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Mechanism, diagnosis, and treatment of outflow tract tachycardia

Nature Reviews Cardiology volume 12, pages 597–608 (2015)Cite this article

Subjects

Key Points

  • Outflow tract tachycardia originates from the right or left ventricular outflow tracts and from the region of the tricuspid and mitral valve annuli

  • In most outflow tract tachycardia, a left bundle branch block inferior axis morphology is observed

  • Outflow tract tachycardia is sensitive to adenosine and is characteristically caused by cAMP-mediated triggered activity

  • Definitive therapy is achieved through catheter ablation of the focal site of origin of the arrhythmia

  • The prognosis of outflow tract arrhythmia is favourable, with two uncommon exceptions: cardiomyopathy or polymorphic ventricular tachycardia induced by outflow tract premature ventricular contractions

Abstract

Idiopathic ventricular arrhythmia is a generic term for a spectrum of arrhythmias that occur in the absence of structural heart disease or ion channelopathy. These arrhythmias include monomorphic premature ventricular contractions (PVCs), nonsustained monomorphic ventricular tachycardia (VT), and sustained VT. Most idiopathic ventricular arrhythmias originate from the right and left ventricular outflow tracts and include sites accessed from the aortic sinuses of Valsalva. Outflow tract arrhythmia is identified by an electrocardiographic pattern consistent with a left bundle branch block inferior axis morphology. Characteristically, outflow tract VT is caused by cAMP-mediated triggered activity, and is terminated by administration of adenosine. Outflow tract arrhythmias are focal and, therefore, are readily amenable to definitive treatment with catheter-based radiofrequency ablation. Although arrhythmia might be associated with reversible PVC-mediated cardiomyopathy, and infrequently with PVC-induced polymorphic VT or ventricular fibrillation, prognosis is generally favourable.

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Figure 1: Anatomical relationship between the RVOT and LVOT.
Figure 2: Anatomical relationship between left ventricular myocardial crescents and the aortic sinuses.
Figure 3: Signal transduction for initiation and termination of outflow tract tachycardia owing to cAMP-mediated triggered activity.
Figure 4: Electrocardiographic characteristics of premature ventricular contractions originating from the anterior free wall of the RVOT, posterior RVOT, and para-Hisian region.
Figure 5: Electrocardiographic patterns of premature ventricular contractions originating from the coronary cusps.
Figure 6: Electrocardiographic characteristics of premature ventricular contractions originating from the LV summit and ventricular crux.
Figure 7: Electrocardiographic characteristics of mitral annular premature ventricular contractions.

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  1. Department of Medicine, Division of Cardiology, Cornell University Medical Centre, 525 East 68th Street, Starr 4, New York, 10021, NY, USA

    Bruce B. Lerman

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Lerman, B. Mechanism, diagnosis, and treatment of outflow tract tachycardia. Nat Rev Cardiol 12, 597–608 (2015). https://doi.org/10.1038/nrcardio.2015.121

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