The adenosine triphosphate test: a bedside diagnostic tool for identifying the mechanism of supraventricular tachycardia in patients with palpitations
Sami Viskin, MD*,
Roman Fish, MD*,
Aharon Glick, MD*,
Michael Glikson, MD, FACC ,
Michael Eldar, MD, FACC and
Bernard Belhassen, MD, FACC*
* Departments of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel
Sheba Medical Center, and the Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel

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Figure 1 (A) Positive adenosine triphosphate (ATP) test demonstrating dual atrioventricular (AV) node physiology in a 22-year-old male with palpitations. The PR and PP intervals are shown in ms. Following injection of ATP, there is gradual acceleration of sinus rate and sudden increment of the PR interval from 160 to 340 ms (arrow). This "PR jump" of 180 ms probably denotes ATP-induced blockade of fast AV nodal conduction with exposure of the slow AV nodal pathway. Moreover, an AV nodal echo (*) is assumed to be present because of the sinus node resetting following the PR jump (the PP interval suddenly increases from 520 to 1,000 ms). This patient had inducible AV nodal re-entry tachycardia. (B) Positive ATP test unmasking a concealed accessory pathway in a 16-year-old male with palpitations. Note the AV re-entry echo beats (arrow heads), which were of identical morphology to the retrograde P waves observed during the atrioventricular re-entry tachycardia that was eventually induced during the electrophysiologic study. (C) ATP test in a 52-year-old male with a 20-year history of episodic palpitations. This ATP test was considered negative, according to our prospectively defined criteria, because II° degree AV block (*) occurred without evidence of dual AV node physiology or a concealed accessory pathway. Interestingly, a few seconds after the onset of paroxysmal AV block, an atrial tachycardia (atrial rate 220 beats/min) ensued (small arrows). Provocation of nonsustained atrial tachycardia by ATP was reproducible. During the electrophysiologic study, this patient spontaneously developed an atrial tachycardia (with identical P-wave morphology) that was ablated in the left atrium.
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