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Junctional ectopic tachycardia

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Junctional ectopic tachycardia

Junctional ectopic tachycardia
Classification and external resources
MeSH D013613

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery.[1] It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node (AV node).[2][3] In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia.

Etymology

Junctional ectopic tachycardia derives its name from the problem it causes. "Junctional" is used as the abnormal tissue driving the ventricular rate is located close junction between the atria and ventricles, known as the AV node. Ectopic (from the Greek ektopos, meaning "out of place") refers to the fact that the ventricles are being triggered by tissue that is not the normal pacemaker tissue within the heart. Tachycardia (from the Greek takhys, meaning "swift", and kardia, meaning heart) means a swift heart rate.[4]

By this definition, junctional ectopic tachycardia is an abnormally swift heart rhythm due to cells firing within the heart near the AV node.

Pathophysiology

In normal individuals, electrical activity in the heart is initiated in the sinoatrial (SA) node (located in the right atrium), propagates to the atrioventricular (AV) node, and then through the bundle of His to the ventricles of the heart. (See electrical conduction system of the heart).

The AV node acts as a gatekeeper, limiting the electrical activity that reaches the ventricles of the heart. This function of the AV node is important, because if the signals generated in the atria of the heart were to increase in rate (as they do during atrial fibrillation or atrial flutter), the AV node will limit the electrical activity that conducts to the ventricles. For instance, if the atria are electrically activated at 300 beats per minute, half those electrical impulses are blocked by the AV node, so that the ventricles are activated at 150 beats per minute (giving a pulse of 150 beats per minute). Another important property of the AV node is that it slows down individual electrical impulses. This is manifest on the ECG as the PR interval, which is about less than 200 milliseconds, the time from activation of the atria (manifest as the P wave) and activation of the ventricles (manifest as the QRS complex).

Individuals with JET have a "short-circuit" in their heart, where the electricity bypasses the AV node, causing the heart to beat faster than normal. The cause of the arrhythmia, the ectopic focus, is usually near the AV node in the triangle of Koch (a rough triangle with points at the coronary sinus, the tendon of Todaro, and the tricuspid valve).[5]

Patients of heart surgery may experience an accelerated narrow complex tachycardia, usually within the first 24–48 hours (but occasionally longer) after surgery. There may be atrio-ventricular disassociation with more ventricular signals then atrial signals. The cause of JET is felt to be due to manipulation of the tissue surrounding the AV node during surgery, however debate exists regarding the exact cause, as it is seen after procedures even without significant manipulation of this area.

JET-like symptoms can also manifest congenitally and in the first six months of life. This syndrome, which may also referred to as His bundle tachycardia, is resistant to therapy and can be difficult to treat.[3][6]

Treatment

Treatment is aimed at slowing the rate by correcting acidosis, correcting electrolytes (especially magnesium and calcium), cooling the patient, and antiarrhythmic medications. Occasionally pacing of the atrium at a rate higher than the JET may allow improved cardiac function by allowing atrial and ventricular synchrony.

A 1994 study at the Adolph Basser Institute of Cardiology found that amiodarone, an antiarrhythmic agent, could be used safely and relatively effectively.[7]

JET occurring after the first six months of life is somewhat more variable, but may still be difficult to control. Treatment of non-post-operative JET is typically with antiarrhythmic medications or a cardiac catheterization with ablation (removal of affected tissue). A cardiac catheterization may be performed to isolate and ablate (burn or freeze) the source of the arrhythmia. This can be curative in the majority of cases. The use of radiofrequency energy is infrequently associated with damage to the normal conduction due to the close proximity to the AV node, the normal conduction tissue. The use of cryotherapy (cold energy) appears to be somewhat safer, and can also be effective for the treatment of JET.[8]

References

  1. ^ Sarubbi B, Vergara P, D'Alto M, Calabro R (2003). "Congenital junctional ectopic tachycardia: presentation and outcome". Indian Pacing Electrophysiol J 3 (3): 143–7.  
  2. ^ "Supraventricular Tachycardia, Junctional Ectopic Tachycardia: Overview - eMedicine". Retrieved 2008-12-21. 
  3. ^ a b Campbell, R. W. F.; Wren, C. (1987). "His bundle tachycardia- arrhythmogenic and antiarrhythmic effects of therapy". European Heart Journal 8 (6): 647–650.  
  4. ^ "Tachycardia". Online Etymology Dictionary. Retrieved 2011-08-29. 
  5. ^ Zhivadinovik J, Lazarova D, Gjorgov N (2006). "Dimensions of the Triangle of Koch". Bratisl Lek Listy 107 (4): 107–9. Retrieved 2013-01-31. 
  6. ^ Sarubbi B, Musto B, Ducceschi V, D’Onofrio A, Cavallaro C, Vecchione F, Musto C, Calabro R. (2002). "Congenital junctional ectopic tachycardia in children and adolescents: a 20 year experience based study". Heart. 
  7. ^ P Raja, R E Hawker, A Chaikitpinyo, S G Cooper, K C Lau, G R Nunn, T B Cartmill, and G F Sholler (September 1994). "Amiodarone management of junctional ectopic tachycardia after cardiac surgery in children". Heart 72 (3): 261–265.  
  8. ^ Law IH, Von Bergen NH, Gingerich JC, Saarel EV, Fischbach PS, Dick M 2nd (August 2006). "Transcatheter cryothermal ablation of junctional ectopic tachycardia in the normal heart". Heart Rhythm 3 (8). 
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