Atrioventricular Nodal Reentrant Tachycardia
AV nodal reentrant tachycardia is the most common type of reentrant paroxysmal SVT, occurring in about 60% of patients with SVT. Symptoms may emerge at any age but are rare in early childhood and most commonly appear in the late teens or early twenties. More women than men are affected for unknown reasons. Patients with AV nodal reentrant tachycardia have no greater incidence of heart disease than the general population.
The AV nodal reentrant circuit involves the AV node and tissue in close proximity to it. Dual conduction pathways within the AV node allow electrical impulses to recycle within the AV nodal region at rate of 150-250 beats per minute after a premature beat encounters one of the pathways during its refractory period. The impulse travels down one pathway to the point where the pathways converge again. If the second pathway has recovered its ability to conduct, the impulse travels back up the second pathway to where the pathways converge "upstream". The impulse then travels down the first pathway again and the cycle repeats
Therapy of AVNRT can be curative or palliative. Because the reentry involves mainly the AV node, AV nodal drugs as well as maneuvers that increase vagal tone can be effective in terminating the arrhythmia. Prevention of this tachycardia with drugs may be more difficult. For patients who are unresponsive or intolerant to medications or who are interested in curative therapy, transcatheter ablation is the preferred treatment. This low risk technique has a very high cure rate and can be performed as an outpatient. During the procedure, one of the two pathways is eliminated so that the potential circuit no longer exists.
Atrioventricular Reentry Tachycardia
Atrioventricular reentry tachycardia (AVRT) results from the presence of two conducting pathways creating a reentry circuit very similar to AV nodal reentrant tachycardia (AVNRT). In AVNRT, the reentry circuit is contained entirely within the AV node and does not require the participation of either the atrium or the ventricle to sustain itself. Atrioventricular reentry tachycardia requires the participation of both atrium and ventricle and a piece of conducting tissue bridging the atrium and ventricles outside of the AV node. This extra piece of tissue is called an accessory pathway. The accessory pathway is an extra piece of conducting heart muscle with which the patient is born. It crosses through or around electrically insulating fibrous tissue that separates the atrial muscle from the ventricular muscle. In atrioventricular reentry tachycardia, the two pathways of the reentry circuit can be composed of one accessory pathway and the AV node or it can be made up of two accessory pathways without the participation of the AV node.
The accessory pathways can conduct either from the atrium to the ventricle (antegrade conduction) or from the ventricle to the atrium (retrograde conduction) or in both directions. The ventricles of patients with antegrade conduction down an accessory pathway are receiving electrical stimulation from both the AV nodal pathway and the accessory pathway. The signal going from the atrium down the accessory pathways often reaches the ventricles before the signal going down the AV node. This results in pre-excitation of the ventricles and can be observed on the ECG trace. The feature seen as an extra bump on the QRS complex is called the delta wave. Patients having a delta wave are said to have a Wolfe-Parkinson-White abnormality (WPW). If patients with a delta wave on the resting ECG develop atrioventricular reentry tachycardia, they are said to have Wolfe-Parkinson-White Syndrome. Patients with atrioventricular tachycardia due to a pathway that only conducts retrograde are said to have a concealed pathway, concealed in the sense that there is no evidence of it on resting ECG. When these patients develop AVRT, they technically are not referred to as having WPW. The presence of the accessory pathways or delta wave does not mean that the patient will have a reentry tachycardia. Certainly not all patients having such delta wave ever have any tachycardia or symptoms of tachycardia.
The prevalence of the WPW abnormality (having a delta wave on the ECG) is estimated to be 0.1-0.3 percent of the general population with males affected twice as often as females. Although the anomaly is thought to be present at birth it often appears sporadically and is only occasionally transmitted genetically. Most persons remain free of symptoms and are incidentally found to have this abnormality. Some individuals with WPW (30-40%) receive medical attention because of associated structural heart disease such as atrial septal defect, mitral valve prolapse, hypertrophic cardiomyopathy, Ebstein's anomaly, or transposition of great the great vessels. Children with WPW treated as infants have an increased risk of recurrence of SVT at 5 to 10 years of age. In general, symptomatic tachycardia does not appear until adolescence or adulthood.
The accessory pathways that conduct antegrade can conduct from the atrium to the ventricle much faster than possible through the AV node. This is a problem when patients have a tachycardia where the atrium may have very rapid rates such as 200 to 300 beats a minute. Normally the AV node would only allow possible 175 to 300 beats a minute to pass to the ventricle. The accessory pathways may transmit all 300 beats a minute, which can result in very low blood pressure and even death. Fortunately this is a rare event. The classic clinical situation is where the patient develops atrial fibrillation and the signals from the atrium go down the accessory pathway at 300 or more beats a minutes. The patients may collapse and may even have a full cardiac arrest.
The severity of the patient's symptoms determines the therapy. Patients with AVRT tachycardia usually complain of a "racing heart," palpitations, shortness of breath, weakness, light-headedness, or syncope with the tachycardia episodes. Reassurance alone may be reasonable for the patient with brief or infrequent attacks of tachycardia that are well tolerated or can be readily self-terminated by vagal maneuvers. As with other forms of SVT, management options include palliative and curative therapies. Palliative therapy includes drug therapy to terminate the tachycardia and/or prevent recurrences and chemical or electrical cardioversion to terminate tachycardia when it occurs. Because multiple cell types with disparate responsiveness to drugs contribute to the macro-reentrant circuit of AVRT, pharmacological interventions are complex and best prescribed by a cardiac electrophysiologist. Curative therapy involves catheter ablation of the bypass tract(s) and has become routine therapy and probably the therapy of first choice for most patients with accessory pathways. Electrophysiologists can, in most cases, localize the bypass tract(s) and destroy them by RF ablation. The use of EP studies for WPW (having a delta wave on ECG ) in patients with no symptoms or history of tachycardia is not currently recommended. Sudden cardiac death from rapid antegrade conduction is a rare especially as a first presentation of the AVRT. The life style or occupation of an individual with no symptoms may warrant the low risk EP study to determine the possibility of troublesome tachycardia.
Junctional (AV Nodal) Tachycardias
The junction tachycardias are rare but still seen occasionally among patients with SVT. Their actual incidence and prevalence are unknown. Two forms of junctional tachycardia are recognized, and each has a different mechanism.
The permanent form of junctional reentrant tachycardia (PJRT) is a reentrant tachycardia in which an accessory pathway lies very close to the AV node. The tachycardia is slower than AV nodal reentrant tachycardia and is often an incessant. This tachycardia has been associated with the development of a reversible cardiomyopathy that resolves when the tachycardia is successfully terminated. PJRT is usually treated by interruption of the tachycardia circuit by RF ablation.
Automatic junctional tachycardia is, as the name suggests, an automatic tachycardia of the AV node. It may be caused by drug toxicity or it may be idiopathic. It is usually controlled with antiarrhythmic drugs.