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Action of ATP on ventricular automaticity
G Stark1, H Domanowits, F Sterz
1Department of Internal Medicine, Karl-Franzens-University, Graz, Austria.
Journal of Cardiovascular Pharmacology
|November 1, 1994
Summary
Adenosine triphosphate (ATP) effectively treats supraventricular tachycardia by temporarily suppressing ventricular automaticity. This effect is short-lived, with rapid recovery of heart function due to ATP's short half-life.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Adenosine triphosphate (ATP) is a known treatment for supraventricular tachycardia involving the atrioventricular node.
- Lower pacemakers in the hierarchy are more sensitive to adenosine, prompting investigation into ATP's effects on ventricular automaticity.
Purpose of the Study:
- To investigate the effects of ATP on ventricular automaticity in both in vivo and in vitro models.
- To assess the efficacy and safety of varying ATP doses in terminating tachycardias.
Main Methods:
- Administered sequential intravenous boluses of 6, 12, and 18 mg ATP to 46 patients with wide and narrow QRS complex tachycardia.
- Utilized isolated spontaneously beating guinea pig hearts perfused with 100 microM ATP to evaluate ventricular automaticity suppression and recovery.
Main Results:
- ATP successfully terminated tachycardias in 67% of patients.
- Intravenous ATP bolus induced transient asystole (<= 6.4 seconds) that was self-limiting.
- In vitro, ATP completely suppressed ventricular automaticity, with recovery of ventricular beats and sinus node activity within seconds after discontinuation.
Conclusions:
- ATP is effective in terminating supraventricular tachycardias.
- ATP causes transient, self-limited asystole and suppresses ventricular automaticity.
- Rapid recovery of cardiac function post-ATP administration is attributed to its short half-life.