Adenosine administration terminated 100% of sustained focal annular ventricular and atrial tachycardias, providing evidence for a shared mechanism of intracellular calcium overload.
Observational (n=49)
Do focal annular atrial and ventricular tachycardias share a common mechanism characterized by adenosine sensitivity?
Peri-annular atrial and ventricular tachycardias share a common mechanism of adenosine sensitivity, consistent with intracellular calcium overload and triggered activity.
BACKGROUND: Based on the 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 comprised the study group. All underwent electrophysiological 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 or terminated or both with programmed stimulation in 46 of 46 patients and most (70%) were catecholamine facilitated. Of the 9 patients with sustained annular ventricular tachycardia, 3 were localized to the tricuspid annulus, and 6 to the mitral annulus. All the 9 ventricular tachycardias (100%) terminated with adenosine, 2 of 2 terminated with verapamil, and 2 of 2 terminated with Valsalva. Of the 40 patients with annular atrial tachycardia, 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 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.
Ip et al. (Sun,) conducted a observational in Sustained focal annular tachycardia (n=49). Adenosine administration during electrophysiological evaluation was evaluated on Tachycardia termination in response to adenosine. Adenosine administration terminated 100% of sustained focal annular ventricular and atrial tachycardias, providing evidence for a shared mechanism of intracellular calcium overload.