Atrioventricular Nodal Reentrant Tachycardia, Atrioventricular Reciprocating Tachycardia, Wolff–Parkinson–White Syndrome, and Junctional Rhythms


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Atrioventricular Nodal Reentrant Tachycardia, Atrioventricular Reciprocating Tachycardia, Wolff–Parkinson–White Syndrome, and Junctional Rhythms


I. Inappropriate Sinus tachycardia (IST) and postural orthostatic tachycardia syndrome (POTS)


Sinus tachycardia is generally not a primary rhythm abnormality. It is secondary to cardiac, pulmonary, septic, or metabolic issues and is often an ominous sign (e.g., HF, large MI, shock, sepsis, acute bleed, anemia, hypoxia).


IST– Inappropriate sinus tachycardia is a non-paroxysmal sinus tachycardia that is present most of the day, at rest and/or mild physical effort, out of proportion to any physiologic need. The resting sinus rate is >100 bpm and the mean 24-hour sinus rate on Holter is  > 90 bpm. IST is due to a dysautonomia that activates the sinus node’s If current and is mainly seen in young women (<50 years of age). IST is associated with symptoms of palpitations, fatigue, and dizziness, that may be improved with drugs blocking the sinus node. In fact, the use of an If current blocker, i.e., a sinus node blocker (ivabradine), eliminated > 70% of IST symptoms in one study (class IIa recommendation in ACC guidelines). β-blockers may also be effective, but may not be well tolerated in dysautonomic patients (class IIb). Sinus node ablation is only temporarily effective, as tachycardia may arise from other sinus sites after ablation, the main issue being autonomic dysfunction.


POTS-POTS is an orthostatic intolerance defined by an increase in sinus rate ≥ 30 bpm within 10 min of standing, without orthostatic hypotension or syncope. The supine heart rate is generally normal, in contradistinction with IST, where the supine heart rate is elevated and only mildly rises upon standing; yet both conditions may coexist. POTS is a form of cardiovascular deconditioning that starts after a period of bedrest (e.g., surgery, acute illness or viral illness) and may have a somewhat acute onset, sometimes in hospitalized patients. This deconditioning leads to reduced stroke volume, reduced renin-angiotensin activation (low blood volume), and peripheral autonomic denervation with lack of vasoconstriction. As such, sinus tachycardia is often useful in POTS because it maintains BP and compensates for the low stroke volume and vascular tone. Thus, β-blocker therapy worsens POTS symptoms, and POTS needs to be ruled out before using β-blockers in IST. Only one form of POTS, hyperadrenergic POTS, may benefit from a small propranolol dose.


II. Atrioventricular nodal reentrant tachycardia (AVNRT)


A. Mechanism (see Figure 12.1)


In AVNRT, the AV node has two pathways: fast pathway and slow pathway. Approximately 20% of normal individuals have dual AV node pathways, but most of them do not manifest AVNRT.


Normally, the AV node conducts impulses through the fast pathway.


The fast pathway conducts faster but has a longer refractory period than the slow pathway. After a PAC, the fast pathway may still be in its refractory period, whereas the slow pathway, having the short refractory period, has already recovered and conducts forward. The impulse then conducts retrogradely through the fast pathway if it has recovered; this leads to a typical “slow-then-fast” (“SF”) AVNRT. If the fast pathway has not recovered its refractory period, the impulse will lead to one QRS having a longer PR interval; arrhythmia is not initiated.


Other, less common forms of AVNRT are the fast-then-slow AVNRT, and the slow-then-slow AVNRT. In the fast-then-slow AVNRT, the slow pathway has a longer refractory period than the fast pathway.


AVNRT usually occurs in patients without underlying heart disease.

Schematic illustration of AVNRT usually starts with a PAC that has a long PR interval as it goes through the slow pathway.

Figure 12.1 AVNRT usually starts with a PAC that has a long PR interval as it goes through the slow pathway. The slow pathway is slower but has a shorter refractory period than the fast pathway, allowing conduction of the PAC. If, at the time the impulse reaches the distal slow pathway, the fast pathway is still in its refractory period, the reentrant circuit of AVNRT will not launch. A few subsequent sinus P waves may keep conducting over the slow pathway (Figure 12.5).


If, at the time the impulse reaches the distal slow pathway, the fast pathway has recovered, AVNRT will be initiated. The R–R interval can shorten over the course of the first few beats; it may lengthen during the last few beats before termination with AV nodal blocking agents.


B. ECG


AVNRT typically manifests as a regular, narrow QRS complex tachycardia, with a ventricular rate of ~150–250 bpm (most often ~180 bpm).


P waves are retrograde and are usually hidden inside the QRS or at the terminal portion of the QRS (Figure 12.2). These P waves manifest as terminal r’ in V1 and pseudo-S in the inferior leads, with a short RP (often < 90 ms). P waves are often simultaneous to the QRS and therefore are clearly visible in only ~1/2 of the cases (Figures 12.2, 12.3). Rarely, P waves may precede QRS, with a short PR interval < 110 ms (Figure 12.4). If P waves cannot be identified in patients presenting with a regular narrow complex tachycardia, AVNRT is the most likely diagnosis.


The tachycardia being initiated by an ectopic atrial beat that goes down the slow pathway, the PR interval of this initial beat is longer than the sinus PR interval. As opposed to automatic atrial tachycardia, this initial ectopic P wave usually differs from the subsequent (retrograde) P waves and does not march out with them.


The atypical forms of AVNRT (fast–slow or slow–slow AVNRT) have a long RP interval, longer than 1/2 RR interval, and may thus simulate atrial tachycardia. The loop is overall slower than in typical AVNRT; thus, the atypical forms tend to be incessant tachycardias.


Occasionally, dual AV nodal pathways manifest on the baseline sinus rhythm. In this case, two different PR intervals are seen in sinus rhythm (Figure 12.5).


C. Treatment


1. Acute therapy


  • Adenosine 6 mg IV (followed by 12 mg IV if the 6 mg dose is ineffective). Adenosine breaks AVNRT and AVRT by blocking the AV node. AVNRT and AVRT are the main arrhythmias that break rather than simply slow down with adenosine; atrial tachycardia can sometimes break with adenosine.
  • Diltiazem IV or β-blocker IV is also effective.

2. Long-term treatment is required in case of frequent recurrences of sustained episodes

There are two options:



  • Chronic β-blockers or CCBs. When AVNRT is infrequent, one dose of these drugs may be used intermittently upon each recurrence (e.g., rapid-release diltiazem 120 mg) (pill-in-the pocket strategy).
  • Radiofrequency ablation of the AV node’s slow pathway is a second-line therapy after failure of drug therapy. It is a first- line therapy in poorly tolerated AVNRT, recurrent AVNRT, or even one or infrequent episodes of well-tolerated AVNRT if the patient wishes complete control of the arrhythmia (class I recommendation).
Image described by caption.

Figure 12.2 (a) Arrows point to the retrograde P wave that is superimposed on the ST segment, appearing as a notch on the ST segment. (b) An ECG of the same patient in sinus rhythm after adenosine therapy: note the difference in V1–V2 and in the inferior leads (no “pseudo-r’” or “pseudo S”).

Schematic illustration of narrow complex tachycardia with retrograde P waves (arrows) seen in leads III and V1.

Figure 12.3 Narrow complex tachycardia with retrograde P waves (arrows) seen in leads III and V1. RP is short, < 1/2 RR interval; hence, atrial tachycardia is unlikely. In AVNRT, P wave typically falls within or immediately after QRS (RP interval < 90 ms), giving a pseudo-S shape in the inferior leads and pseudo-r’ shape in V1. In this case, P wave falls a bit further away and RP is > 90 ms; thus, the arrhythmia could be either AVNRT or AVRT.

Schematic illustration of p waves.

Figure 12.4 P waves are seen just before the QRS, with a PR interval < 110 ms. In a narrow complex tachycardia, this suggests AVNRT, although it is only seen in 4% of AVNRTs.

Schematic illustration of sinus rhythm is present throughout the tracing.

Figure 12.5 Sinus rhythm is present throughout the tracing. Vertical lines indicate P waves. Initially, the PR interval is normal (0.20 s), but after a couplet of PVCs (4th and 5th QRS complexes), the PR interval lengthens markedly. The AV conduction shifts from the fast pathway to the slow pathway. With the 7th sinus P wave after the couplet, the PR returns to normal. Reproduced with permission from Glancy DL, Hanna EB, Jain N. Long P-R intervals following certain ventricular premature complexes. J La State Med Soc 2010; 162: 185–6.

Schematic illustration of anatomy of the slow pathway, fast pathway, and compact AV node.

Figure 12.6 Anatomy of the slow pathway, fast pathway, and compact AV node. Note their potential relationship with a His catheter and coronary sinus catheter. The Koch triangle, where the slow pathway lies, is bordered by the His, the coronary sinus, and the tricuspid annulus. The crista terminalis is behind the Koch triangle. A slow potential recorded across the slow pathway is shown. CS, coronary sinus.


Anatomically, the slow pathway is located inferiorly, along the tricuspid annulus in front of the coronary sinus os, whereas the fast pathway is located superior to the coronary sinus os. They both coalesce more distally to form the compact AV node then His, which is located anteriorly (Figure 12.6). The slow pathway is located anatomically using a His catheter and coronary sinus catheter, and electrically by searching for an area where both A and V deflections are recorded, along with a slow potential in between, not a His potential.


D. Termination


Spontaneous termination may occur if a PAC occurs at a time when it can enter the slow-pathway arm of the reentrant circuit without fully penetrating it. This PAC gets blocked and stops the reentry (Figure 12.7). Spontaneous termination may also occur when the vagal tone blocks the slow pathway.


Vagal tone and AV nodal blocking agents block the slow pathway, usually in a Wenckebach pattern. They terminate the AVNRT after a few cycles, when an impulse that has conducted retrogradely fails to reenter the slow pathway (Wenckebach block). The tachycardia ends with a P wave.


In AVNRT, the atria and ventricles are not required for AV nodal reentry. Thus, if a PAC, a PVC, or atrial or ventricular pacing does not penetrate the AV nodal reentry, AVNRT will not be disrupted. On ECG, AVNRT appears to resume at the same rate after the PAC or PVC; in fact, the reentry circuit has not been affected at any time by this premature beat.


III. Atrioventricular reciprocating tachycardia (AVRT) and Wolff–Parkinson–White (WPW) syndrome


A. Pathophysiology


AVRT and WPW syndrome are characterized by an accessory pathway (AP), also called bypass tract, that connects one atrium to one ventricle.



  1. Approximately 30–60% of diagnosed APs are concealed pathways, meaning they can only conduct retrogradely from the ventricle to the atrium. A concealed AP is silent when the patient is in sinus rhythm and only manifests itself during a tachycardia that involves its retrograde conduction (orthodromic AVRT).
  2. The remaining APs are manifest pathways, meaning that they conduct from the atrium to the ventricle on a regular basis, bypassing the slower AV nodal conduction. The manifest AP conducts faster than the AV node. The normal sinus impulse conducts through both the AV node and the AP. The relative contributions of the AP and the AV node depend on the conduction speed across the AP vs. AV node and how far left/laterally the AP originates. The conduction over the pathway leads to a delta wave and PR shortening, more evident when relatively more ventricle is stimulated through the AP.

    This pathway conducts from the atrium to the ventricle and can conduct from the ventricle to the atrium. There are four possible AP locations: (1) left lateral, free wall (the most common, ~50% of APs); (2) right free wall (10–20%); (3) posteroseptal (20–30%); (4) anteroseptal (least common, ~5%). Approximately 5–10% of patients have multiple APs.


    This AP “pre-excites” the ventricles and the phenomenon is called pre-excitation. WPW pattern is used to describe the baseline pre-excitation, while WPW syndrome is used when arrhythmias occur as a result of the manifest AP. WPW pattern is seen in ~0.2% of the population. It has a higher prevalence in Ebstein’s anomaly and HOCM.


B. Baseline ECG is not affected by a concealed accessory pathway


C. Baseline ECG is affected by a manifest accessory pathway (pre-excitation or WPW pattern) (see Figures 12.8, 12.9, 12.10)



  1. The baseline ECG is characterized by:
    Schematic illustration of an appropriately timed PAC conducts down the slow pathway but cannot go deep enough as the distal parts of this pathway (1) or the fast pathway (2) are in the refractory period.

    Figure 12.7 An appropriately timed PAC conducts down the slow pathway but cannot go deep enough as the distal parts of this pathway (1) or the fast pathway (2) are in the refractory period. Eventually, the reentrant cycle is broken and the next P wave is a sinus P wave. Depending on where the block occurs:



    • There is no conduction to the ventricles or the atria (block 1), the tachycardia ends with the premature P wave.
    • There is conduction downstream to the ventricle but no retrograde conduction to the atria (block 2); the tachycardia ends with a QRS.

    A PAC may not penetrate the reentrant circuit at all if the whole slow and fast pathways are in the refractory period; in this case, the PAC does not affect the AVNRT, which continues unaffected. The tachycardia also ends with a P wave when the spontaneous vagal tone or AV nodal agents interrupt the tachycardia (they block the slow pathway).

    Schematic illustration of electrocardiographic features of pre-excitation.

    Figure 12.8 Electrocardiographic features of pre-excitation. Arrows point to the positive and negative delta waves.



    • Short PR interval (< 120 ms). The pre-excited PR is shorter than the AV nodal conduction but may not be short in the absolute sense.
    • Delta wave, which corresponds to the early onset of ventricular activation through the AP. Delta wave is a slur on the initial portion of QRS, usually riding the P wave. This slur may be negative, mimicking a Q wave.
    • Wide QRS > 120 ms, with secondary ST–T abnormalities (directed opposite to QRS). As opposed to RBBB and LBBB, QRS is slurred and delayed in its initial rather than terminal portion. QRS may be narrower than 120 ms in up to half of pre-excitation cases, whenever the ventricular excitation spreading down the AP does not occur long enough before the excitation spreading down the AV node.

  2. The degree of pre-excitation depends on (Figure 12.9):

    • The relative amount of ventricular tissue stimulated through the AP versus the AV node, which depends on the relative conduction speed through the AP versus the AV node. PR may be normal and delta wave may be absent in patients who have a fast AV nodal conduction and a left lateral AP. In the latter case, it takes a long time for the atrial impulse to reach the atrial insertion of the AP, by which time a slick AV node would have stimulated most of the myocardium: an increasing amount of ventricular muscle is excited through the normal AV pathway and a decreasing amount is excited through the anomalous pathway, which results in a less pre-excited QRS complex.
    • The refractory period of the AP, which is longer than the refractory period of the AV node. An AP with a long refractory period is more likely to block at a relatively slow heart rate (e.g., 100 bpm).

  3. When antegrade AP conduction and delta wave only manifest intermittently, or when the ECG criteria of pre-excitation are not completely fulfilled (PR slightly > 120 ms, QRS 100–120 ms), pre-excitation and delta wave may be unveiled by:

    • Slowing the conduction over the AV node, which leads to proportionately larger amount of myocardium stimulated through the AP (adenosine, carotid sinus massage). This leads to a shorter PR interval and a wider delta wave. Since sinus bradycardia is many times associated with slowing of the AV nodal conduction (high vagal tone, drugs), delta wave is often more prominent during sinus bradycardia.
      Image described by caption.

      Figure 12.9 Amount of myocardium depolarized by the accessory pathway (gray circle) vs. the AV node (blue circle) depends on the speed of AV conduction, how far laterally the AP originates, and the refractory period of the AP. A PAC is slowly conducted through the AV node, which allows more ventricular mass to be depolarized through the AP. However, a very premature PAC may get blocked across the AP which, although faster than the AV node, has a longer refractory period and is more likely to block its conduction.

      Schematic illustration of a slur is seen on the upslope of the QRS complex (e.g., leads II, III, aVF, V2–V6, as marked by the arrows).

      Figure 12.10 A slur is seen on the upslope of the QRS complex (e.g., leads II, III, aVF, V2–V6, as marked by the arrows). Also, note how the P wave is very close to the QRS complex (almost abuts it). The QRS seems negative in V1 but the initial deflection, i.e., delta wave, is positive. The accessory pathway is left-sided, as delta is positive in V1–V2; it is left lateral, as delta wave is negative (pseudo-Q wave) in aVL.


    • PAC. Delta wave is typically wider during a PAC, and a progressive increase in prematurity of the PAC usually results in a progressive increase in the pre-excitation of the QRS complex. PAC results in prolongation of the conduction time through the AV node (increased AH interval), whereas the AP keeps a constant conduction time; thus, relatively more ventricular muscle gets excited through the AP. However, with a further increase in prematurity, the refractory period of the anomalous pathway is reached, and conduction is achieved through the AV node without any pre-excitation; this actually allows estimation of the refractory period of the AP (Figure 12.9). A similar phenomenon may be seen with progressively faster atrial pacing, wherein AV nodal conduction slows down allowing delta wave to become more prominent, until the AP refractory period is reached.
    • In exertional sinus tachycardia, delta wave may diminish as a result of: (1) increased AV conduction; or (2) long AP refractory period leading to a block of conduction in AP. A consistent lack of delta wave during tachycardia suggests the latter alternative.
    • As opposed to aberrancy, the pre-excitation/delta wave is more likely to manifest after a long R–R interval. If, despite those maneuvers, the only abnormality seen on the ECG is a short PR interval, the patient simply has accelerated AV nodal conduction rather than pre-excitation, i.e., a short AV delay that is within the spectrum of normal AV delays. It was suggested previously that this may be due to an atriofascicular bypass tract, especially if the patient develops SVT (Long–Ganong–Levine syndrome). However, this is very rarely the case.

D. Localization of the accessory pathway according to the baseline ECG


In order to localize the AP, it is key to identify the leads with negative delta waves. Delta is negative in the leads surrounding the origin of the AP, as AP will be pointing away from those leads. Analyze the right-sided lead V1, the inferior leads, and the left lateral leads I and aVL:



  • Lead V1 provides an assessment of right vs. left pathway. A negative delta in lead V1 (QS pattern) implies that AP is pointing away from the right side, and thus the pathway is right-sided. A positive delta wave in lead V1 (R, RS, or RSr’ pattern) implies a left-sided pathway.
  • The inferior leads provide an assessment of anterior vs. inferior pathway. A negative delta in the inferior leads implies an AP that points away from the inferior wall, often a posteroseptal pathway.
  • The lateral leads provide an assessment of left lateral vs. septal or RV pathway. A negative delta wave in the left lateral leads I and aVL often implies a left lateral pathway (Table 12.1).

The same rules apply to localizing the origin of VT. The orientation of QRS is analyzed in those same leads. There is one additional rule in VT: negative QRS concordance in all precordial leads V1–V6 implies an apical origin, a pattern not seen with delta wave or pre-excited SVT.


E. Types of tachyarrhythmias: mechanisms and initiation


1. Concealed accessory pathway (see Figure 12.11 )

The pathway cannot conduct antegradely, and therefore it does not conduct during sinus rhythm; no delta wave is seen. However, partial, concealed penetration of the AP occurs at baseline and puts it in a refractory period, so that retrograde impulses coming from the ventricle cannot get conducted and cannot initiate reentry. This is called concealed conduction into the AP.


The AP has a longer refractory period than the AV node; thus, when a very premature PAC occurs, it cannot penetrate the AP to any degree, allowing the AP to rest. When the electrical activation reaches the ventricle, it can conduct retrogradely through the AP for two reasons: (1) the AP is capable of conducting retrogradely; (2) the AP has had time to rest and recover from the refractory period, since the PAC did not penetrate it at all. This initiates a reentry called orthodromic AVRT. As opposed to AVNRT, in orthodromic AVRT the atria and the ventricles are depolarized sequentially rather than simultaneously and distinct P waves are almost always seen, with a short RP interval <1/2 RR, but not too short (>90 ms). The ventricular rate is ~150–250 bpm.


Also, a PVC can initiate retrograde AP conduction and reentry because it occurs after the sinus-originating ventricular stimulation, at a time when the AP has recovered from the refractory period.


2. Manifest accessory pathway (see Figure 12.12 )

The AP can conduct both antegradely and retrogradely.



  1. The AP is a myocardial structure that conducts faster than the AV node; however, it has a longer refractory period than the AV node. When a very early PAC occurs, orthodromic AVRT may occur (similar mechanism to the concealed AP). PVC can also propagate up the AP and initiate reentry.
  2. It is rare for the PAC to solely conduct down the AP and not the AV node, because the AP usually has a longer refractory period than the AV node. However, the refractory period of the AP is occasionally very short, shorter than the AV node’s refractory period; in this case, the impulse of a PAC can conduct down through the AP then up through the AV node (antidromic AVRT). Since the ventricle is stimulated through a ventricular focus rather than the His bundle, the tachycardia is a wide complex tachycardia that has VT morphology. As opposed to VT, the pre-excited QRS complex cannot be negative in leads V4–V6, as the pre-excitation is usually basal rather than apical

    Table 12.1 Electrocardiographic localization of the AP.






























    V1 II/III/aVF I, aVL
    Left lateral (+) (+) (–)
    Right free wall (–) (±)
    (e.g., + in II, – in III)    		 (+)
    Posteroseptal (near the coronary sinus) (–) with sharp transition to (+) in V2 if right posteroseptal (+) if left posteroseptal (–) (+)
    Anteroseptal (right) (–), isoelectric, or biphasic (+) (+)

    Those rules may apply to localizing the origin of PVC or VT based on the voltage of QRS in those leads. Lead I is more important than aVL in AP localization. Since the AP is basal, i.e., not close to the apex in any form, the QRS cannot be negative in leads V4–V6.

    Schematic illustration of concealed accessory pathway (AP).

    Figure 12.11 Concealed accessory pathway (AP).


    The pathway cannot fully conduct antegradely; thus, it does not conduct during sinus rhythm and no delta wave is seen. Yet, partial penetration of the AP occurs at baseline and puts it in a refractory period, so that retrograde impulses coming from the ventricle get blocked and cannot initiate reentry. This is called concealed conduction into the AP. The AP has a longer refractory period than the AV node; thus, when a very early PAC occurs (right), it cannot penetrate the AP to any degree, allowing the AP to rest. When the electrical activation reaches the ventricle, it can conduct retrogradely through the AP, which has had time to rest and recover from the refractory period, since the PAC did not penetrate it at all. This initiates reentry (orthodromic AVRT).

    Schematic illustration of manifest accessory pathway.

    Figure 12.12 Manifest accessory pathway.


    The AP can conduct both antegradely and retrogradely. The normal sinus impulse conducts through both the AV node and the AP. The conduction over AP leads to delta wave and PR shortening, more evident when relatively more ventricle is stimulated through the AP. The AP conducts faster than the AV node but has a longer refractory period than the AV node. Thus, when a very premature PAC occurs, the PAC conducts solely through the AV node without any delta wave and initiates reentry (orthodromic AVRT). The larger the difference in refractory period between the AV node and the AP, the more likely it is for a PAC to get blocked in the AP and initiate AVRT. Occasionally, the PAC conducts down the AP and leads to antidromic AVRT. AF or atrial flutter may conduct rapidly and antegradely over the accessory pathway.


  3. Pre-excited AF or atrial flutter: in this case, AF or atrial flutter conducts at a high rate from A to V over the accessory pathway (Figure 12.13). This leads to very fast (> 200 bpm), very wide, bizarre-looking QRS complexes, without a typical bundle branch block morphology. By using the SVT/VT differentiation algorithm, pre-excited SVT typically has morphological VT features, yet the irregularity and the variable QRS morphology (variable pre-excitation) point to a pre-excited AF. This is the most dangerous tachycardia associated with the accessory pathway. Sudden death is, fortunately, rare, seen in < 1% of patients with WPW pattern over the course of 10 years.

Patients with WPW are prone to develop AF, possibly because of reentry around the atrial insertion of the AP (prevalence of AF in young patients with WPW ~15–30%). Also, any AVRT can trigger AF and become poorly tolerated.

Schematic illustration of irregular tachycardia with wide, polymorphic, bizarre-looking QRS, with VT rather than SVT features.

Figure 12.13 Irregular tachycardia with wide, polymorphic, bizarre-looking QRS, with VT rather than SVT features (positive QRS concordance in V1–V6, QRS morphology not consistent with RBBB or LBBB). This is a pre-excited AF in a patient with WPW. Note that, as opposed to aberrancy, QRS becomes wider after a longer R–R interval (arrows). AP is likely left posteroseptal (delta wave is negative in the inferior leads).

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Nov 27, 2022 | Posted by in CARDIOLOGY | Comments Off on Atrioventricular Nodal Reentrant Tachycardia, Atrioventricular Reciprocating Tachycardia, Wolff–Parkinson–White Syndrome, and Junctional Rhythms

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