Preexcitation, Atrioventricular Reentry, and Variants

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Preexcitation, Atrioventricular Reentry, and Variants





Definitions


Atrioventricular (AV) reentry is the second most common cause of paroxysmal supraventricular tachycardia (PSVT) among patients referred for catheter ablation. In most cases of AV reentrant tachycardia (AVRT), the reentrant circuit involves the AV node and the accessory pathway (AP) for anterograde and retrograde conduction, respectively. The electrocardiogram (ECG) typically shows a regular, narrow complex rhythm referred to as orthodromic reciprocating tachycardia (ORT). Less commonly, a wide-complex rhythm may be observed when anterograde conduction occurs over the AP and retrograde conduction over the AV node or another AP, referred to as antidromic reciprocating tachycardia (ART).


If the AP is capable of anterograde conduction, the baseline ECG demonstrates a short PR interval and a slurred upstroke of the QRS complex referred to as a delta wave, hallmarks of ventricular preexcitation. The AP thus is considered to be manifest (Figure 76-1). In approximately 50% of patients with AVRT, the accessory pathway is capable of only retrograde conduction. The ECG during sinus rhythm in these patients shows a normal QRS complex, and therefore the accessory connection is considered to be concealed. Patients with evidence of preexcitation on the resting ECG and symptomatic tachycardia are said to have the Wolff-Parkinson-White (WPW) syndrome. An asymptomatic patient who incidentally is found to have preexcitation on the ECG is said to have a WPW “pattern.”




Accessory Pathways


Accessory pathways are anomalous bypass tracts that are typically composed of working myocardial cells. Most APs insert along the mitral or tricuspid valve and are referred to as AV accessory pathways. Approximately 60% of APs insert along the mitral valve and are referred to as left free-wall pathways. About one-fourth insert along the septal aspect of the tricuspid or mitral valve and are classified as septal pathways. The remaining 15% are right free-wall pathways.


Occasionally one may encounter APs that do not insert along the AV valves. Examples include atriofascicular, nodoventricular, nodofascicular, and atrionodal pathways. Atriofascicular pathways connect the right atrium to the distal ramifications of the right bundle branch and are capable of only anterograde conduction. Nodoventricular and nodofascicular pathways connect the AV node to the right ventricular myocardium and the specialized conduction system, respectively. Atriofascicular and nodoventricular/nodofascicular connections are also notable for their decremental conduction properties. Atrionodal pathways are rare and connect the right atrial myocardium to the AV node. The fact that these unusual pathways do not insert along the AV annulus calls for a mapping approach that is different from that of typical AV pathways.



Presentation and Evaluation


The presentation of patients with AVRT is clinically indistinguishable from that of patients with other mechanisms of PSVT. Symptoms commonly include rapid palpitations, chest discomfort, dizziness/light-headedness, dyspnea, weakness, neck pulsations, and presyncope. Syncope is an uncommon symptom of AVRT. Occasionally, patients with AVRT develop atrial fibrillation (AF), which may lead to hemodynamic deterioration as the result of rapid anterograde conduction over the accessory pathway (Figure 76-2). This may cause syncope, cardiac arrest, or sudden death.



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Figure 76-2 Preexcited Atrial Fibrillation (AF)
This ECG was recorded from the same patient as in Figure 76-1. He presented to the hospital with palpitations and near-syncope. Note the wide-complex QRS morphology, which is very similar to that during sinus rhythm (Figure 76-1). The QRS morphology is not uniform (asterisks), reflecting a varying degree of fusion of ventricular activation over the AP and the specialized conduction system. The ventricular rate is irregular and at times is as short as 200 ms. The AP was successfully ablated at the lateral mitral annulus. Paper speed = 25 mm/s.


Although AVRT may occur at any age, it is usually seen in young patients without evidence of structural heart disease. Therefore, patients typically do not require an extensive cardiac evaluation. Nonetheless, frequent or incessant episodes of AVRT, such as may occur with permanent junctional reciprocating tachycardia (PJRT, see later), may be associated with tachycardia-related cardiomyopathy. Rarely, AVRT may be associated with other cardiac conditions such as hypertrophic cardiomyopathy or Ebstein’s anomaly. The physical examination and the resting ECG are helpful in screening for these unusual associations. Although the ECG during AVRT (or other causes of supraventricular tachycardia [SVT]) may reveal ST-segment depression, such changes usually are tachycardia related and are not indicative of myocardial ischemia. Thus, barring symptoms consistent with angina, coronary angiography usually is not required. As compared with patients with atrioventricular nodal reentrant (AVNRT) or atrial tachycardia, patients with AVRT are more likely to be male and to develop symptoms at a younger age.



Management


The acute treatment of supraventricular tachycardia in the emergency room is straightforward. Patients without hemodynamic instability can be treated with intravenous adenosine, a highly effective agent with an extremely short half-life. Although the risks of adenosine and other AV nodal blocking agents in patients with preexcited atrial fibrillation are well known, some caution should be exercised in patients with narrow QRS complex tachycardia as well. Adenosine may induce atrial fibrillation in about 10% of patients undergoing electrophysiological evaluation for SVT. If a patient presenting to the emergency room with a narrow QRS complex tachycardia also has manifest preexcitation during sinus rhythm, adenosine administration may result in AF with a very rapid ventricular response and hemodynamic deterioration. Therefore, when adenosine is administered in this situation, emergency resuscitation equipment and appropriately trained personnel should be available. Patients presenting with a narrow QRS complex tachycardia who have a history of asthma should not receive adenosine and can be treated with intravenous calcium blockers. Patients with preexcited atrial fibrillation who are hemodynamically stable may be treated with intravenous procainamide or ibutilide. Patients who present with hemodynamic instability should undergo urgent direct current cardioversion.


Long-term treatment of patients with SVT should be individualized. In a patient with a first episode or infrequent, well-tolerated episodes of tachycardia and no evidence of preexcitation on the ECG, abortive maneuvers and reassurance are reasonable options. Alternatively, these patients may be offered a “pill-in-the-pocket” approach, which involves self-administration of oral AV nodal agents at the onset of symptoms. If the patient prefers, an electrophysiological procedure may be a reasonable option. Patients with recurrent SVT should be considered for an electrophysiological evaluation and catheter ablation.


Supraventricular tachycardia in association with ventricular preexcitation is considered a class I indication for electrophysiological evaluation and catheter ablation.1 Catheter ablation is highly effective in eliminating AP conduction, thereby eliminating symptoms caused by SVT and the small risk of sudden death associated with the WPW syndrome. Patients with WPW syndrome in whom ablation would be likely to result in high-grade AV block should be treated with a combination of rhythm- and rate-controlling medications.


One study found that after a first episode of tachycardia in patients with WPW syndrome, a large proportion of patients remained asymptomatic over the next several years.2 The risk of adverse events during follow-up was very low. Investigators identified high-risk features including a short AP effective refractory period, inducible AVRT triggering preexcited AF, and the presence of multiple accessory pathways. The low event rate after a first episode of AVRT suggests that long-term pharmacologic treatment may not be needed until the tachycardia becomes recurrent.


Most asymptomatic patients in whom the ECG incidentally shows evidence of preexcitation do not require an electrophysiological evaluation because their risk of sudden death is very low.1,3 However, data suggest that catheter ablation in this group reduces the risk of arrhythmic events.4 The decision to perform catheter ablation in asymptomatic patients with “high-risk” occupations, for example, pilots and bus drivers, should be individualized.



ECG Characterization


In patients referred for an electrophysiological evaluation for PSVT, the ECG during sinus rhythm and during tachycardia may be helpful in identifying the mechanism of the tachycardia. Evidence of preexcitation during sinus rhythm in a patient with a history of tachycardia makes AVRT very likely. The degree of preexcitation may be subtle, especially in patients with a left free wall or with slowly conducting APs. In the former, it is helpful to analyze the QRS morphology in the lateral precordial leads. In patients with subtle preexcitation due to a left free-wall AP, a “septal” Q wave is not inscribed in the lateral precordial leads (Figure 76-3). The left-sided location of the pathway allows ventricular activation to proceed over the AV node more than would be possible with right-sided pathways. Right-sided APs are associated with a greater degree of preexcitation. In patients with an equivocal ECG, administration of adenosine is helpful in unmasking preexcitation.



In most patients with ORT, the ECG shows a regular, narrow QRS complex tachycardia. The timing of the P wave with respect to the QRS is a useful clue. During ORT, atrial activation can occur only after ventricular activation, and therefore the P wave is inscribed shortly after the QRS complex, frequently within the ST segment. This feature is suggestive but not diagnostic of ORT as it may be seen with AVNRT or atrial tachycardia. During typical (“slow-fast”) AVNRT, the atrium and the ventricle are activated nearly simultaneously. The P wave is inscribed within or at the end of the QRS complex, resulting in a pseudo R′ in lead V1 and a pseudo S wave in lead II. These features help to rule out ORT as the mechanism.


In patients with PJRT, the accessory pathway is usually located in the posteroseptal region and has a long conduction time. As a result, the ECG shows a long RP tachycardia, with inverted P waves in the inferior leads. PJRT can be incessant and can result in a tachycardia-induced cardiomyopathy that generally resolves after accessory pathway ablation.


The mode of tachycardia initiation and termination is also helpful. If tachycardia is initiated with anterograde conduction block in the AP, the mechanism is very likely to be ORT. If the tachycardia persists despite AV block, ORT is ruled out because the ventricle is an obligatory component of the reentrant circuit. If the tachycardia reliably terminates with AV block, atrial tachycardia is unlikely.


Beat-to-beat alternation of the QRS amplitude is more common in ORT than in AVNRT and atrial tachycardia. However, QRS alternans is not specific for ORT and probably is related to the higher heart rate during ORT. Although the ECG is a helpful guide, it often does not provide unambiguous diagnostic features. In fact, approximately 20% of tachycardias are misclassified when the diagnosis is based only on the ECG.

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Jun 5, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Preexcitation, Atrioventricular Reentry, and Variants

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