Torsade de pointes

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Classification according to ICD-10
I47.2 Ventricular tachycardia
ICD-10 online (WHO version 2019)

As torsades de pointes (TdP), torsades de pointes tachycardia, Spitzenumkehrtachykardie, Schraubentachykardie or short torsade tachycardia (z. T. as plural torsades ) is in the cardiology a special form of ventricular tachycardia called that by a wave- or helical (also referred to as spindle-shaped) image of the ventricular complexes in the electrocardiogram (EKG) and has heart rates above 150 bpm . Since it can turn into ventricular fibrillation , it is a potentially life-threatening cardiac arrhythmia .

history

Torsade tachycardia was first identified in 1932 by Schwartz et al. have been described. The first ECG recording of a drug-induced torsade tachycardia was published in 1964 by the American cardiologists Arthur Selzer and H. Wesley Wray.

In 1966, the French cardiologist François Dessertenne coined the term Torsade de pointes, which is used today . The French term describes the helical winding of the ECG curve around the isoelectric line .

Emergence

Telemetric recording of a torsade tachycardia. The blue line illustrates the characteristic helical winding around the isoelectric line.

Favoring factors

Pathomechanism of drugs that prolong the QT time

The main target of these drugs is usually the hERG potassium channel , which due to its size and structure (large pore) is very susceptible to various substances but also to large molecules. By blocking the channel, the repolarization of the heart muscle cell is delayed and the plateau phase is lengthened and the action potential is lengthened . In addition, there is an intracellular accumulation of calcium ions (due to a delayed inactivation or reactivation of cardiac calcium channels ), which favors early after depolarizations (EADs). These can appear as pathological U-waves in the ECG.

The delayed repolarization can, in addition to the occurrence of the above. EADs also encourage excessive spatial spreading (dispersion) of repolarization. Both mechanisms thus contribute to the development of torsade tachycardia.

Not all drugs that increase QT time cause torsade tachycardia. A facility in Arizona maintains a detailed English-language database (see web links ).

trigger

The trigger of tachycardia with pre-existing beneficial factors is usually an extrasystole falling into the vulnerable phase (which of course becomes all the more likely with a prolonged vulnerable phase).

clinic

  • dizziness
  • Syncope
  • nausea

therapy

Torsade tachycardias often end on their own after a short time, but can recur. Cardioversion should be performed if the torsade tachycardia persists . To stabilize the membrane, magnesium and potassium are administered up to highly normal levels.

In drug-induced torsade tachycardia, the identification and discontinuation of the triggering drug are of crucial importance. In the acute situation, the increase in heart rate can e.g. B. prevent renewed tachycardias with orciprenaline or a temporary pacemaker .

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

literature

  • Gerd Herold: Internal Medicine. Self-published, Cologne 2007, ISBN 978-3-89019-704-3 .
  • P. Schweikert-Wehner: Antidepressants, beware of arrhythmias . In: Pharmazeutische Zeitung , Volume 159, Issue 44, pp. 22–24, Eschborn, 2014

Web links

Individual evidence

  1. ^ NS Moise: As Americans, we should get this right. In: Circulation , 1999, 100, p. 1462. PMID 10500317
  2. ^ SP Schwartz, A. Jetzer: Transient ventricular fibrillation. The clinical and electrocardiographic manifestations of the syncopal seizures in a patient with auriculoventricular dissociation. In: Arch Intern Med . , 1932, 50, pp. 450-469.
  3. ^ SP Schwartz, J. Orloff, C. Fox: Transient ventricular fibrillation: I. The prefibrillatory period during established auriculoventricular dissociation with a note on the phonocardiograms obtained at such time. In: Am Heart J . 1949; 37, pp. 21-35. PMID 18104378
  4. ^ A. Selzer, HW Wray: Quinidine Syncope. Paroxysmal Ventricular Fibrillation Occurring during Treatment of Chronic Atrial Arrhythmias. (PDF; 2.3 MB). In: Circulation , 1964, 30, pp. 17-26. PMID 14197832
  5. ^ F. Dessertenne: La tachycardie ventriculaire a deux foyers opposes variables. In: Arch Mal Coeur Vaiss. , 1966, 59, pp. 263-272. PMID 4956181
  6. F. Dessertenne, A. Fabiato, P. Coumel: Un nouveau chapitre d'electrocardiographie: les variations de l'progressive amplitude de l'electrocardiogram programs. In: Actual Cardiol Angeiol Int (Paris) , 1966, 15, pp. 241-258. PMID 5985594
  7. ^ P. Schweikert-Wehner: Antidepressants: Beware of arrhythmias . Ed .: Pharmaceutical newspaper. tape 159 , no. 44 . Govi Verlag, Eschborn October 30, 2014, p. 22, 24 .
  8. Johannes-Martin Hahn: Checklist internal medicine . Thieme, 2013, ISBN 978-3-13-152287-0 ( google.com [accessed May 31, 2016]).
  9. C. Antzelevitch: Role of transmural dispersion of repolarization in the genesis of drug-induced torsades de pointes. In: Heart Rhythm , 2005, 2 (2 Suppl), pp. S9-S15. PMID 16253930