Elsevier

Journal of Electrocardiology

Volume 51, Issue 2, March–April 2018, Pages 163-169
Journal of Electrocardiology

Review
Noninvasive clues for diagnosing ventricular tachycardia mechanism,☆☆

https://doi.org/10.1016/j.jelectrocard.2017.11.009Get rights and content

Highlights

  • The electrophysiologic mechanism of ventricular tachycardia (VT) are enhanced automaticity, triggered activity and reentry.

  • Understanding the VT mechanism is relevant for the prognosis, pharmacological therapy and ablation strategy.

  • We review clues from the history, 12-lead ECG, monitoring and response to pharmacologic agents, to predict the VT mechanism.

Abstract

The electrophysiologic mechanisms responsible for the initiation and maintenance of ventricular tachycardia (VT) include enhanced automaticity, triggered activity and reentry. Differentiating between these three mechanisms can be challenging for the clinician and usually requires an invasive electrophysiology study. Establishing the underlying VT mechanism in a particular patient is helpful to define the optimal therapeutic approach, including the selection of pharmacologic agents or delineation of an ablation strategy. The purpose of this review is to provide insight into the possible VT mechanisms based on noninvasive clues from the clinical history, 12-lead electrocardiogram, tachycardia onset and termination and the response to pharmacologic manipulation.

Introduction

The electrophysiologic mechanisms responsible for ventricular tachycardia (VT) fall in one of 3 categories: [1] abnormal automaticity; [2] triggered activity; and [3] reentry [1]. (See Tables 1 and 2.)

Understanding the cellular mechanism of VT in a particular patient is relevant for the prognosis, pharmacological management and also to define the optimal mapping and ablation strategies. Most focal VTs, due to a triggered or automatic mechanism, are amenable to betablockade therapy. In contrast, reentrant VTs usually require membrane active antiarrhythmic agents that slow conduction or prolong refractoriness to prevent reentry. In focal VTs the 12-lead electrocardiogram (ECG) provides a powerful tool for localizing the focal origin and the target for ablative therapy. In reentrant VTs the 12-lead ECG may only identify an exit for a larger macro-reentrant circuit. Activation mapping to define the site of earliest ventricular activation is the mainstay for mapping of focal VTs, typically complemented with pacemapping. On the other side, macro-reentrant VTs are better mapped with a combination of voltage mapping to delineate the arrhythmogenic substrate and entrainment maneuvers to define the critical components of the circuit. Focal VTs can be ablated with a single ablation lesion, whereas macro-reentrant VTs require linear lesions between unexcitable boundaries aimed at interrupting the width of the reentrant circuit.

Correct identification of the mechanism can be difficult in clinical practice and the 12-lead ECG by itself is limited for this purpose [2]. In this article we review some noninvasive clues from the clinical history, 12-lead ECG, telemetry monitoring or response to pharmacologic agents that may help the clinician to recognize the potential VT mechanism.

Section snippets

Abnormal automaticity

Automaticity is the property of cardiac cells to generate spontaneous action potentials and is the result of diastolic depolarization caused by a net inward current during phase 4 of the action potential [3]. Normal automaticity is a property of the sinoatrial and atrioventricular nodes and depends mainly on 2 phenomena: [1] diastolic activation of If (funny current), a mixed Na-K inward current, which unlike most voltage-sensitive currents, is activated by hyperpolarization rather than

Conclusion

Identifying the electrophysiologic mechanism of VT is important to define a therapeutic strategy. Although this is challenging without an invasive electrophysiology study, several elements from the clinical history, 12-lead ECG in sinus rhythm or during tachycardia and analysis of Holter recordings and/or device electrograms, may provide insight about the most likely mechanism. Adenosine, due to its mechanism-specific effect is a valuable tool for the diagnosis of VT due to triggered activity.

References (29)

  • R. Li et al.

    Adrenergic signaling and cardiac ion channels

  • J. Hai et al.

    Mechanisms of ventricular tachycardia: impact for successful mapping and ablation

  • W. Grimm

    Accelerated idioventricular rhythm

    Card Electrophysiol Rev

    (2001)
  • Y.T. Tai et al.

    Incessant automatic ventricular tachycardia complicating acute coxsackie B myocarditis

    Cardiology

    (1992)
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    Funded in part by The Richard T. and Angela Clark Innovation Fund in Cardiac Electrophysiology.

    ☆☆

    Disclosures: None.

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