Therapy Efficacy Antitachycardia Pacing

In addition to terminating rhythms by high-voltage shocks, ICDs are also capable of terminating tachyarrhythmias by pacing-strength stimulation. Antitachycardia pacing (ATP) works through the extinguishing of reentrant activity by overdrive pacing. By pacing faster than the tachycardia rate, the activations driven from the pacing site capture increasing areas of the ventricles. If the reentrant circuit is entered by paced activations and is driven to an unsustainable rate, the resulting conduction block terminates the tachycardia.41 However, ATP is ineffective for polymorphic tachycardias and fibrillation.42 ATP therapy can be applied using many different algorithmic methods that set the timing of each pacing pulse.43'44 ICD diagnostics have played a vital role in understanding the different aspects of ATP therapy and in broadening its application.

Specialized pacemakers, not ICDs, were the first devices to apply automatic ATP.45 However, like shock therapies, ATP has a number of possible failure modes. It can fail to terminate the tachyarrhythmia or only slow the tachycardia rate. ATP can also accelerate the rhythm to a faster tachycardia or fibrillation (see Fig. 5 for an example). Acceleration failures resulting in lethal rhythms indicated that shock backup was needed for automatic ATP devices. Thus, ATP for ventricular tachyarrhythmias is now exclusively delivered by ICDs.

The efficacy of ATP for monomorphic ventricular tachycardia (MVT), the predominant rhythm treated by ICDs, is the same as low-energy cardioversion.46 In recent large studies, ATP efficacy for MVT was approximately 90%.35'47 The rate of ATP failures that result in acceleration of the rhythm is related to ATP aggressiveness, the amount by which the tachycardia is overdriven.44 In studies using predominantly burst pacing (single-cycle length stimulation trains) at 88% of the tachycardia cycle length, acceleration ranged from 2 to 3% of treated episodes.

The initial ICD trials proved ATP was a reliable therapy option and established that ATP success in the laboratory setting carried over to the ambulatory setting.48 Many of the major events that drove increased ATP utilization would not have been possible without ICD diagnostic data. The first major expansion in ATP use was triggered by findings that ATP efficacy was not completely predicted by induced tachycardia efficacy. A patient could benefit from ATP without having demonstrated successful ATP in the laboratory. This also meant that tailoring ATP parameters based on laboratory testing was not required, and empirically programmed parameters were sufficient.49 Another limitation of laboratory studies of ATP was demonstrated by the discovery that ATP efficacy for spontaneous MVT exceeds the efficacy for induced MVT in the laboratory.50'51 A partial explanation for these findings came from examination of ICD electrograms of both induced and spontaneous episodes. It was found that the MVT induced in the laboratory for a patient was often different from the tachycardia EGM morphology of the ambulatory episodes (see examples in Fig. 6).52

The large proportion of rapid MVT (> 200 bpm) observed in ICD diagnostics, coupled with the efficacy of empirically programmed ATP, motivated an investigation of the application of ATP for rapid MVT.42 Prior programming strategies reflected concerns that syncope

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Figure 5: Antitachycardia pacing (ATP) accelerates a fast ventricular tachycardia (VT) to ventricular fibrillation (VF). The top signal is the shock coil to the implantable cardioverter-defibrillator (ICD) can electrogram (EGM). The second signal is the Vtip-Vring EGM. Marker annotations of "TP" indicate ATP pulses, the rest below the marker line are intrinsic ventricular events. The atrial intervals measured from an atrial lead bipole (waveform not shown) are all due to intrinsic events and are shown above the marker line. The pacing train prior to acceleration ("TP" markers) consists of eight pulses at 88% of the average VT cycle length

Figure 5: Antitachycardia pacing (ATP) accelerates a fast ventricular tachycardia (VT) to ventricular fibrillation (VF). The top signal is the shock coil to the implantable cardioverter-defibrillator (ICD) can electrogram (EGM). The second signal is the Vtip-Vring EGM. Marker annotations of "TP" indicate ATP pulses, the rest below the marker line are intrinsic ventricular events. The atrial intervals measured from an atrial lead bipole (waveform not shown) are all due to intrinsic events and are shown above the marker line. The pacing train prior to acceleration ("TP" markers) consists of eight pulses at 88% of the average VT cycle length c-l

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