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

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

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1098-1102
Number of pages5
JournalJournal of the American College of Cardiology
Volume42
Issue number6
DOIs
StatePublished - Sep 17 2003

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Adenosine A1 Receptor Agonists
Paroxysmal Tachycardia
Supraventricular Tachycardia
Atrioventricular Node
Tachycardia
Hypotension
Adenosine A2 Receptors
Purinergic P1 Receptor Agonists
Blood Pressure
Adenosine A1 Receptors
tecadenoson
Purinergic P1 Receptors
Bronchoconstriction
Electrophysiology
Vasodilation
Adenosine

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Prystowsky, Eric N. ; Niazi, Imran ; Curtis, Anne B. ; Wilber, David J. ; Bahnson, Tristram ; Ellenbogen, Kenneth ; Dhala, Anwer ; Bloomfield, Daniel M. ; Gold, Michael ; Kadish, Alan ; Fogel, Richard I. ; Gonzalez, Mario ; Belardinelli, Luiz ; Shreeniwas, Revati ; Wolff, Andrew A. / Termination of paroxysmal supraventricular tachycardia by tecadenoson (CVT-510), a novel A1-adenosine receptor agonist. In: Journal of the American College of Cardiology. 2003 ; Vol. 42, No. 6. pp. 1098-1102.
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abstract = "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.",
author = "Prystowsky, {Eric N.} and Imran Niazi and Curtis, {Anne B.} and Wilber, {David J.} and Tristram Bahnson and Kenneth Ellenbogen and Anwer Dhala and Bloomfield, {Daniel M.} and Michael Gold and Alan Kadish and Fogel, {Richard I.} and Mario Gonzalez and Luiz Belardinelli and Revati Shreeniwas and Wolff, {Andrew A.}",
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Prystowsky, EN, Niazi, I, Curtis, AB, Wilber, DJ, Bahnson, T, Ellenbogen, K, Dhala, A, Bloomfield, DM, Gold, M, Kadish, A, Fogel, RI, Gonzalez, M, Belardinelli, L, Shreeniwas, R & Wolff, AA 2003, 'Termination of paroxysmal supraventricular tachycardia by tecadenoson (CVT-510), a novel A1-adenosine receptor agonist', Journal of the American College of Cardiology, vol. 42, no. 6, pp. 1098-1102. https://doi.org/10.1016/S0735-1097(03)00987-2

Termination of paroxysmal supraventricular tachycardia by tecadenoson (CVT-510), a novel A1-adenosine receptor agonist. / Prystowsky, Eric N.; Niazi, Imran; Curtis, Anne B.; Wilber, David J.; Bahnson, Tristram; Ellenbogen, Kenneth; Dhala, Anwer; Bloomfield, Daniel M.; Gold, Michael; Kadish, Alan; Fogel, Richard I.; Gonzalez, Mario; Belardinelli, Luiz; Shreeniwas, Revati; Wolff, Andrew A.

In: Journal of the American College of Cardiology, Vol. 42, No. 6, 17.09.2003, p. 1098-1102.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Termination of paroxysmal supraventricular tachycardia by tecadenoson (CVT-510), a novel A1-adenosine receptor agonist

AU - Prystowsky, Eric N.

AU - Niazi, Imran

AU - Curtis, Anne B.

AU - Wilber, David J.

AU - Bahnson, Tristram

AU - Ellenbogen, Kenneth

AU - Dhala, Anwer

AU - Bloomfield, Daniel M.

AU - Gold, Michael

AU - Kadish, Alan

AU - Fogel, Richard I.

AU - Gonzalez, Mario

AU - Belardinelli, Luiz

AU - Shreeniwas, Revati

AU - Wolff, Andrew A.

PY - 2003/9/17

Y1 - 2003/9/17

N2 - 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.

AB - 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.

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