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CLINICAL RESEARCH: ELECTROPHYSIOLOGIC DISORDERS

Termination of paroxysmal supraventricular tachycardia by tecadenoson (CVT-510),a novel A₁-adenosine receptor agonist

Eric N. Prystowsky, MD^*,*, Imran Niazi, MD, Anne B. Curtis, MD, David J. Wilber, MD, Tristram Bahnson, MD^||, Kenneth Ellenbogen, MD^¶, Anwer Dhala, MD^#, Daniel M. Bloomfield, MD^**, Michael Gold, MD, Alan Kadish, MD, Richard I. Fogel, MD^*, Mario D. Gonzalez, MD, Luiz Belardinelli, MD, Revati Shreeniwas, MD and Andrew A. Wolff, MD

^* Care Group, Indianapolis, Indiana, USA
Cardiology Division, St. Luke's Hospital, Milwaukee, Wisconsin, USA
Cardiology Division, University of Florida, Gainesville, Florida, USA
Cardiology Division, Loyola University Medical Center, Chicago, Illinois, USA
^|| Cardiology Division, Duke Medical Center, Durham, North Carolina, USA
^¶ Cardiology Division, Medical College of Virginia, Richmond, Virginia, USA
^# Heart Care Associates, Milwaukee, Wisconsin, USA
^** Cardiology Division, Columbia University, New York, New York, USA
Cardiology Division, University of Maryland, Baltimore, Maryland, USA
Cardiology Division, Northwestern University, Chicago, Illinois, USA
CV Therapeutics, Inc., Palo Alto, California, USA

Manuscript received August 7, 2002; revised manuscript received May 30, 2003, accepted June 13, 2003.

^* Reprint requests and correspondence: Dr. Eric N. Prystowsky, The Care Group, LLC, 8333 Naab Road, Suite 400, Indianapolis, Indiana 46260, USA.
eprystow{at}thecaregroup.com

OBJECTIVES: The aim of this study was to evaluate tecadenoson safety and efficacy during conversion of paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm.

BACKGROUND: Tecadenoson (CVT-510), a novel adenosine receptor (Ado R) agonist, selectively activates the A₁ Ado R and prolongs atrioventricular (AV) nodal conduction at doses lower than those required to cause A₂ Ado R-mediated coronary and peripheral vasodilation. Unlike adenosine, which non-selectively activates all four Ado R subtypes and produces unwanted effects, tecadenoson appears to terminate AV node-dependent supraventricular tachycardias without hypotension and bronchoconstriction.

METHODS: In this open-label, multicenter, dose escalation study, tecadenoson was administered to 37 patients (AV node re-entrant tachycardia, n = 29; AV re-entrant tachycardia, n = 8) with inducible PSVT sustained for 1 min during an electrophysiology study. Seven regimens (0.3 to 15 µg/kg) of up to two identical tecadenoson intravenous bolus doses were administered.

RESULTS: After the first or second bolus, PSVT converted to sustained sinus rhythm for 5 min in 86.5% (32/37) of the patients, with 91% (29/32) of the conversions occurring after the first bolus (most within 30 s), coincident with anterograde conduction block in the AV node. No effects on sinus cycle length (SCL) or systolic blood pressure were observed. The atrial-His (AH), but not the His-ventricular (HV) interval was prolonged up to 5 min after the final tecadenoson bolus, returning to baseline by 10 min. Tecadenoson was generally well tolerated.

CONCLUSIONS: In this study, tecadenoson rapidly terminated sustained PSVT by depressing AV nodal conduction without causing hypotension. After sinus rhythm restoration, there was minimal AH interval prolongation without HV interval or SCL prolongation.

Abbreviations and Acronyms   Ado R   adenosine receptor   AH   atrial-His   AV   atrioventricular   AVNRT   atrioventricular node re-entrant tachycardia   AVRT   atrioventricular re-entrant tachycardia   Cmax   maximum plasma level   HV   His-ventricular   IV   intravenous   PSVT   paroxysmal supraventricular tachycardia   SCL   sinus cycle length   S-H   stimulus-to-His bundle interval   SNRT   sinus node recovery time

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