1:1 Tachycardia initiated by a premature ventricular contraction: The curious appeal of the peel

Key Teaching Points.

• •Gap phenomena can occur when the effective refractory period of a distal site is longer than the functional refractory period of a proximal site. It can be observed when an appropriately timed early stimulus propagates with conduction delay through the proximal site, allowing improved conduction at the distal site.
• •Peeling back of refractoriness refers to pre-excitation of proximal tissue by retrograde conduction from a premature ventricular contraction that shortens the absolute refractory period of the His-Purkinje system, allowing conduction of a previously nonconducted supraventricular input.
• •Gap phenomena is not synonymous with excitable gap. The term “excitable gap” is used to describe a window of time when a tissue is excitable before the arrival of the next stimulus in a re-entrant circuit.

Introduction

Stored electrograms (EGMs) retrieved from cardiac implantable devices provide a rich source of diagnostic information. Current algorithms discriminate supraventricular tachycardia (SVT) from ventricular tachycardia (VT) with positive predictive values greater than 90%, based on passive analysis of detected rhythms.¹ However, the incidence of inappropriate therapies for SVT varies from 16% to 31% based on some studies.² Careful analysis of EGMs can elucidate the arrhythmic mechanism to guide appropriate treatment.

Case report

We present a 69-year-old man with a past medical history of hypertension, diabetes mellitus, human immunodeficiency virus, left bundle branch block, heart failure with reduced ejection fraction, and a primary prevention cardiac resynchronization defibrillator who presented to the emergency department for multiple cardiac resynchronization defibrillator shocks. Device interrogation disclosed multiple episodes labeled as VT. Figure 1A displays tachycardia initiation.

Figure 1.

1:1 Tachycardia initiation. A: Supraventricular tachycardia (SVT) at a cycle length of 280–300 ms and biventricular pacing at a rate of ∼560 ms. A premature ventricular contraction starts a 1:1 tachycardia at a cycle length similar to the SVT. The device is demonstrating upper rate behavior, with 2:1 pacing owing to every other atrial beat falling in the post ventricular atrial refractory period, designated (AF) on the marker channel. B: Response to antitachycardia pacing (ATP). The atrial activity is dissociated during ATP. C: Electrogram during native rhythm. Red circles show right ventricle–left ventricle time 33 ms in both SVT and native rhythm. Red arrows show AV interval 170 ms in both SVT and sinus tachycardia.

For reference, all the EGMs shown are displayed in an A-V-Shock configuration, where the first EGM shows the atrial lead recording, the second EGM displays the ventricular lead, and the last EGM shows the shock lead. The response to antitachycardia pacing (ATP) is shown in Figure 1B. The interrogation also demonstrated intact antegrade and retrograde conduction (not pictured). What is the differential diagnosis of the arrhythmia? What is the mechanism of the tachycardia initiation by the premature ventricular contraction (PVC)?

Discussion

Figure 1 depicts an atrial arrhythmia with a cycle length of 280–300 ms with biventricular pacing. The device demonstrates upper rate behavior, with 2:1 pacing owing to every other atrial beat falling in the post ventricular atrial refractory period. After the antitachycardia response duration is fulfilled, the device triggers a mode switch (ATR-Fallback). Notably, the mode switch is not instantaneous but is governed by Fallback Time, nominally 30 seconds. Before the switch to DDI, a single PVC initiates a 1:1 tachycardia, detected as VT.

The differential diagnosis of 1:1 tachycardia includes SVT, VT with 1:1 retrograde conduction, and double tachycardia with simultaneous SVT and VT. The 1:1 tachycardia cycle length is identical to the atrial rate of the atrial arrhythmia during biventricular pacing. Double tachycardia is an unlikely diagnosis, as there is a low probability that a PVC would trigger ventricular tachycardia at the exact cycle length of the atrial arrhythmia. Similarly, the PVC does not perturb the atrial cycle length, nor does the atrial EGM morphology change, making VT with 1:1 retrograde conduction less likely.

In addition to its therapeutic utility in the termination of tachycardia, the response to ATP provides additional diagnostic information that may aid in diagnosing an arrhythmia. ATP is analogous to the fundamental maneuver in the electrophysiology laboratory, ventricular overdrive pacing (VOP) during SVT. Both techniques can document atrial entrainment, postpacing interval, post-VOP response, and transition zone. Both the success and failure to terminate an arrhythmia yield diagnostic information. When properly exploited, VOP can provide the SVT diagnosis in most cases.³

Figure 1B demonstrates that ATP does not terminate the arrhythmia. There is wobble in the atrial rate during ATP, suggesting retrograde penetration but not entrainment, as the atrium is not accelerated to the paced cycle length. Ventriculoatrial dissociation during ATP excludes atrioventricular reentrant tachycardia. AV nodal reentrant tachycardia (AVNRT) with upper or lower common pathway block is a less likely consideration. However, AVNRT with persistent complete VA dissociation is highly unusual.

If the arrhythmia is not VT, then the PVC unexpectedly facilitates 1:1 conduction of SVT. This phenomenon is sometimes dubbed “supernormal conduction.”⁴ The term implies conduction through cardiac tissue that is relatively better than anticipated or conduction that improves despite underlying conduction disease. The definition of supernormal conduction is not well agreed upon and is often filed under Miscellaneous. In some instances, it is used as an umbrella description covering several mechanisms, and other times is used to invoke a specific phenomenon. To avoid confusion, we will avoid this term and focus on 3 potential mechanistic explanations, “gap phenomenon,” “equal bundle branch delay,” and “peeling of refractoriness.”

Gap phenomenon

The “gap phenomenon” can occur when the effective refractory period of a distal site is longer than the functional refractory period of a proximal site.⁵ The gap phenomenon can be observed when an appropriately timed early stimulus propagates with conduction delay through the proximal site, allowing improved conduction at the distal site. Both antegrade and retrograde gap phenomena have been observed. Examples exist between most adjacent conduction tissues, more commonly between the AV node and the His-Purkinje system.

In this example, there is an atrial arrhythmia with biventricular pacing. The antegrade impulses are blocked somewhere along the conduction system. Hypothetically, the PVC, via delayed retrograde concealed conduction over the left bundle branch block and His-Purkinje system (“proximal site”), could promote recovery at the AV node (“distal site”) and thereby facilitate conduction of the antegrade atrial impulses. The gap phenomenon requires the prolongation of a component of the conduction system.⁶ However, the interventricular time is ∼33 ms in both native rhythm and SVT (Figure 1B and 1C), and the shock lead EGM is unchanged during SVT. These findings argue against gap phenomena driven by further delay in the left bundle, where a change in the interventricular time or EGM would be expected. Similarly, the AV interval is ∼170 ms in both native rhythm and SVT. These findings argue against delay at the infranodal level or at the AV node owing to dual AV nodal physiology, where a prolongation of the AV interval would be expected (Figure 1B and 1C).

There are inherent limitations to this interpretation. Without a His bundle catheter, we cannot exclude that there may be balanced changes between the AH and HV intervals, not reflected in the interventricular or AV intervals. Also, the temporal resolution of the intervals detected by implantable cardioverter-defibrillators (ICDs) has limited accuracy in discriminating minute changes.

Equal bundle branch delay

In some instances, bundle branch block is caused by conduction delay rather than complete bundle branch block. Conditions can occur that cause slowing in the contralateral bundle branch, leading to normalization in the QRS owing to balanced conduction delay. The phenomenon has been observed in appropriately timed atrial or ventricular coupling intervals and changes in the conduction of the contralateral bundle branch owing to medical conditions, such as pulmonary embolism.

Figure 2 shows the induction of 1:1 tachycardia by 1 PVC. The post-PVC beat on the shock EGM is narrower than during the tachycardia. The marker channel indicates the PVC originated closer to the left ventricular sensing electrode (sensing vector was left ventricle tip to left ventricle ring) and is ipsilateral to the left bundle. The contralateral bundle may be delayed by early retrograde concealed conduction, leading to equal bundle branch delay and promotion of 1:1 conduction. While this mechanism may explain the narrower post-PVC beat, it does not explain the sustained 1:1 tachycardia while the QRS returns to its baseline wide morphology.

Figure 2.

Initiation of 1:1 supraventricular tachycardia with premature ventricular contraction (PVC). Red arrow shows PVC that initiates 1:1 arrhythmia. The red circle shows the post-PVC beat is narrower than the QRS during that tachycardia. The V-V interval of the PVC is 478 ms to the left ventricle (LV) channel and 518 ms to the right ventricle (RV) channel, suggesting the PVC originated closer to the LV. Electrogram (EGM) shows atrial tachycardia with 2:1 ventricular pacing. The PVC (1) sets up a long-short sequence (green and red lines). The refractory period of His-Purkinje tissue directly related to the cycle length of the preceding R-R interval. The shorted refractory period of His-Purkinje tissue facilitates results in resolution of functional block and facilitates conduction of the next atrial beat (2). This mechanism is termed the “peeling back” effect. Note the relatively narrow shock EGM (red circle), possibly due to transient shortened His-Purkinje refractory period. The next atrial beat (3) conducts with the baseline wide QRS on the shock electrogram. AVN = atrioventricular node; BB = bundle branch; His = His bundle.

Peeling back of refractoriness

A more likely mechanistic explanation is the peeling-back effect. Pre-excitation of proximal tissue by retrograde conduction from a PVC shortens the absolute refractory period of the His-Purkinje system, allowing conduction of a previously nonconducted supraventricular input.⁵ Intact antegrade and retrograde conduction was demonstrated on ICD interrogation. We hypothesize that at the transition from normal sinus rhythm with biventricular pacing to atrial tachycardia with biventricular pacing, functional infranodal block was initiated by a long-short sequence in the His-Purkinje system. Presumably, during the atrial arrhythmia, there is retrograde concealed conduction during ventricular pacing (Figure 3). Because of concealed conduction with partial penetration of the His-Purkinje system during 2:1 ventricular pacing, the long-short sequence is perpetuated, and the functional block continues.

Figure 3.

Initiation of functional block at onset of atrial tachycardia. Electrogram shows interruption of biventricular pacing at onset of atrial ectopy. The first early atrial beat (1) is conducted and sets up a long-short-long sequence (green and red lines). The refractory period of His-Purkinje tissue directly related to the cycle length of the preceding R-R interval. The shorted refractory period of His-Purkinje tissue facilitates conduction of the next atrial beat (2). This relatively longer interval results in a prolongation of the refractory period of His-Purkinje tissue. The third atrial beat (3) is not conducted, likely owing to functional block in the His-Purkinje tissue. The persistence of functional block is caused by both antegrade penetration of the His-Purkinje tissue from atrial tachycardia and repetitive concealed transseptal conduction during 2:1 ventricular pacing. The distal left bundle branch is activated retrogradely late in the QRS complex via right-to-left transseptal conduction. AVN = atrioventricular node; BB = bundle branch; His = His bundle.

The spontaneous PVC, also by retrograde concealed conduction, sets up a long-short sequence and “peels back” the absolute refractory period of the tissue (Figure 2). Since the refractory period of His-Purkinje tissue is directly related to the cycle length of the preceding R-R interval, the shorted refractory period of His-Purkinje tissue results in resolution of functional block and facilitates the conduction of the next atrial beat. Ventricular pacing is first inhibited by the PVC and then by the first conducted beat post-PVC. A 1:1 conduction likely continues after the PVC owing to the resolution of His-Purkinje functional block that was perpetuated by 2:1 pacing during the atrial arrhythmia. Similar sustained improvement in conduction during SVT after PVCs has been reported in 2:1 AVNRT, where the PVC peels back His-Purkinje refractoriness, restoring 1:1 AV conduction during tachycardia.⁷

The moniker inappropriately appropriate or pseudo appropriate is sometimes used in case studies to describe fortuitous events of cardiac devices behaving according to their programming—for instance, when SVT is classified as VT and is terminated by inappropriate ATP. This case represents a species of inappropriately appropriate therapy, where 2:1 pacing upper rate behavior perpetuated functional block, preventing the inappropriate therapies that followed after the resolution of the His-Purkinje functional block by the PVC. The same initiation of 1:1 SVT with a single PVC was repeatedly observed on other stored episodes. In our case, the patient declined an electrophysiologic study and preferred medical therapy.

Conclusion

Unfortunately, despite improvements in ICD programming and discrimination algorithms, inappropriate ICD shocks remain common. The short time frame of a standard electrocardiogram is frequently not long enough to capture examples of transient unusual electrophysiologic phenomena. Electrograms (EGMs) summarize extended events and allow opportunities to observe illustrations of these fundamental principles. Although a His bundle recording is the gold-standard diagnostic tool, combining EGM findings with fundamental electrophysiologic concepts can frequently lead to a correct diagnosis and guide interventions. With the proliferation of conduction system pacing, we expect an updated catalog of thought-provoking EGMS.