsade cardioversion should be performed. For membrane stabilization, administration of magnesium and potassium takes place up to high normal values.

In drug -induced torsade tachycardia are the identification and discontinuation of the triggering drug is crucial. In the acute situation may prevent re tachycardia, the increase in heart rate, for example by orciprenaline or by a transient pacemaker.

In the congenital long QT syndrome, in contrast, reduces a lowering of heart rate with beta blockers (without ISA) and oral administration of magnesium, the incidence of torsade de pointes. If this is not sufficient, the implantation of a cardioverter - defibrillator (ICD) is shown.

France Premature ventricular contraction Active ingredient Circulation (journal)
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