Unifying Mechanism of Sustained Idiopathic Atrial and Ventricular Annular Tachycardia
Background—Based on current understanding of cardiac conduction system development and the observation that arrhythmogenic foci can originate in areas near the atrioventricular annuli, we hypothesized that focal annular tachycardias, whether atrial or ventricular, share a common mechanism. We therefore prospectively evaluated this hypothesis in patients with sustained atrial and ventricular tachycardia originating from the peri-tricuspid and mitral annuli.
Methods and Results—Forty-nine consecutive patients with sustained, focal annular tachycardia comprise the study group. All underwent electrophysiologic evaluation and the mode of tachycardia initiation, termination, sensitivity to catecholamine infusion and response to adenosine/verapamil were evaluated. Electroanatomical activation maps identified the sites of arrhythmia origin. Tachycardias could be initiated and/or terminated with programmed stimulation in 46/46 patients and most (70%) were catecholamine facilitated. Of the 9 patients with sustained annular VT, 3 were localized to the tricuspid annulus, and 6 to the mitral annulus. All 9 VTs (100%) terminated with adenosine, 2/2 terminated with verapamil, and 2/2 terminated with Valsalva. Of the 40 patients with annular AT, 4 tachycardias were localized to the mitral annulus and 37 to the tricuspid annulus (including 9 para-Hisian), and all were adenosine-sensitive.
Conclusions—Peri-annular atrial and ventricular tissue correspond to a region enriched with arrhythmogenic foci, which may reflect to a common developmental origin. Furthermore, the sensitivity of these tachycardias to adenosine provides evidence for a shared arrhythmia mechanism, consistent with intracellular calcium overload and triggered activity.
- Received December 20, 2013.
- Revision received March 6, 2014.
- Accepted April 11, 2014.