Goldilocks Principle for Antitachycardia Pacing Therapy

Michelle White
Oct 6, 2019 · 6 min read

In a previous post of mine I briefly mentioned the different basic algorithms for antitachycardia pacing (ATP) therapy. In this post I would like to delve deeper into other parameters of ATP therapy besides algorithm. More specifically, I want to talk about the cycle length at which ATP is delivered. ATP can be either too slow or too fast; it can even be TOO too fast. Here I’ll go into the details of what happens when ATP is set to different cycle lengths, but first let’s review the basic ATP algorithms.

Basic Antitachycardia Pacing

Basic ATP comes in 3 different flavors: burst, scan, and ramp.

Burst ATP has a constant, predetermined cycle length for each train that is sent. Multiple trains can be sent before tachycardia is terminated. A train is just a fixed number of impulses sent within quick succession of one another. There are two types of burst pacing: asynchronous and rate-adaptive.

Asynchronous burst pacing sends trains at the same cycle length no matter what. With rate-adaptive burst pacing, the train cycle length changes according to changes in the tachycardia cycle length. Trains are delivered at a certain percentage of the detected tachycardia cycle length — usually no shorter than 88% in order to avoid acceleration or degeneration into fibrillation. I will talk about acceleration and fibrillation in more detail later.

Scan ATP is similar to rate-adaptive burst ATP in that the cycle length changes between trains. However, with scan ATP those changes are preprogrammed and will happen regardless of the tachycardia cycle length.

Ramp ATP, on the other hand, sees changes in cycle length within the train. A crude diagram, courtesy of the author, is provided below.

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Drawing of the different types of basic ATP sequences. VTCL stands for ventricular tachycardia cycle length.

ATP That is Too Fast

ATP can be delivered at cycle lengths that are too short to be effective for terminating tachycardia. When ATP is too fast, it can cause tachycardia to accelerate or degenerate into fibrillation. There are three main mechanisms behind tachycardia acceleration: double-wave reentry, functional reentry, or transition to a faster anatomical pathway.

If tachycardia accelerates or degenerates into fibrillation, then it becomes more dangerous. It makes it harder for the heart to function properly and becomes harder to terminate with ATP.

Double-wave reentry occurs when two impulses circulate through the same circuit. These impulses must be circulating in the same direction, otherwise they would crash head-on and reentry would not persist. In order for double-wave reentry to occur, the circuit must have a large excitable gap. If the excitable gap is large enough then two premature impulses can penetrate the circuit and create two independently-circulating wave fronts. An anatomical circuit is defined as a reentrant circuit whose core is an anatomical obstacle, usually scar tissue.

One might think that double-wave reentry would result in a tachycardia that is twice as fast as single-wave reentry. This is not the case, however. In experiments by Brugada et al. it was shown that, on average, the cycle length of double-wave reentry was approximately 56% of the cycle length of single-wave reentry.

Functional reentry it reentry without an anatomical obstacle. Instead, an impulse anchors to a microheterogeneity in the myocardium and revolves around and around, using the microheterogeneity as its pivot point/axis. Such functional obstacles can be visualized as points in 2D scenarios and as filaments in 3D scenarios.

Functional reentry is much faster than anatomical reentry because functional circuits are smaller than anatomical circuits. The less tissue an impulse has to travel through, the shorter its rotational period around the circuit. Functional circuits are smaller because they are anchored to microscopic obstacles as opposed to macroscopic scar tissue.

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Examples of microheterogeneities. A: myocyte-free regions; B: mechanical damage from forceps; C: areas of higher density; D: clusters of damaged cells; E: areas of lesser/uneven density.

Photo credits:

Agladze, K., Kay, M. W., Krinsky, V., & Sarvazyan, N. (2007). Interaction between spiral and paced waves in cardiac tissue. American Journal of Physiology-Heart and Circulatory Physiology, 293(1), H503-H513.

Functional circuits can come about when anatomical circuits are disturbed in some way. For example, if ATP is delivered too quickly to an anatomical circuit then it could usurp the circuit’s rhythm. Then, outgoing wave fronts can pin to microheterogeneities and functional reentry will occur. If there are many heterogeneities, fibrillation will result from the many functional circuits crashing into each other. Fibrillation is characterized by chaotic electrical patterns.

If there is a lot of scar tissue present in the myocardium, then reentrant circuits can transition from obstacle to obstacle. If an impulse moves to a new circuit with greater conduction velocity, then tachycardia will accelerate.

When a premature impulse encounters an already-existing circuit, then it can terminate that circuit. However, if there’s another obstacle nearby, that premature impulse can simultaneously terminate the existing circuit AND initiate a new circuit around the other obstacle. This is how reentry can transition among obstacles. This is also the underlying concept for figure 8 reentry involving two obstacles.

Brugada, J., Brugada, P., Boersma, L., Mont, L., Kirchhof, C., Wellens, H. J., & Allessie, M. A. (1991). On the mechanisms of ventricular tachycardia acceleration during programmed electrical stimulation. Circulation, 83(5), 1621–1629.

Sometimes, ATP can be so fast that it doesn’t even accelerate tachycardia. In fact, it will never even reach the reentrant circuit at all. When the cycle length of ATP is less than the refractory period of the tissue it’s delivered to, then ATP will block itself.

ATP That is Too Slow

ATP can also be so slow that it’s ineffective for terminating tachycardia. Without a full electrophysiology (EP) study, the precise location of a reentrant circuit cannot be determined. There may even be several reentrant circuits within a single chamber. Because of this, the electrodes that deliver ATP impulses from implantable devices are usually never placed directly on the circuit. ATP must therefore travel through some intervening tissue before reaching the circuit.

The purpose of the ATP train is to break that intervening tissue barrier. If a reentrant circuit is sending out impulses at a certain rate, then the ATP train must be sent at a slightly faster rate. This is because each outgoing tachy impulse must be terminated by an incoming ATP impulse. Also, each incoming impulse needs to get a bit closer to the circuit than the previous one. This is precisely why ATP is set at a fraction of the tachycardia cycle length, usually around 88%.

Kaiser et al. sought to mathematically determine the number of train impulses needed to reach a reentrant circuit in the paper cited below.

Kaiser, D. W., Hsia, H. H., Dubin, A. M., Liem, L. B., Viswanathan, M. N., Zei, P. C., … & Turakhia, M. P. (2016). The precise timing of tachycardia entrainment is determined by the postpacing interval, the tachycardia cycle length, and the pacing rate: theoretical insights and practical applications. Heart rhythm, 13(3), 695–703.

So, if the ATP cycle length is too large then it will never reach the reentrant circuit and therefore be unable to terminate the tachycardia from its source. ATP therapy thus exhibits the Goldilocks Principle in that it cannot be too fast nor too slow. The margins for the most effective ATP cycle length are currently studied empirically, but perhaps we can figure out away to determine these margins with our computer models.

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