ReviewNoninvasive clues for diagnosing ventricular tachycardia mechanism☆,☆☆
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.
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Ventricular tachycardia as a consequence of triggered activity
2021, American Journal of Emergency MedicineCitation Excerpt :Delayed afterdepolarization is classically associated with outflow tract (OT) tachycardia [2]. The ECG in the case is consistent with a triggered, OT tachycardia, as the tachydysrhythmia starts with a PVC that is similar to the ensuing complexes (as opposed to reentrant VT where the initiating PVC is dissimilar) [3] and there is an inferior axis and left bundle branch block pattern. Baseline echocardiography will also help to distinguish between types of monomorphic VT, as OT tachycardia is the most common in patients without structural heart disease [4,5].
Ventricular Arrhythmias
2019, Medical Clinics of North AmericaCitation Excerpt :If the chain is broken, the tachycardia terminates. Repetitive MMVT is the pathognomonic form of a triggered mechanism (see Fig. 1B).7 Accelerated idioventricular rhythm is the pathognomonic form of an abnormal automatic mechanism.
Genetically Determined Serum Calcium Levels and Markers of Ventricular Repolarization: A Mendelian Randomization Study in the UK Biobank
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2018, Revue Medicale de Liege
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Funded in part by The Richard T. and Angela Clark Innovation Fund in Cardiac Electrophysiology.
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Disclosures: None.